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1.
Int. j. morphol ; 41(2): 625-633, abr. 2023. ilus, tab
Article in English | LILACS | ID: biblio-1440306

ABSTRACT

SUMMARY: One of the reasons for acute kidney damage is renal ischemia. Nevertheless, there are limited protective and therapeutic approaches for this problem. Diacerein is an anti-inflammatory drug characterized by numerous biological activities. We aimed to determine the ameliorative impact of diacerein on renal ischemia/reperfusion injury (I/R) condition, exploring the underlying mechanisms. Twenty-four male rats were allotted into four groups (n= 6): sham group; Diacerein (DIA) group; I/R group, in which a non-crushing clamp occluded the left renal pedicle for 45 min, and the right kidney was nephrectomized for 5 min before the reperfusion process; I/R + diacerein group, injected intraperitoneally with 50 mg diacerein/kg i.m 30 minutes prior to I/R operation. Ischemia/ reperfusion was found to affect renal function and induce histopathological alterations. The flow cytometry analysis demonstrated an elevated expression of innate and mature dendritic cells in I/R renal tissues. Moreover, upregulation in the expression of the inflammatory genes (TLR4, Myd88, and NLRP3), and overexpression of the pro-inflammatory cytokines (IL-1β), apoptotic (caspase-3) and pyroptotic (caspase-1) markers were observed in I/R-experienced animals. The aforementioned deteriorations were mitigated by pre-I/R diacerein treatment. Diacerein alleviated I/R-induced inflammation and apoptosis. Thus, it could be a promising protective agent against I/R.


La isquemia renal es una de los motivos del daño renal agudo. Sin embargo, los enfoques protectores y terapéuticos para este problema son limitados. La diacereína es un fármaco antiinflamatorio caracterizado por numerosas actividades biológicas. Nuestro objetivo fue determinar el impacto de mejora de la diacereína en la condición de lesión por isquemia/ reperfusión renal (I/R), explorando los mecanismos subyacentes. Veinticuatro ratas macho se distribuyeron en cuatro grupos (n= 6): grupo simulado; grupo de diacereína (DIA); grupo I/R, en el que una pinza no aplastante ocluyó el pedículo renal izquierdo durante 45 min, y el riñón derecho fue nefrectomizado durante 5 min antes del proceso de reperfusión; Grupo I/R + diacereína, inyectado por vía intraperitoneal con 50 mg de diacereína/kg i.m. 30 min antes de la operación I/R. Se encontró que la isquemia/ reperfusión afecta la función renal e induce alteraciones histopatológicas. El análisis de citometría de flujo demostró una expresión elevada de células dendríticas innatas y maduras en tejidos renales I/R. Además, se observó una regulación positiva en la expresión de los genes inflamatorios (TLR4, Myd88 y NLRP3) y una sobreexpresión de las citoquinas proinflamatorias (IL-1β), marcadores apoptóticos (caspasa-3) y piroptóticos (caspasa-1) en animales con experiencia en I/R. Los deterioros antes mencionados fueron mitigados por el tratamiento previo a la diacereína I/R. La diacereína alivió la inflamación y la apoptosis inducidas por I/R. Por lo tanto, podría ser un agente protector prometedor contra I/R.


Subject(s)
Animals , Rats , Reperfusion Injury/drug therapy , Anthraquinones/administration & dosage , Kidney Diseases/drug therapy , Anti-Inflammatory Agents/administration & dosage , Dendritic Cells/drug effects , Reperfusion Injury/immunology , Signal Transduction , NF-kappa B/metabolism , Anthraquinones/immunology , Apoptosis/drug effects , Oxidative Stress , Toll-Like Receptor 4/metabolism , Interleukin-1beta/metabolism , Flow Cytometry , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , Inflammation , Injections, Intraperitoneal , Kidney Diseases/immunology
2.
Article in English | WPRIM | ID: wpr-971675

ABSTRACT

10,11-Dehydrocurvularin (DCV) is a natural-product macrolide that has been shown to exert anti-inflammatory activity. However, the underlying mechanism of its anti-inflammatory activity remains poorly understood. Aberrant activation of the NLRP3 inflammasome is involved in diverse inflammation-related diseases, which should be controlled. The results showed that DCV specifically inhibited the activation of the NLRP3 inflammasome in association with reduced IL-1β secretion and caspase-1 activation, without effect on the NLRC4 and AIM2 inflammasomes. Furthermore, DCV disturbed the interaction between NEK7 and NLRP3, resulting in the inhibition of NLRP3 inflammasome activation. The C=C double bond of DCV was required for the NLRP3 inflammasome inhibition induced by DCV. Importantly, DCV ameliorated inflammation in vivo through inhibiting the NLRP3 inflammasome. Taken together, our study reveals a novel mechanism by which DCV suppresses inflammation, which indicates the potential role of DCV in NLRP3 inflammasome-driven inflammatory disorders.


Subject(s)
Animals , Mice , Inflammasomes , NLR Family, Pyrin Domain-Containing 3 Protein/genetics , Inflammation/drug therapy , Anti-Inflammatory Agents/pharmacology , Interleukin-1beta/genetics , Mice, Inbred C57BL
3.
Article in Chinese | WPRIM | ID: wpr-969969

ABSTRACT

OBJECTIVE@#To observe the effects of moxibustion at "Baihui" (GV 20) and "Dazhui" (GV 14) at different time points on the serum level of β-endorphin (β-EP), substance P (SP) and expression of interleukin-1β (IL-1β) and cyclooxygenase-2 (COX-2) protein in brainstem in rats with migraine, and to explore the effect and mechanism of moxibustion in preventing and treating migraine.@*METHODS@#Forty male SD rats were randomly divided into a blank group, a model group, a prevention+treatment (PT) group and a treatment group, 10 rats in each group. Except the blank group, the rats in the remaining groups were injected with nitroglycerin subcutaneously to prepare migraine model. The rats in the PT group were treated with moxibustion 7 days before modeling (once a day) and 30 min after modeling, while the rats in the treatment group were treated with moxibustion 30 min after modeling. The "Baihui" (GV 20) and "Dazhui" (GV 14) were taken for 30 minutes each time. The behavioral scores in each group were observed before and after modeling. After intervention, ELISA method was used to detect the serum level of β-EP and SP; the immunohistochemistry method was used to detect the number of positive cells of IL-1β in brainstem; the Western blot method was used to detect the expression of COX-2 protein in brainstem.@*RESULTS@#Compared with the blank group, the behavioral scores in the model group were increased 0-30 min, 60-90 min and 90-120 min after modeling (P<0.01); compared with the model group, in the treatment group and the PT group, the behavioral scores were decreased 60-90 min and 90-120 min after modeling (P<0.01). Compared with the blank group, in the model group, the serum level of β-EP was decreased (P<0.01), while the serum level of SP, the number of positive cells of IL-1β in brainstem and the expression of COX-2 protein were increased (P<0.01). Compared with the model group, in the PT group and and the treatment group, the serum level of β-EP was increased (P<0.01), while the serum level of SP, the number of positive cells of IL-1β and the expression of COX-2 protein in brainstem were decreased (P<0.01, P<0.05). Compared with the treatment group, in the PT group, the serum level of β-EP was increased and COX-2 protein expression was decreased (P<0.05).@*CONCLUSION@#Moxibustion could effectively relieve migraine. The mechanism may be related to reduce the serum level of SP, IL-1β and COX-2 protein expression in brainstem, and increase the serum level of β-EP, and the optimal effect is observed in the PT group.


Subject(s)
Rats , Male , Animals , Moxibustion , Rats, Sprague-Dawley , Cyclooxygenase 2 , beta-Endorphin , Substance P , Interleukin-1beta , Migraine Disorders , Brain Stem
4.
Article in English | WPRIM | ID: wpr-971327

ABSTRACT

OBJECTIVE@#To investigate the effect of electroacupuncture (EA) at Neiguan (PC 6) on myocardial fibrosis in spontaneously hypertensive rats (SHRs), and to explore the contribution of interleukin-1 β (IL-1 β), insulin-like growth factor 1 (IGF-1), and transforming growth factor β 1 (TGF- β 1) to the effects.@*METHODS@#Nine 12-weeks-old Wistar Kyoto (WKY) male rats were employed as the normal group. Twenty-seven SHRs were equally randomized into SHR, SHR+EA, and SHR + sham groups. EA was applied at bilateral PC 6 once a day 30 min per day in 8 consecutive weeks. After 8-weeks EA treatment at PC 6, histopathologic changes of collagen type I (Col I), collagen type 1 (Col 1) and the levels of IGF-1, 1L-1 β, TGF- β 1, matrix metalloproteinase (MMP)-2 and MMP-9 were examined in myocardial tissure respectively.@*RESULTS@#After 8-weeks EA treatment at PC 6, the enhanced myocardial fibrosis in SHRs were characterized by the increased mean fluorescence intensity of Col I and Col 1 in myocardium tissue (P<0.01). All these abnormal alterations above in SHR + EA group was significantly lower compared with the SHR group (P<0.01). Meanwhile, the increased levels of IL-1 β, IGF-1, TGF-β 1 in serum or myocardial tissue of SHRs, diminished MMP 9 mRNA expression in SHRs were also markedly inhibited after 8 weeks of EA treatment (P<0.05 or P<0.01). Furthermore, the contents of IL-1 β, IGF-1, TGF-β 1 in myocardial tissue were positively correlated with the systolic blood pressure and hydroxyproline respectively (P<0.01).@*CONCLUSION@#EA at bilateral PC 6 could ameliorate cardiac fibrosis in SHRs, which might be mediated by regulation of 1L-1 β/IGF-1-TGF- β 1-MMP9 pathway.


Subject(s)
Rats , Animals , Male , Rats, Inbred WKY , Electroacupuncture , Hypertension/therapy , Insulin-Like Growth Factor I , Interleukin-1beta , Rats, Inbred SHR , Essential Hypertension , Myocardium/pathology , Collagen Type I , Fibrosis
5.
Article in Chinese | WPRIM | ID: wpr-981385

ABSTRACT

This study aims to explore the effect of "Trichosanthis Fructus-Allii Macrostemonis" combination(GX) on the activation of NOD-, LRR-, and pyrin domain-containing protein 3(NLRP3) inflammasome, the release of inflammatory cytokines, and the level of autophagy in RAW264.7 macrophage damaged by lipopolysaccharide(LPS), and the mechanism of GX against inflammatory response in macrophages. To be specific, LPS was used to induce the injury of RAW264.7 cells. Cell Counting Kit-8(CCK-8) assay was employed to measure the survival rate of cells, and Western blot to detect the protein expression of NLRP3, apoptosis-associated speck-like protein(ASC), cysteine-aspartic acid protease(caspase)-1, interleukin(IL)-18, IL-1β, microtubule-associated protein light chain 3(LC3)-Ⅱ, and selective autophagy junction protein p62/sequestosome 1 in RAW264.7 macrophages. ELISA was used to measure the levels of IL-18 and IL-1β in RAW264.7 cells. Transmission electron microscopy was applied to observe the number of autophagosomes in RAW264.7 cells. Immunofulourescence staining was used to detect the expression of LC3-Ⅱ and p62 in RAW264.7 cells. The result showed that GX significantly reduced the protein expression of NLRP3, ASC, and caspase-1 in RAW264.7 cells, significantly increased the protein expression of LC3Ⅱ, decreased the expression of p62, significantly inhibited the secretion of IL-18 and IL-1β, significantly increased the number of autophagosomes, significantly enhanced the immunofluorescence of LC3Ⅱ, and reduced the immunofluorescence of p62. Furthermore, 3-methyladenine(3-MA) could reverse the inhibitory effect of GX on NLRP3, ASC, and caspase-1 and reduce the release of IL-18 and IL-1β. In summary, GX can increase of the autophagy activity of RAW264.7 and inhibit the activation of NLRP3 inflammasome, thereby reducing the release of inflammatory cytokines and suppressing inflammatory response in macrophages.


Subject(s)
Inflammasomes/metabolism , NLR Family, Pyrin Domain-Containing 3 Protein/metabolism , Interleukin-18/metabolism , Lipopolysaccharides/pharmacology , Macrophages , Cytokines/metabolism , Caspase 1/metabolism , Autophagy , Interleukin-1beta/metabolism
6.
Araçatuba; s.n; 2023. 82 p. ilus, tab.
Thesis in English | LILACS, BBO | ID: biblio-1510540

ABSTRACT

A infecção endodôntica ocorre a após contaminação do tecido pulpar levando à uma colonização bacteriana dos canais radiculares resultando em uma resposta inflamatória dos tecidos periapicais e formação de uma lesão periapical, a periodontite apical (PA). O tabagismo, por sua vez, tem impactos prejudiciais à saúde oral e sistêmica sendo considerado um importante fator de risco para as doenças periodontais. Este trabalho tem por finalidade investigar a influência do tabagismo no desenvolvimento da periodontite apical em ratos. Trinta e dois ratos machos Wistar foram divididos em 4 grupos experimentais (n=8): Controle (sem periodontite apical induzida e sem inalação da fumaça do cigarro); FU (com inalação a fumaça do cigarro); PA (com periodontite apical induzida); FU+PA (com inalação a fumaça do cigarro e periodontite apical induzida). Para a inalar a fumaça do cigarro, grupo de cinco animais permaneceram em uma câmara de tabagismo inalando a fumaça de 10 cigarros por 8 minutos, três vezes ao dia, durante 50 dias. Decorridos 20 dias de inalação de fumaça do cigarro, foi realizada a cirurgia para indução da periodontite apical nos animais do grupo PA e FU+PA, no primeiro molar inferior direto, o qual permaneceu aberto na cavidade bucal por 30 dias. Nesses 30 dias subsequentes da indução da PA, os animais do grupo FU+PA e FU continuaram com a inalação a fumaça do cigarro. No 50º dia, os animais foram eutanasiados e coletados amostras de tecido hematológico para avalição dos níveis séricos de nicotina, cotinina, fosfatase alcalina, cálcio, fósforo, série vermelha e série branca. As hemimandibula removidas foram escaneadas em microtomógrafo para avaliar o volume da destruição óssea e processadas histologicamente para avaliação do perfil inflamatório e expressão das citocinas IL-6, IL-1ß, TNF-α e dos marcadores do metabolismo ósseo RANKL e OPG. Os dados foram tabulados e aplicados os testes estatísticos de Mann-Whitney para os dados não paramétricos e teste t para os dados paramétricos, a um nível de significância de P< 0.05. Com relação a análise histológica o grupo FU+PA apresentou infiltrado inflamatório mais intenso em relação aos demais grupos (P< 0,05). As citocinas pró-inflamatórias IL-6, IL-1ß, TNF-α apresentaram alto padrão de imunomarcação para o grupo FU+PA (P< 0,05). A análise histométrica mostrou maior área de reabsorção óssea no grupo FU+PA, assim como na análise microtomográfica (P< 0,05). As citocinas RANKL esteve mais expressa no grupo FU+PA (P< 0,05) e OPG teve maior expressão no grupo PA (P< 0,05). Na análise hematológica houve um aumento na concentração de hemácias, hemoglobina e leucócitos para o FU+PA (P< 0,05). Os níveis séricos de cálcio foram menores no FU+PA (P> 0,05), a fosfatase alcalina e o cálcio se manteve constante em todos os grupos experimentais (P> 0,05). A concentração sérica de nicotina e cotinina no grupo FU e FU+PA foram compatíveis com fumante humano(AU)


Endodontic infection occurs mainly after pulp tissue contamination by a carious process, leading to bacterial colonization of root canal system and inflammatory response of periapical tissues, followed by formation of apical periodontitis (AP). It is widely known that smoking has harmful impacts on oral and systemic health and is considered a risk factor for periodontal diseases. The objective of this research was to investigate the influence of smoking on the development of AP in rats. Thirty-two male Wistar rats were divided into 4 experimental groups (n = 8): C - Control (no induced AP and no cigarette smoke inhalation); CSI (cigarette smoke inhalation); AP (induced apical periodontitis); CSI + AP (cigarette smoke inhalation and induced apical periodontitis). To inhale cigarette smoke, group with five animals remained in a smoking chamber inhaling smoke from 10 cigarettes for 8 minutes, three times daily, for 50 days. After 20 days of cigarette smoke inhalation, pulp chamber access was performed to induce apical periodontitis in the first mandibular right molar, which remained with pulp chamber exposed to oral cavity for 30 days in animals in the AP and CSI + AP group. During these 30 days after the AP induction, animals in the CSI + AP and CSI group continued to inhale cigarette smoke. On the 50th day, animals were euthanized and blood sample collected to assess serum levels of nicotine, cotinine, alkaline phosphatase, calcium, phosphorus, red series and white series. The hemimandibles were removed and scanned in microtomograph to assess bone volume and histologically processed to assess inflammatory profile and expression of cytokines IL-6, IL-1ß, TNF-α and bone metabolism markers RANKL and OPG. Data were tabulated and statistically analyzed using Mann-Whitney tests for nonparametric data and analysis of variation test for parametric data, with a significance level of P< 0.05. Regarding histological analysis, CSI+AP group showed more intense inflammatory infiltrate compared to other groups (P < 0.05). Histometric analysis showed a larger area of bone resorption in the CSI + AP group, also observed in the microtomographic analysis (P< 0.05). Group CSI+AP had elevated pro-inflammatory cytokines IL-6, IL-1ß, TNF-α expression (P< 0.05). The RANKL cytokines were also more expressed in the CSI+AP group (P< 0.05), while OPG was more expressed in the AP group (P< 0.05). The hematological analysis revealed an increase in the concentration of red blood cells, hemoglobin, and leukocytes for CSI+AP (P< 0.05). Serum calcium levels were lower in CSI+AP (P> 0.05), and alkaline phosphatase and calcium remained constant in all experimental groups (P> 0.05). The serum concentrations of nicotine and cotinine in the CSI and CSI+AP group were compatible with human smokers(AU)


Subject(s)
Animals , Rats , Phosphorus , Calcium , Oral Health , Interleukin-6 , Tumor Necrosis Factor-alpha , Cotinine , Alkaline Phosphatase , Interleukin-1beta , Nicotine
7.
Article in English | WPRIM | ID: wpr-982292

ABSTRACT

OBJECTIVE@#To examine the anti-inflammatory effect of grape seed extract (GSE) in animal and cellular models and explore its mechanism of action.@*METHODS@#This study determined the inhibitory effect of GSE on macrophage inflammation and Th1 and Th17 polarization in vitro. Based on the in vitro results, the effects and mechanisms of GSE on multiple sclerosis (MS)-experimental autoimmune encephalomyelitis (EAE) mice model were further explored. The C57BL/6 mice were intragastrically administered with 50 mg/kg of GSE once a day from the 3rd day to the 27th day after immunization. The activation of microglia, the polarization of Th1 and Th17 and the inflammatory factors such as tumor necrosis factor- α (TNF- α), interleukin-1 β (IL-1 β), IL-6, IL-12, IL-17 and interferon-γ (IFN-γ) secreted by them were detected in vitro and in vivo by flow cytometry, enzyme linked immunosorbent assay (ELISA), immunofluorescence staining and Western blot, respectively.@*RESULTS@#GSE reduced the secretion of TNF-α, IL-1 β and IL-6 in bone marrow-derived macrophages stimulated by lipopolysaccharide (P<0.01), inhibited the secretion of TNF-α, IL-1 β, IL-6, IL-12, IL-17 and IFN-γ in spleen cells of EAE mice immunized for 9 days (P<0.05 or P<0.01), and reduced the differentiation of Th1 and Th17 mediated by CD3 and CD28 factors (P<0.01). GSE significantly improved the clinical symptoms of EAE mice, and inhibited spinal cord demyelination and inflammatory cell infiltration. Peripherally, GSE downregulated the expression of toll-like-receptor 4 (TLR4) and Rho-associated kinase (ROCKII, P<0.05 or P<0.01), and inhibited the secretion of inflammatory factors (P<0.01 or P<0.05). In the central nervous system, GSE inhibited the infiltration of CD45+CD11b+ and CD45+CD4+ cells, and weakened the differentiation of Th1 and Th17 (P<0.05). Moreover, it reduced the secretion of inflammatory factors (P<0.01), and prevented the activation of microglia (P<0.05).@*CONCLUSION@#GSE had a beneficial effect on the pathogenesis and progression of EAE by inhibiting inflammatory response as a potential drug and strategy for the treatment of MS.


Subject(s)
Mice , Animals , Encephalomyelitis, Autoimmune, Experimental/pathology , Grape Seed Extract/therapeutic use , Interleukin-17 , Interleukin-1beta , Tumor Necrosis Factor-alpha/metabolism , Interleukin-6/metabolism , Th1 Cells , Mice, Inbred C57BL , Interferon-gamma/therapeutic use , Th17 Cells/metabolism , Interleukin-12/therapeutic use , Cytokines/metabolism
8.
Article in Chinese | WPRIM | ID: wpr-981883

ABSTRACT

Objective To investigate the neuroprotective effect of methylene blue on diabetic retinopathy in rats. Methods Thirty SD rats were randomly divided into blank, control and experimental groups. The control and experimental groups were induced with diabetes by streptozotocin (STZ) intraperitoneal injection. After 6 weeks of successful modeling, the experimental group received intravitreal injection of methylene blue at a dose of [0.2 mg/(kg.d)], while the control group received an equal amount of dimethyl sulfoxide (DMSO) intravitreal injection, both continuously injected for 7 days. ELISA was used to detect the levels of retinal superoxide dismutase (SOD), 8-iso-prostaglandin F2alpha (iPF2α) and interleukin-1β (IL-1β) in rats. Western blot analysis was used to detect the expression of retinal extracellular signal-regulated kinase 1/2 phosphorylation (p-ERK1/2) and phosphorylated protein kinase B (p-AKT), and PAS staining was used to detect retinal morphological changes. Results Compared with the blank group rats, the retinal SOD activity in the control and experimental group rats was significantly reduced. iPF2α, IL-1β and p-ERK1/2 level increased, while p-AKT level decreased. Compared with the control group, the SOD activity of the experimental group rats increased. iPF2α and IL-1β level went down, while p-ERK1/2 and p-AKT level went up significantly. The overall thickness of the retinal layer and the number of retinal ganglion cells were significantly reduced. Conclusion Methylene blue improves diabetic retinopathy in rats by reducing retinal oxidative stress and enhancing ERK1/2 and AKT phosphorylation.


Subject(s)
Rats , Animals , Diabetic Retinopathy/metabolism , Proto-Oncogene Proteins c-akt/metabolism , Mitogen-Activated Protein Kinase 3/metabolism , Interleukin-1beta/metabolism , Methylene Blue/pharmacology , Phosphorylation , Rats, Sprague-Dawley , MAP Kinase Signaling System , Diabetes Mellitus, Experimental/drug therapy , Superoxide Dismutase/metabolism
9.
Int. j. morphol ; 40(1): .84-90, feb. 2022.
Article in English | LILACS | ID: biblio-1385595

ABSTRACT

SUMMARY: Rheumatoid arthritis (RA), an inflammatory autoimmune disease that causes cartilage degradation and tissue destruction, can affect synovial joints such as the knee joint. The link between the nitrosative stress enzyme inducible nitric oxide synthase (iNOS) and the cytokine interleukin-1 (IL-1β) in RA-induced knee joint synovial membrane damage with and without the incorporation of the GSK3β inhibitor TDZD-8 has never been studied. As a result, we used active immunization method with collagen type II (COII) for twenty one days to induce RA in rats. TDZD-8 (1 mg/kg; i.p.) was given daily into matched immunized rats for three weeks after day 21 (COII+TDZD-8). Blood and tissue samples were taken 42 days after immunization. A dramatic increase in rheumatoid factor (RF) blood levels, as well as considerable synovial tissue damage and inflammatory cell infiltration of the synovial membrane, were used to validate the onset of RA following COII immunization. COII immunization increased tissue levels of iNOS protein and IL- 1β mRNA and protein expression, which TDZD-8 suppressed considerably (p<0.0001). Furthermore, there was a significantly (p<0.001) positive correlation between iNOS, inflammatory biomarkers, and RF. We concluded that TDZD-8 reduced RA-induced IL-1β -iNOS axis-mediated arthritis in the rat knee joint synovium.


RESUMEN: La artritis reumatoide (AR), es una enfermedad autoinmune inflamatoria que causa la degradación del cartílago y la destrucción del tejido, pudiendo afectar las articulaciones sinoviales, como la articulación de la rodilla. No se ha estudiado el vínculo entre la óxido nítrico sintasa inducible por la enzima del estrés nitrosativo (iNOS) y la citocina interleucina-1 (IL-1β) en el daño de la membrana sinovial de la articulación de la rodilla provocado por AR con y sin la incorporación del inhibidor de GSK3β TDZD-8. Utilizamos el método de inmunización activa con colágeno tipo II (COII) durante veintiún días para inducir AR en ratas. Se administró TDZD-8 (1 mg/kg; i.p.) diariamente a ratas inmunizadas emparejadas durante tres semanas después del día 21 (COII+TDZD- 8). Se tomaron muestras de sangre y tejido 42 días después de la inmunización. Se observó un gran aumento de los niveles sanguíneos del factor reumatoideo (FR), así como un daño considerable del tejido sinovial e infiltración de células inflamatorias en la membrana sinovial, para validar la aparición de la AR después de la inmunización con COII. La inmunización con COII aumentó los niveles tisulares de la proteína iNOS y la expresión de proteína y ARNm de IL-1β, que TDZD-8 suprimió considerablemente (p<0,0001). Además, hubo una correlación positiva significativa (p<0,001) entre iNOS, biomarcadores inflamatorios y FR. Concluimos que TDZD- 8 redujo la artritis mediada por el eje IL-1β-iNOS inducida por la AR en la sinovial de la articulación de la rodilla de rata.


Subject(s)
Animals , Rats , Arthritis, Rheumatoid/immunology , Thiadiazoles/administration & dosage , Glycogen Synthase Kinase 3 beta/antagonists & inhibitors , Arthritis, Rheumatoid/chemically induced , Immunohistochemistry , Rats, Wistar , Collagen Type II/administration & dosage , Disease Models, Animal , Interleukin-1beta , Glycogen Synthase Kinase 3 beta/administration & dosage , Nitrosative Stress/drug effects , Inflammation
10.
Asian Journal of Andrology ; (6): 213-218, 2022.
Article in English | WPRIM | ID: wpr-928528

ABSTRACT

Experimental autoimmune prostatitis (EAP)-induced persistent inflammatory immune response can significantly upregulate the expression of N-methyl-D-aspartic acid (NMDA) receptors in the paraventricular nucleus (PVN). However, the mechanism has not yet been elucidated. Herein, we screened out the target prostate-derived inflammation cytokines (PDICs) by comparing the inflammatory cytokine levels in peripheral blood and cerebrospinal fluid (CSF) between EAP rats and their controls. After identifying the target PDIC, qualified males in initial copulatory behavior testing (CBT) were subjected to implanting tubes onto bilateral PVN. Next, they were randomly divided into four subgroups (EAP-1, EAP-2, Control-1, and Control-2). After 1-week recovery, EAP-1 rats were microinjected with the target PDIC inhibitor, Control-1 rats were microinjected with the target PDIC, while the EAP-2 and Control-2 subgroups were only treated with the same amount of artificial CSF (aCSF). Results showed that only interleukin-1β(IL-1β) had significantly increased mRNA-expression in the prostate of EAP rats compared to the controls (P < 0.001) and significantly higher protein concentrations in both the serum (P = 0.001) and CSF (P < 0.001) of the EAP groups compared to the Control groups. Therefore, IL-1β was identified as the target PDIC which crosses the blood-brain barrier, thereby influencing the central nervous system. Moreover, the EAP-1 subgroup displayed a gradually prolonged ejaculation latency (EL) in the last three CBTs (all P < 0.01) and a significantly lower expression of NMDA NR1 subunit in the PVN (P = 0.043) compared to the respective control groups after a 10-day central administration of IL-1β inhibitors. However, the Control-1 subgroup showed a gradually shortened EL (P < 0.01) and a significantly higher NR1 expression (P = 0.004) after homochronous IL-1β administration. Therefore, we identified IL-1β as the primary PDIC which shortens EL in EAP rats. However, further studies should be conducted to elucidate the specific molecular mechanisms through which IL-1β upregulates NMDA expression.


Subject(s)
Animals , Male , Rats , Cytokines/metabolism , Disease Models, Animal , Ejaculation/physiology , Interleukin-1beta/metabolism , N-Methylaspartate/metabolism , Prostate/metabolism , Prostatitis/metabolism , Receptors, N-Methyl-D-Aspartate/metabolism
11.
Int. j. morphol ; 39(1): 311-317, feb. 2021. ilus, graf
Article in English | LILACS | ID: biblio-1385290

ABSTRACT

SUMMARY: Rheumatoid arthritis (RA) is considered an autoimmune disease distinguished by chronic synovial membrane inflammation, degraded cartilage, as well as bone destruction, which lead to joints pain and stiffness. The pathogenesis of RA involved at least two mechanisms: Cellular proliferation and activation of glycogen synthase kinase-3β (GSK3β) enzyme. Thus, we tested the hypothesis that the GSK3binhibitor, TDZD-8, can treat the synovial tissue toward collagen type II (COII)-mediated RA linked to apoptosis induction and biomarker suppression of inflammation. Wistar rats were immunized with COII (the model group) for 21 days. Matched immunized rats were daily injected with TDZD-8 (1 mg/kg; i.p) for three additional weeks (COII+TDZD- 8).After 42 days of post-immunization, blood and tissues were collected. Histology (H&E) and immunohistochemistry (CD45; leukocyte common antigen) images showed that COII induced RA was demonstrated by profound damage to the synovial tissue and infiltration of the inflammatory cells, which were substantially ameliorated with TDZD-8. In addition, COII immunization caused the induction of rheumatoid factor (RF), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin 1 beta (IL-1β) that were substantially (p<0.05) suppressed by TDZD-8. Whereas, TDZD-8 augmented the apoptotic biomarker, Bcl-2-associated X protein (Bax), which was significantly (p<0.05) ameliorated by RA. We also showed a substantial relationship (p<0.001) between the blood levels of RF and the synovial tissue levels of TNF-α (r = 0.759), IL-1b (r = 0.969), IL-6 (r = 0.749), and Bax (r = - 0.914). These results indicate effective treatment of the injured synovial tissue by TDZD-8 against COII-induced RA in rats, which also decreases inflammatory biomarkers and augmentation of apoptosis.


RESUMEN: La artritis reumatoide (AR) es una enfermedad autoinmune que se distingue por la inflamación crónica de la membrana sinovial, el cartílago degradado y la destrucción de los huesos, lo que provoca dolor y rigidez en las articulaciones. La patogenia de la AR involucra al menos dos mecanismos: la proliferación celular y la activación de la enzima glucógeno sintasa quinasa-3b (GSK3β) Por lo tanto, probamos la hipótesis de que el inhibidor de GSK3β, TDZD-8, puede tratar el tejido sinovial hacia el colágeno tipo II (COII) - AR mediada por inducción de apoptosis y supresión de biomarcadores de inflamación. Se inmunizaron ratas Wistar con COII (el grupo modelo) durante 21 días. Se inyectaron diariamente ratas emparejadas inmunizadas con TDZD-8 (1 mg / kg; i.p) durante tres semanas adicionales (COII + TDZD-8). Después de 42 días de post-inmunización, se recolectó sangre y tejidos. Las imágenes de histología (H&E) e inmunohistoquímica (CD45; antígeno común de leucocitos) mostraron que la AR inducida por COII presentaba un daño profundo en el tejido sinovial e infiltración de las células inflamatorias, las que mejoraron con TDZD-8. Además, la inmunización con COII provocó la inducción de factor reumatoide (FR), factor de necrosis tumoral alfa (TNF-α), interleucina-6 (IL-6) e interleucina 1 beta (IL-1β) que fueron suprimidos por TDZD-8 de manera significativa (p < 0.05). Considerando que TDZD-8 aumentó el biomarcador apoptótico, la proteína X asociada a Bcl-2 (Bax), que fue mejorado (p <0,05) por RA. También se observó una relación sustancial (p <0,001) entre los niveles sanguíneos de RF y los niveles de tejido sinovial de TNF-α (r = 0,759), IL-1β (r = 0,969), IL-6 (r = 0,749), y Bax (r = -0,914). Estos resultados indicaron un tratamiento eficaz del tejido sinovial lesionado por TDZD-8 contra la AR inducida por COII en ratas, que también disminuye los biomarcadores inflamatorios y el aumento de la apoptosis.


Subject(s)
Animals , Male , Rats , Arthritis, Rheumatoid/drug therapy , Thiadiazoles/administration & dosage , Collagen Type II/adverse effects , Arthritis, Experimental/drug therapy , Thiadiazoles/pharmacology , Immunohistochemistry , Blotting, Western , Rats, Wistar , Apoptosis , Disease Models, Animal , Interleukin-1beta , Inflammation
12.
Arq. bras. oftalmol ; 84(1): 67-73, Jan.-Feb. 2021. graf
Article in English | LILACS | ID: biblio-1153097

ABSTRACT

ABSTRACT Purpose: Diabetic retinopathy is currently considered a chronic inflammatory disease involving NOD-like receptor family pyrin domain containing 3 inflammasome activation and retinal microglial pyroptosis. In this study, we aimed to investigate whether NOD-like receptor family pyrin domain containing 3 inflammasome signaling induces pyroptotic death of retinal microglia under high-glucose conditions. Methods: Retinal microglia were stimulated by high glucose levels for 24 h. Cell viability, lactate dehydrogenase release, and caspase-1 activity were detected in vitro. The expression of pro-inflammatory cytokine (interleukin-1β, activated microglia marker ionized calcium-binding adapter molecule-1), NOD-like receptor family pyrin domain containing 3, cleaved caspase-1, and cleaved gasdermin D were examined. Subsequently, retinal microglia were pretreated with the inhibitors of NOD-like receptor family pyrin domain containing 3 inflammasome signaling prior to stimulation with high glucose, and their molecular and functional changes were evaluated. Results: High-glucose (25, 50, or 100 mM) stimulation decreased cell viability, but enhanced lactate dehydrogenase release and caspase-1 activity in a dose-dependent manner. Moreover, high glucose upregulated the protein expression of interleukin-1β, ionized calcium-binding adapter molecule-1, NOD-like receptor family pyrin domain containing 3, cleaved caspase-1, and cleaved gasdermin D. However, pretreatment with the inhibitors of NOD-like receptor family pyrin domain containing 3 inflammasome signaling inhibited high glucose (25 mM)-induced cytotoxicity, NOD-like receptor family pyrin domain containing 3 inflammasome activation, and pyroptosis of retinal microglia. Conclusions: NOD-like receptor family pyrin domain containing 3 inflammasome signaling may modulate retinal microglia-related inflammation and pyroptosis under high-glucose conditions.


RESUMO Objetivo: Atualmente, a retinopatia diabética é considerada uma doença inflamatória crônica envolvendo a ativação de inflamassomas NLRP3 e piroptose da micróglia da retina. Neste estudo, objetivamos investigar se a sinalização de inflamassomas NLRP3 induz a morte da micróglia da retina sob condições de alta glicose. Métodos: A micróglia da retina foi estimulada por altos níveis de glicose durante 24 horas. A viabilidade celular, a liberação de LDH e a atividade da caspase1 foram analisadas in vitro. Avaliou-se a expressão de citocina pró-inflamatória (IL1β), de marcador de micróglia ativado (Iba1), de NLRP3, de caspase1 clivada e de GSDMD clivada. Subsequentemente, a micróglia da retina foi pré-tratada com inibidores da sinalização de inflamassomas NLRP3 antes da estimulação com altos níveis de glicose e suas alterações moleculares e funcionais foram avaliadas. Resultados: A estimulação com altos níveis de glicose (25 mM, 50 mM ou 100 mM) diminuiu a viabilidade celular, mas aumentou a liberação de LDH e a atividade da caspase1 de forma dependente da dose. Além disso, os altos níveis de glicose aumentaram a expressão das proteínas IL1β, Iba1, NLRP3, caspase1 clivada e GSDMD clivada. No entanto, o pré-tratamento com inibidores da sinalização de inflamassomas NLRP3 e a posterior estimulação com altos níveis de glicose (25 mM) induziu citotoxicidade, a ativação de inflamassomas NLRP3 e a piroptose da micróglia da retina. Conclusão: A sinalização de inflamassomas NLRP3 pode modular a inflamação e a piroptose da micróglia da retina na presença de altos níveis de glicose.


Subject(s)
Humans , Inflammasomes , Pyroptosis , Microglia , Interleukin-1beta , NLR Family, Pyrin Domain-Containing 3 Protein , Glucose
13.
Article in Chinese | WPRIM | ID: wpr-921648

ABSTRACT

The rats were exposed to chronic unpredictable mild stress(CUMS) and kept in separate cages for inducing depressive disorder, which was judged by behavioral indicators. The number and morphology of neurons in hippocampal CA3 area and prefrontal cortex were observed by hematoxylin-eosin(HE) staining. The levels of brain-derived neurotrophic factor(BDNF), 5-hydroxytryptamine(5-HT), 5-hydroxyindoleacetic acid(5-HIAA), dopamine(DA), norepinephrine(NE), glutamic acid(GLU), interleukin-1β(IL-1β), interleukin-18(IL-18), and tumor necrosis factor-α(TNF-α) were detected by enzyme-linked immunosorbent assay(ELISA). Real-time polymerase chain reaction(RT-PCR) and Western blot were conducted to determine the mRNA and protein expression levels of related molecules in NLRP3 pathway. The results showed that compared with the model group, acidic polysaccharides from Poria at the low-, medium-, and high-doses(0.1, 0.3 and 0.5 g·kg~(-1)·d~(-1)) all improved the depression-like behavior of rats, increased the number of neurons and the levels of BDNF, 5-HT, 5-HIAA, DA, and NE in the hippocampus, and reduced GLU and serum IL-1β, IL-18, and TNF-α levels. The mRNA expression levels of ASC, caspase-1, IL-1β, and IL-18 and the protein expression levels of NLRP3, ASC, caspase-1, IL-1β, and IL-18 in each medication group were down-regulated, whereas the protein expression levels of pro-caspase-1, pro-IL-1β, and pro-IL-18 were up-regulated. All these have indicated that acidic polysaccharides from Poria exerted the antidepressant effect possibly by regulating neurotransmitters and NLRP3 inflammasome signaling pathway.


Subject(s)
Animals , Rats , Antidepressive Agents , Depression/drug therapy , Interleukin-1beta , NLR Family, Pyrin Domain-Containing 3 Protein/genetics , Neurotransmitter Agents , Polysaccharides/pharmacology , Poria
14.
Braz. arch. biol. technol ; 64: e21210256, 2021. tab, graf
Article in English | LILACS | ID: biblio-1339311

ABSTRACT

Abstract While the role of cytokines in celiac disease has been investigated in detail, cytokine release in the event of the exposure of healthy subjects to glutens has only recently been studied. This study was aimed at determining the effects of corn and wheat glutens, incorporated as protein sources into the diet, on serum interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) levels and the immunohistochemical distribution of CD3 and CD8 receptors in the small intestine in male rats. The study material comprised 24 twenty-day-old male Wistar albino rats, which were randomly assigned in equal numbers to three groups (2 rats/replicate and 4 replicates/group). The feed rations provided to all three groups contained high levels of proteins, which were soybean meal, corn gluten and wheat gluten in the control, corn and wheat groups, respectively. The in Control, Corn and Wheat groups serum IL-1 beta and TNF-alpha levels respectively 55.83 - 46.37; 81.65 - 61.95 and 81.65-61.31 was determined but these differences were statistically insignificant. Furthermore, immunohistochemical examination demonstrated a mathematical increase to have occurred in the distribution of the CD3 and CD8 receptors in the duodenum, jejunum and ileum samples of the corn and wheat groups. In result, based on the findings obtained in this study, we suggest that the long-term feeding of rats on high levels of gluten causes systemic adverse effects.


Subject(s)
Animals , Rats , Cytokines/drug effects , Tumor Necrosis Factor-alpha/drug effects , Interleukin-1beta/drug effects , Glutens/pharmacology , Immunohistochemistry , Rats, Wistar
15.
J. appl. oral sci ; 29: e20210160, 2021. tab, graf
Article in English | LILACS | ID: biblio-1340107

ABSTRACT

Abstract Objective This study aims to evaluate the effect of ellagic acid (EA) by measuring the levels of alveolar bone resorption and inflammatory and oxidative stress markers in the periodontal tissues and serum on the periodontal repair process related to experimental periodontitis in rats. Methodology Forty Wistar rats were divided into four study groups as follows: Group 1=healthy control (n=10); Group 2=EA control (15 mg/kg)(n=10); Group 3=periodontitis (n=10); Group 4=periodontitis+EA (15 mg/kg) (n=10). The periodontitis model was established by ligating bilateral mandibular first molars for 14 days. Then, rats were given normal saline or EA for another 14 days by gavage administration. Serum and gingiva myeloperoxidase (MPO) activity, 8-hydroxydeoxyguanosine(8-OHdG), and glutathione (GSH) levels were analyzed by ELISA. İmmunohistochemical analysis was used to detect Interleukin (IL)-6, IL-10, and tumor necrosis factor-alpha (TNF-α) immunoreactivities in the periodontal tissues. Alveolar bone loss (ABL) and attachment loss (AL) was evaluated by histomorphometry analysis. Results ABL and AL were statistically higher in group 3 than in groups 1, 2 and 4 and in group 4 than in groups 1 and 2 (p<0.05). MPO activities in gingival tissue and serum were significantly increased in group 3 compared to groups 1 and 2 (p<0.05). Significantly higher serum GSH levels, lower gingiva, and serum 8-OHdG levels, and MPO activity were observed in group 4 compared to group 3 (p<0.05). Rats with periodontitis (group 3) expressed significantly higher immunoreactivities of IL-6 and TNF-α and lower IL-10 immunoreactivity compared to those other groups (p<0.05). IL-6 and TNF-α immunoreactivities significantly decreased and IL-10 immunoreactivity increased in group 4 after the use of EA compared to group 3 (p<0.001). Conclusions Our findings showed that EA provides significant improvements on gingival oxidative stress and inflammatory markers and alveolar bone resorption in the repair process associated with experimental periodontitis. Therefore, EA may have a therapeutic potential on periodontitis.


Subject(s)
Animals , Rats , Periodontitis/drug therapy , Alveolar Bone Loss , Tumor Necrosis Factor-alpha , Rats, Wistar , Ellagic Acid/pharmacology , Interleukin-1beta
16.
Article in English | WPRIM | ID: wpr-880636

ABSTRACT

OBJECTIVES@#Inflammation especially the overexpression of inflammasome and inflammatory cytokines, is one of the important reasons that affect the occurrence and development of acute cerebral infarction, including the initiation of cerebral infarction, the progress and recovery of post-infarction injury. This study aims to explore expressions of absent in melanoma 2 (AIM2), interleukin-1β (IL-1β), and interleukin-18 (IL-18) in plasma of patients with acute cerebral infarction and its significance.@*METHODS@#A total of 85 patients with acute cerebral infarction were enrolled in the cerebral infarction group. They were assigned into mild, moderate, and severe groups according to the severity of neurological deficits. They were assigned into small, middle, and large cerebral infarction groups according to the area of cerebral infarction. They were assigned into a good prognosis group and a poor prognosis group according to the Modified Rankin Scale (mRS) score on the 90th day after the onset. A total of 85 healthy controls were selected as a control group. The levels of AIM2, IL-1β, and IL-18 in plasma of the cerebral group and the control group were detected by enzyme-linked immunosorbent assay (ELISA).@*RESULTS@#The levels of plasma AIM2, IL-1β, and IL-18 in the cerebral infarction group were significantly higher than those in the control group (all @*CONCLUSIONS@#Expressions of AIM2, IL-1β, and IL-18 are up-regulated in the plasma of patients with acute cerebral infarction, and they are closely related to the severity of neurological deficit, cerebral infarction area, and prognosis in patients with acute cerebral infarction, suggesting that AIM2, IL-1β, and IL-18 may play an important role in the occurrence and development of acute cerebral infarction.


Subject(s)
Humans , Cerebral Infarction , DNA-Binding Proteins , Interleukin-18 , Interleukin-1beta , Melanoma , Plasma , Stroke
17.
Article in English | WPRIM | ID: wpr-880618

ABSTRACT

OBJECTIVES@#Chondrocyte apoptosis is an important process in the pathogenesis of osteoarthritis. Mangiferin exerts multiple pharmacological effects such as anti-inflammatory and anti-apoptosis. However, the role of mangiferin in chondrocyte apoptosis is not clear. In this study, we aimed to explore the role of mangiferin in IL-1β-induced chondrocyte apoptosis.@*METHODS@#ATDC5 cells were randomly divided into a control group, a IL-1β group, a MFN-L group, a MFN-M group, a MFN-H group and a MFN+LY294002 group. Cells in the control group were treated with IL-1β (10 ng/mL) for 24 h; cells in the MFN-L group, the MFN-M group and the MFN-H group were pretreated with 5, 10 and 20 μmol/L mangiferin for 1 h respectively, and then they were treated with IL-1β (10 ng/mL) for 24 h; cells in the MFN+LY294002 group were treated with LY294002 (25 μmol/L) for 1 h, then mangiferin (20 μmol/L) and IL-1β (10 ng/mL) for 1 h and 24 h, respectively. Cell viability was detected by CCK-8 assay and cell apoptosis was measured by flow cytometry. Colorimetric assay was conducted to measure the caspase-3 activity. The protein levels of Bcl-2, Bax, and phosphoinositide 3-kinase (PI3K)/Akt signaling pathway related proteins were detected by Western blotting.@*RESULTS@#Compared to the control group, cell viability was significantly decreased; cell apoptosis, caspase-3 activity and Bax protein expression were significantly increased; the protein levels of Bcl-2, p-PI3K, and p-Akt were significantly decreased in the IL-1β group (all @*CONCLUSIONS@#Mangiferin could attenuate IL-1β-induced apoptosis of the mice chondrocytes, which is mediated by the activation of PI3K/Akt signaling pathway.


Subject(s)
Animals , Mice , Apoptosis , Chondrocytes , Interleukin-1beta , Phosphatidylinositol 3-Kinases , Proto-Oncogene Proteins c-akt , Xanthones
18.
Article in English | WPRIM | ID: wpr-878441

ABSTRACT

OBJECTIVES@#To study the effect and mechanism of low-level laser irradiation (LLLI) on lipopolysaccharide (LPS)-induced inflammatory injury of human periodontal ligament fibroblasts (hPDLFs).@*METHODS@#hPDLFs were inoculated into well plates and randomly divided into the normal group, LPS group, and LPS+LLLI group. The cells in the normal group were cultured in conventional medium. The hPDLFs in the LPS and LPS+LLLI groups were cultured in RPMI1640 medium containing 1 mg·L@*RESULTS@#Compared with the normal group, the LPS group showed increased apoptosis rate of hPDLFs and intracellular free Ca@*CONCLUSIONS@#LLLI has a protective effect on the inflammatory injury of hPDLFs induced by LPS, and the effect is most obvious when the irradiation intensity is 4 J·cm


Subject(s)
Humans , Cells, Cultured , Fibroblasts , Interleukin-1beta , Lasers , Lipopolysaccharides , Periodontal Ligament , Tumor Necrosis Factor-alpha
20.
Chinese Medical Journal ; (24): 963-970, 2021.
Article in English | WPRIM | ID: wpr-878129

ABSTRACT

BACKGROUND@#Histone deacetylase 4 (HDAC4) regulates chondrocyte hypertrophy and bone formation. The aim of the present study was to explore the effects of HDAC4 on Interleukin 1 beta (IL-1β)-induced chondrocyte extracellular matrix degradation and whether it is regulated through the WNT family member 3A (WNT3A)/β-catenin signaling pathway.@*METHODS@#Primary chondrocytes (CC) and human chondrosarcoma cells (SW1353 cells) were treated with IL-1β and the level of HDAC4 was assayed using Western blotting. Then, HDAC4 expression in the SW1353 cells was silenced using small interfering RNA to detect the effect of HDAC4 knockdown on the levels of matrix metalloproteinase 3 (MMP3) and MMP13 induced by IL-1β. After transfection with HDAC4 plasmids, the overexpression efficiency was examined using Real-time quantitative polymerase chain reaction (qRT-PCR) and the levels of MMP3 and MMP13 were assayed using Western blotting. After incubation with IL-1β, the translocation of β-catenin into the nucleus was observed using immunofluorescence staining in SW1353 cells to investigate the activation of the WNT3A/β-catenin signaling pathway. Finally, treatment with WNT3A and transfection with glycogen synthase kinase 3 beta (GSK3β) plasmids were assessed for their effects on HDAC4 levels using Western blotting.@*RESULTS@#IL-1β downregulated HDAC4 levels in chondrocytes and SW1353 cells. Furthermore, HDAC4 knockdown increased the levels of MMP3 and MMP13, which contributed to the degradation of the extracellular matrix. Overexpression of HDAC4 inhibited IL-1β-induced increases in MMP3 and MMP13. IL-1β upregulated the levels of WNT3A, and WNT3A reduced HDAC4 levels in SW1353 cells. GSK-3β rescued IL-1β-induced downregulation of HDAC4 in SW1353 cells.@*CONCLUSION@#HDAC4 exerted an inhibitory effect on IL-1β-induced extracellular matrix degradation and was regulated partially by the WNT3A/β-catenin signaling pathway.


Subject(s)
Humans , Cell Line, Tumor , Cells, Cultured , Chondrocytes/metabolism , Glycogen Synthase Kinase 3 beta/genetics , Histone Deacetylases/genetics , Interleukin-1beta/pharmacology , Matrix Metalloproteinase 13/metabolism , Matrix Metalloproteinase 3 , Repressor Proteins , Wnt Signaling Pathway , Wnt3A Protein/genetics , beta Catenin/metabolism
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