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1.
Rev. ADM ; 79(1): 38-47, ene.-feb. 2022. tab
Article in Spanish | LILACS | ID: biblio-1361906

ABSTRACT

Las urgencias odontológicas son, quizá, las razones principales de atención en el consultorio, muchas veces el significado de dolor se encuentra acompañado por inflamación; el uso de antiinflamatorios no esteroideos (AINES) es común en el ejercicio de la odontología por la excelente respuesta analgésica y antiinflamatoria que tiene, por lo que es importante conocer la fisiopatología de la inflamación y el dolor y cómo actúan los AINES, ya que algunos de estos fármacos tienen respuestas adversas y sitios de acción importantes. Los factores de riesgo por inflamación y dolor nos obligan a conocer la variedad de fármacos que no entran en la clasificación de AINES y que tenemos a disposición, hay más opciones para la elección ante la presencia de inflamación por un factor en particular, cada uno de éstos tienen indicaciones y contraindicaciones que conoceremos, lo cual nos ampliará el conocimiento para dar una prescripción ante la presencia de eventos inflamatorios. Se realizó un estudio detallado de artículos bibliográficos de cada tema, los fármacos más usados en odontología son los AINES, hay poco uso y conocimiento de antiinflamatorios que podemos usar en urgencias, el porcentaje de uso de los AINES derivados del ácido propiónico es alto por la excelente respuesta en pacientes y otras veces por el desconocimiento de más opciones (AU)


Dental emergencies are perhaps the main reasons for care in the office, many times the meaning of pain is accompanied by inflammation, the use of non-steroidal anti-inflammatory drugs is common in the practice of dentistry due to the excellent analgesic and anti-inflammatory response it has, important is knowing the pathophysiology of inflammation and pain, how NSAIDs act, some of these drugs have adverse responses and important sites of action, risk factors for inflammation and pain require us to know the variety of drugs that do not enter the classification of NSAIDs and we have at our disposal, there are more options for choosing in the presence of inflammation due to a particular factor, each of these have indications and contraindications that we will know, it expands our knowledge to give a prescription in the presence of inflammatory events. A detailed study of bibliographic articles on each topic was carried out, the drugs most used in dentistry are NSAIDs, there is little use and knowledge of anti-inflammatories that we can use in the emergency room, the percentage of use of NSAIDs derived from propionic acid is high, due to the excellent response in patients and others due to lack of knowledge of more options (AU)


Subject(s)
Humans , Male , Female , Toothache , Pharmaceutical Preparations , Anti-Inflammatory Agents, Non-Steroidal , Inflammation , Pain/pathology , Pain, Postoperative , Propionates , Prostaglandins/physiology , Statistical Analysis , Drug Interactions , Cyclooxygenase 1/pharmacology , Cyclooxygenase 2 , Cyclooxygenase 2 Inhibitors , Narcotics
3.
Article in Chinese | WPRIM | ID: wpr-887978

ABSTRACT

Through literature analysis of Pheretima and its origin-related earthworm,this study summarized the progress on Pheretima in textual criticism of origin,origin identification,effective components,detection of harmful components,and pharmacological effects,which can lay a basis for further research on Pheretima. Through literature research,the authors found that Pheretima was first recorded in Secret Formulary for Traumatology and Fracture Taught by Immortal written by LIN Daoren in Tang Dynasty rather than the Taiping Holy Prescriptions for Universal Relief in Song Dynasty. The latest techniques for origin identification include microscopic trait identification,DNA barcoding,and HPLC. The main effective components of Pheretima are proteins,polypeptides,enzymes,nucleotides,amino acids,and trace elements. According to recent studies,Pheretima has anti-pulmonary and anti-renal interstitial fibrosis,respiratory syncytial virus-inhibiting,human hypertrophic scar fibroblast proliferation-suppressing,and mouse embryonic fibroblast proliferation-promoting effects. Moreover,Pheretima can prevent colitis-induced colon cancer by inhibiting the activation of COX-2/PGE2/β-catenin signaling pathway. METHODS:: for detecting the harmful components and their residues( organic pollutant polychlorinated biphenyl,heavy metals) and bacteria in Pheretima,have been established. Pheretima,mainly derived from wild earthworms,has remarkable clinical efficacy. However,the wild resource is in short supply and artificial culture is expected to be a promising solution.


Subject(s)
Animals , Chromatography, High Pressure Liquid , Cyclooxygenase 2 , DNA , Fibroblasts , Mice , Oligochaeta
4.
Article in English | WPRIM | ID: wpr-787141

ABSTRACT

Neuroinflammation is an important process underlying a wide variety of neurodegenerative diseases. Carvacrol (CAR) is a phenolic monoterpene commonly used as a food additive due to its antibacterial properties, but it has also been shown to exhibit strong antioxidative, anti-inflammatory, and neuroprotective effects. Here, we sought to investigate the effects of CAR on inflammation in the hippocampus and prefrontal cortex, as well as the molecular mechanisms underlying these effects. In our study, lipopolysaccharide was injected into the lateral ventricle of rats to induce memory impairment and neuroinflammation. Daily administration of CAR (25, 50, and 100 mg/kg) for 21 days improved recognition, discrimination, and memory impairments relative to untreated controls. CAR administration significantly attenuated expression of several inflammatory factors in the brain, including interleukin-1β, tumor necrosis factor-α, and cyclooxygenase-2. In addition, CAR significantly increased expression of brain-derived neurotrophic factor (BDNF) mRNA, and decreased expression of Toll-like receptor 4 (TLR4) mRNA. Taken together, these results show that CAR can improve memory impairment caused by neuroinflammation. This cognitive enhancement is due to the anti-inflammatory effects of CAR medicated by its regulation of BDNF and TLR4. Thus, CAR has significant potential as an inhibitor of memory degeneration in neurodegenerative diseases.


Subject(s)
Animals , Brain , Brain-Derived Neurotrophic Factor , Cyclooxygenase 2 , Cytokines , Discrimination, Psychological , Food Additives , Hippocampus , Inflammation , Lateral Ventricles , Lipopolysaccharides , Memory , Necrosis , Neurodegenerative Diseases , Neuroprotective Agents , Phenol , Prefrontal Cortex , Rats , RNA, Messenger , Toll-Like Receptor 4
5.
J. appl. oral sci ; 28: e20190699, 2020. graf
Article in English | LILACS, BBO | ID: biblio-1134770

ABSTRACT

Abstract Purpose To evaluate the kinetics of apical periodontitis development in vivo , induced either by contamination of the root canals by microorganisms from the oral cavity or by inoculation of bacterial lipopolysaccharide (LPS) and the regulation of major enzymes and receptors involved in the arachidonic acid metabolism. Methodology Apical periodontitis was induced in C57BL6 mice (n=96), by root canal exposure to oral cavity (n=48 teeth) or inoculation of LPS (10 µL of a suspension of 0.1 µg/µL) from E. coli into the root canals (n= 48 teeth). Healthy teeth were used as control (n=48 teeth). After 7, 14, 21 and 28 days the animals were euthanized and tissues removed for histopathological and qRT-PCR analyses. Histological analysis data were analyzed using two-way ANOVA followed by Sidak's test, and qRT-PCR data using two-way ANOVA followed by Tukey's test (α=0.05). Results Contamination by microorganisms led to the development of apical periodontitis, characterized by the recruitment of inflammatory cells and bone tissue resorption, whereas inoculation of LPS induced inflammatory cells recruitment without bone resorption. Both stimuli induced mRNA expression for cyclooxygenase-2 and 5-lipoxygenase enzymes. Expression of prostaglandin E 2 and leukotriene B 4 cell surface receptors were more stimulated by LPS. Regarding nuclear peroxisome proliferator-activated receptors (PPAR), oral contamination induced the synthesis of mRNA for PPARδ, differently from inoculation of LPS, that induced PPARα and PPARγ expression. Conclusions Contamination of the root canals by microorganisms from oral cavity induced the development of apical periodontitis differently than by inoculation with LPS, characterized by less bone loss than the first model. Regardless of the model used, it was found a local increase in the synthesis of mRNA for the enzymes 5-lipoxygenase and cyclooxygenase-2 of the arachidonic acid metabolism, as well as in the surface and nuclear receptors for the lipid mediators prostaglandin E2 and leukotriene B4.


Subject(s)
Animals , Male , Periapical Periodontitis/microbiology , Dinoprostone/metabolism , Lipopolysaccharides/metabolism , Leukotriene B4/metabolism , Dental Pulp Cavity/microbiology , Periapical Periodontitis/metabolism , Periapical Periodontitis/pathology , Time Factors , Bone Resorption/metabolism , Bone Resorption/microbiology , Arachidonate 5-Lipoxygenase/analysis , Arachidonate 5-Lipoxygenase/metabolism , RNA, Messenger/analysis , RNA, Messenger/metabolism , Dinoprostone/analysis , Random Allocation , Gene Expression , Leukotriene B4/analysis , Reverse Transcriptase Polymerase Chain Reaction , Dental Pulp Cavity/metabolism , Dental Pulp Cavity/pathology , Cyclooxygenase 2/analysis , Cyclooxygenase 2/metabolism , Mice, Inbred C57BL
6.
Article in English | WPRIM | ID: wpr-786072

ABSTRACT

OBJECTIVE: Inflammation is crucial to limiting vascular disease. Previously we reported that acrolein, a known toxin in tobacco smoke, might play an important role in the progression of atherosclerosis via an inflammatory response involving cyclooxygenase-2 (COX-2) and prostaglandin production in human umbilical vein endothelial cells (HUVECs). Curcumin has been known to improve vascular function and have anti-inflammatory properties. In this study, we investigated whether curcumin prevents the induction of inflammatory response caused by acrolein.METHODS: Anti-inflammatory effects of curcumin were examined in acrolein-stimulated HUVECs. Induction of proteins, mRNA, prostaglandin and reactive oxygen species (ROS) were measured using immunoblot analysis, real-time reverse-transcription polymerase chain reaction, enzyme-linked immunosorbent assay and flow cytometry, respectively.RESULTS: Curcumin attenuates inflammatory response via inhibition of COX-2 expression and prostaglandin production in acrolein-induced human endothelial cells. This inhibition by curcumin results in the abolition of phosphorylation of protein kinase C, p38 mitogen-activated protein kinase, and cAMP response element-binding protein. Furthermore, curcumin suppresses the production of ROS and endoplasmic reticulum stress via phosphorylation of eukaryotic initiation factor-2α caused by acrolein.CONCLUSION: These results suggest that curcumin might be a useful agent against endothelial dysfunction caused by acrolein-induced inflammatory response.


Subject(s)
Acrolein , Atherosclerosis , Curcumin , Cyclic AMP Response Element-Binding Protein , Cyclooxygenase 2 , Endoplasmic Reticulum Stress , Endothelial Cells , Enzyme-Linked Immunosorbent Assay , Flow Cytometry , Human Umbilical Vein Endothelial Cells , Humans , Inflammation , Phosphorylation , Polymerase Chain Reaction , Protein Kinase C , Protein Kinases , Reactive Oxygen Species , RNA, Messenger , Smoke , Tobacco , Vascular Diseases
7.
Iatreia ; 32(1): 52-63, ene.-mar. 2019. tab
Article in Spanish | LILACS | ID: biblio-1002139

ABSTRACT

RESUMEN El desarrollo del carcinoma colorrectal es un proceso secuencial asociado con la inestabilidad cromosómica y con mutaciones de oncogenes como KRAS, de genes supresores de tumor como p53, o con pérdida del gen APC, causando transformación y proliferación celular descontrolada. La ciclooxigenasa-2 (COX-2) es una enzima inducible, cuya expresión puede ser influenciada por estímulos proinflamatorios y mitógenos como los ocasionados por citoquinas y factores de crecimiento. Esta ha sido propuesta como reguladora de la proliferación celular y se ha planteado que puede jugar un papel importante en el desarrollo del tejido metaplásico y displásico, así como en el desarrollo y progresión de diferentes tipos de tumores, entre ellos el carcinoma colorrectal. Se han utilizado diferentes técnicas para identificar el nivel de COX-2 en neoplasias colorrectales, una de las más utilizadas es la inmunohistoquímica, que ha permitido demostrar mayor expresión de la enzima en el tejido tumoral en comparación con la mucosa colorrectal normal. La mayoría de los estudios publicados han sugerido que la sobreexpresión común de COX-2 en el carcinoma colorrectal podría ser utilizada como biomarcador para esta neoplasia.


SUMMARY The development of colorectal carcinoma is a sequential process associated to chromosomic instability and to mutations of oncogenes as KRAS, of tumor suppressor gene as p53, or loss of APC, leading to uncontrolled cell proliferation and transformation. Cyclooxygenase 2 (COX-2) is an inducible enzyme, whose expression can be influenced by proinflammatory and mitogenic stimuli such as those caused by cytokines and growth factors, has been proposed as an enzyme regulating cell proliferation, and therefore carcinogenesis, which can play an important role in the development of metaplastic and dysplastic tissues, as well as in the development and progression of cancer as colorectal tumors. Different techniques have been used to identify COX-2 expression in colorectal neoplasms, one of the most widely used is the immunohistochemistry, whose results have generally shown higher staining in tumor tissue compared to normal colorectal mucosa. Most published studies have suggested that the common overexpression of COX-2 in colorectal carcinoma could be used as a biomarker for this neoplasm.


Subject(s)
Humans , Carcinoma , Cyclooxygenase 2 , Neoplasms
8.
Braz. dent. j ; 30(2): 133-138, Mar.-Apr. 2019. graf
Article in English | LILACS | ID: biblio-1001441

ABSTRACT

Abstract In the present study we compared the effects of the selective COX-2 inhibitor etoricoxib with those of the classical non-selective NSAID diclofenac on the inflammatory process and alveolar bone loss in an experimental model of periodontitis in rats. Ninety male Holtzman rats (250 g) were randomly sorted into four experimental groups: Sham+CMC and Ligature+CMC (control) groups which received 0.5% carboxymethylcellulose sodium (CMC) solution; Ligature+Diclofenac and Ligature+Etoricoxib groups which received Potassium Diclofenac and Etoricoxib, respectively, suspended in 0.5% CMC (10 mg/kg/day). At 7, 14 and 21 days after placing ligatures in the cervical region of both the lower right and left first molars, the animals were euthanized. At the end of each period, the mandibles were collected for radiographic examination of alveolar bone loss. In addition, alveolar bone and periodontal ligament tissue samples were collected for COX-2 expression analysis and gingival tissues were collected for measurement of PGE2 contents. Animals with ligature-induced periodontal disease showed significant increased COX-2 gene expression at days 7, 14 and 21 (p<0.05) on alveolar bone and periodontal ligament. However, both treatments resulted in significantly reduced alveolar bone loss when compared to the untreated Ligature group (p<0.05), with no statistical difference between Etoricoxib and Diclofenac Potassium groups. This study shows that both drugs were able to reduce alveolar bone loss after periodontal disease induction.


Resumo No presente estudo nós comparamos os efeitos de um inibidor seletivo da COX-2 (etoricoxibe) com um anti-inflamatório não esteroidal não seletivo (AINE) (diclofenaco de potássio) no processo inflamatório e perda óssea alveolar em modelo de periodontite experimental. Noventa ratos Holtzman machos (250 g) foram randomizados em quatro grupos experimentais: Sham+CMC e Ligadura+CMC (controle) que receberam solução de carboximetilcelulose de sódio (CMC) a 0,5%; Ligadura+Diclofenaco e Ligadura+Etoricoxibe que receberam diclofenaco de potássio e etoricoxibe, respectivamente, suspensos em CMC 0,5% (10 mg/kg/dia). 7, 14 e 21 dias após colocação de ligadura bilateral na região cevical dos primeiros molares inferiores, os animais foram submetidos à eutanásia. No fim de cada período, as mandíbulas foram coletadas para exame radiográfico de perda óssea alveolar. Em adição, osso alveolar e ligamento periodontal foram coletados para determinar a expressão da enzima COX-2, e o tecido gengival foi coletado para determinar a expressão de PGE2. Animais submetidos à indução da doença periodontal pela ligadura (Grupo Ligadura) apresentaram um aumento significativo da expressão gênica de COX-2 nos dias 7, 14 e 21 (p<0,05). Todavia, ambos os tratamentos resultaram em uma significativa redução da perda óssea alveolar em comparação ao grupo Ligadura (p<0,05). Esse estudo mostrou que ambos os fármacos foram capazes de reduzir a perda óssea alveolar após indução da doença periodontal.


Subject(s)
Animals , Male , Rats , Periodontitis , Alveolar Bone Loss , Rats, Wistar , Cyclooxygenase 2 , Gingiva
9.
Pesqui. bras. odontopediatria clín. integr ; 19(1): 4773, 01 Fevereiro 2019. tab, graf
Article in English | LILACS, BBO | ID: biblio-998267

ABSTRACT

Objective: To elicit the structure of isolated compounds from roots of sidaguri (Sida rhombifolia Linn). Material and Methods: Several organic standard protocols were involved, including extraction, fractionation, and phytochemical testing. Further spectroscopy methods, FTIR and 1HNMR, were used to determine the predicted structure of molecules, while their ability to inhibit cyclooxygenase (COX 1 and 2) were tested using in vitro method. Results: Overall assessments showed that the structure of the sidaguri is a long chain aliphatic carboxylic acid and identified as Z-3, 6, 6 trimethylhept-2-en-1-ol (T12) and nonanoic (T13). Both isolates significantly inhibit COX-1 and COX-2 non-selectively (the COX-1/COX-2 ratio for T12 was 0.91 and 0.82; while COX-1/COX-2 ratio for T13 was 0.89 and 0.87 at concentrations of 0.05 and 0.025 µg/mL respectively). Conclusion: The active compounds of Sidaguri have antiinflammatory effect by inhibiting COX non-selectively.


Subject(s)
Spectrum Analysis/methods , Cyclooxygenase 1 , Cyclooxygenase 2 , Anti-Inflammatory Agents , In Vitro Techniques/methods , Indonesia
10.
Säo Paulo med. j ; 137(1): 33-38, Jan.-Feb. 2019. tab
Article in English | LILACS | ID: biblio-1004740

ABSTRACT

ABSTRACT BACKGROUND: There are cases of colorectal tumors that, although small, show more aggressive evolution than large tumors. This motivated us to study whether there are any proteins capable of alerting about these changes. The aim here was to correlate the immunoexpression of the TS, p53, COX2, EGFR, MSH6 and MLH1 biomarkers in tumors in patients with colorectal adenocarcinoma, with the degree of cell differentiation, tumor staging and clinical-pathological prognostic factors. DESIGN AND SETTING: Retrospective observational study at a public tertiary-level hospital. METHODS: We analyzed tissue-microarray paraffin blocks of tumor tissues that had been resected from 107 patients. We used Fisher's exact test to study associations between tumor differentiation/staging and the immunoexpression of biomarkers. We also used Kaplan-Meier estimation, the log-rank test and the adjusted Cox regression model to investigate the patients' overall survival (in months) according to biomarkers and disease-free interval. RESULTS: The degree of tumor differentiation and tumor staging were not associated with the biomarkers, except in cases of patients in stages III or IV, in which there was a correlation with MLH1 expression (P=0.021). Patient survival and disease-free interval were not associated with the biomarkers. CONCLUSION: There were no associations between the degree of tumor differentiation, staging, length of survival or disease-free interval and the immunoexpression of the TS, p53, COX2, EGFR or MSH6 tumor markers. In advanced cases of colorectal adenocarcinoma (stages III and IV), there was a higher percentage of MLH1-negative results.


Subject(s)
Humans , Male , Female , Adult , Middle Aged , Aged , Aged, 80 and over , Young Adult , Colorectal Neoplasms/mortality , Colorectal Neoplasms/pathology , Adenocarcinoma/pathology , Biomarkers, Tumor/analysis , Reference Values , Thymidylate Synthase/analysis , Immunohistochemistry , Adenocarcinoma/mortality , Proportional Hazards Models , Retrospective Studies , Longitudinal Studies , Tumor Suppressor Protein p53/analysis , Tissue Array Analysis , DNA-Binding Proteins/analysis , Cyclooxygenase 2/analysis , Kaplan-Meier Estimate , ErbB Receptors/analysis , MutL Protein Homolog 1/analysis , Neoplasm Staging
11.
Article in English | WPRIM | ID: wpr-741650

ABSTRACT

Inula helenium L. is rich source of eudesmane-type sesquiterpene lactones, mainly alantolactone and isoalantolactone, which have the various pharmacological functions. In this study, we examined the inhibitory effects of nitric oxide (NO) production of hexane, methylene chloride, ethyl acetate, butanol, and water fractions from I. helenium and investigated the anti-inflammatory effect of hexane fraction of I. helenium (HFIH) in LPS-induced RAW 264.7 cells. Quantification of alantolactone and isoalantolactone from HFIH was carried out for the standardization by multiple reaction monitoring using triple quadrupole mass spectrometer. HFIH significantly inhibited inducible NO synthase (iNOS) and cyclooxygenase-2 (COX-2) protein as well as their downstream products NO and prostaglandin E₂ (PGE₂) in LPS-stimulated RAW 264.7 cells. Moreover, HFIH suppressed NF-κB transcriptional activity by decreasing the translocation of p65 to the nucleus. The in vivo study further confirmed that HFIH attenuated the paw edema induced by carrageenan in an acute inflammation model. These findings suggest that HFIH may be useful as a promising phytomedicine for inflammatory-associated diseases.


Subject(s)
Carrageenan , Cyclooxygenase 2 , Edema , Inflammation , Inula , Lactones , Methylene Chloride , Nitric Oxide , Nitric Oxide Synthase , Staphylococcal Protein A , Water
12.
Article in English | WPRIM | ID: wpr-741642

ABSTRACT

The present study was conducted to investigate anti-nociceptive and anti-inflammatory effects of the leaves of Ilex latifolia Thunb (I. latifolia) in in vivo and in vitro. Writhing responses induced by acetic acid and formalin- and thermal stimuli (tail flick and hot plate tests)-induced pain responses for nociception were evaluated in mice. I. latifolia (50 – 200 mg/kg, p.o.) and ibuprofen (100 mg/kg, p.o.), a positive non-steroidal anti-inflammatory drug (NSAID), inhibited the acetic acid-induced writhing response and the second phase response (peripheral inflammatory response) in the formalin test, but did not protect against thermal nociception and the first phase response (central response) in the formalin test. These results show that I. latifolia has a significant anti-nociceptive effect that appears to be peripheral, but not central. Additionally, I. latifolia (50 and 100 µg/mL) and 3,5-di-caffeoyl quinic acid methyl ester (5 µM) isolated from I. latifolia as an active compound significantly inhibited LPS-induced NO production and mRNA expression of the pro-inflammatory mediators, iNOS and COX-2, and the pro-inflammatory cytokines, IL-6 and IL-1β, in RAW 264.7 macrophages. These results suggest that I. latifolia can produce antinociceptive effects peripherally, but not centrally, via anti-inflammatory activity and supports a possible use of I. latifolia to treat pain and inflammation.


Subject(s)
Acetic Acid , Animals , Cyclooxygenase 2 , Cytokines , Ibuprofen , Ilex , In Vitro Techniques , Inflammation , Interleukin-6 , Macrophages , Mice , Nitric Oxide , Nociception , Pain Measurement , Quinic Acid , RNA, Messenger
13.
Article in Korean | WPRIM | ID: wpr-766388

ABSTRACT

There have been no published studies concerning the anti-inflammatory effects of corn silk on colon cancer cells. Thus, this study was conducted to investigate the effect of corn silk extract containing high levels of maysin on inflammation and its mechanism of action in colon cancer cells. SW 480 human colon cancer cells were treated with 1 µg/mL of lipopolysaccharide (LPS) to induce inflammation, and next they were treated with different concentrations of corn silk extract (0, 5, 10 and 15 µg/mL). The concentrations of nitric oxide (NO) were determined. The mRNA expressions of inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor α (TNF-α), interleukin-1beta (IL-1β) and interleukin-6 (IL-6), were determined. Western blot analysis was performed to determine the protein expressions of nuclear factor-kappa B (NF-κB) and mitogen-activated protein kinases, and the latter consists of extracellular signal-related kinase (ERK), c-jun NH2-terminal kinase (JNK) and p38 MAP kinase (p38). The concentration of NO and the mRNA expression of iNOS were significantly and dose-dependently decreased in the corn silk-treated groups (P<0.05). The mRNA expression of TNF-α, IL-1β and IL-6 were significantly increased in the LPS-treated group (P<0.05), but these expressions were significantly and dose-dependently decreased in the corn silk treated groups (P<0.05). The protein expressions of NF-κB (in a dose-dependent fashion), ERK (at 10 and 15 µg/mL), JNK (at 15 µg/mL) and p38 (at 10 and 15 µg/mL) were significantly decreased with corn silk treatments (P<0.05). In conclusion, corn silk extract containing high levels of maysin seems to inhibit the LPS-induced inflammatory responses in SW480 colon cancer cells via the NF-κB pathway.


Subject(s)
Blotting, Western , Colon , Colonic Neoplasms , Cyclooxygenase 2 , Cytokines , Gene Expression , Humans , Inflammation , Interleukin-1beta , Interleukin-6 , Mitogen-Activated Protein Kinases , Nitric Oxide , Nitric Oxide Synthase Type II , p38 Mitogen-Activated Protein Kinases , Phosphotransferases , RNA, Messenger , Saccharin , Silk , Tumor Necrosis Factor-alpha , Zea mays
14.
Acta Physiologica Sinica ; (6): 361-370, 2019.
Article in Chinese | WPRIM | ID: wpr-777178

ABSTRACT

Prostaglandin E2 (PGE2) is a cyclooxygenase metabolite of arachidonic acid. It acts as a bioactive lipid and plays an important role in regulating many biological processes. PGE2 binds to 4 different G protein-coupled receptors including prostaglandin E2 receptor subtypes EP1, EP2, EP3 and EP4. The EP4 receptor is widely expressed in most of human organs and tissues. Increasing evidence demonstrates that EP4 is essential for cardiovascular homeostasis and participates in the pathogenesis of many cardiovascular diseases. Here we summarize the role of EP4 in the regulation of cardiovascular function and discuss potential mechanisms by which EP4 is involved in the development of cardiovascular disorders with a focus on its effect on inflammation.


Subject(s)
Cardiovascular Diseases , Cyclooxygenase 2 , Dinoprostone , Physiology , Humans , Receptors, Prostaglandin E, EP4 Subtype , Physiology
15.
Acta Physiologica Sinica ; (6): 689-697, 2019.
Article in English | WPRIM | ID: wpr-777142

ABSTRACT

The aim of the present study was to investigate the role of ferroptosis in acute lung injury (ALI) mouse model induced by oleic acid (OA). ALI was induced in the mice via the lateral tail vein injection of pure OA. The histopathological score of lung, lung wet-dry weight ratio and the protein content of bronchoalveolar lavage fluid (BALF) were used as the evaluation indexes of ALI. Iron concentration, glutathione (GSH) and malondialdehyde (MDA) contents in the lung tissues were measured using corresponding assay kits. The ultrastructure of pulmonary cells was observed by transmission electron microscope (TEM), and the expression level of prostaglandin-endoperoxide synthase 2 (PTGS2) mRNA was detected by quantitative polymerase chain reaction (q-PCR). Protein expression levels of glutathione peroxidase 4 (GPX4), ferritin and transferrin receptor 1 (TfR1) in lung tissues were determined by Western blot. The results showed that histopathological scores of lung tissues, lung wet-dry weight ratio and protein in BALF in the OA group were higher than those of the control group. In the OA group, the mitochondria of pulmonary cells were shrunken, and the mitochondrial membrane was ruptured. The expression level of PTGS2 mRNA in the OA group was seven folds over that in the control group. Iron overload, GSH depletion and accumulation of MDA were observed in the OA group. Compared with the control group, the protein expression levels of GPX4 and ferritin in lung tissue were down-regulated in the OA group. These results suggest that ferroptosis plays a potential role in the pathogenesis of ALI in our mouse model, which may provide new insights for development of new drugs for ALI.


Subject(s)
Acute Lung Injury , Pathology , Animals , Apoptosis , Bronchoalveolar Lavage Fluid , Chemistry , Cyclooxygenase 2 , Metabolism , Ferritins , Metabolism , Glutathione , Glutathione Peroxidase , Metabolism , Iron , Iron Overload , Lung , Cell Biology , Pathology , Malondialdehyde , Mice , Microscopy, Electron, Transmission , Mitochondrial Membranes , Oleic Acid
16.
Article in English | WPRIM | ID: wpr-776865

ABSTRACT

In the present study, we investigated anti-inflammatory effect of Cardamine komarovii flower (CKF) on lipopolysaccharide (LPS)-induced acute lung injury (ALI). We determined the effect of CKF methanolic extracts on LPS-induced pro-inflammatory mediators NO and prostaglandin E2 (PGE2), production of pro-inflammatory cytokines (IL-1β, TNF-α, and IL-6), and related protein expression levels of MyD88/TRIF signaling pathways in peritoneal macrophages (PMs). Nuclear translocation of NF-κB-p65 was analyzed by immunofluorescence. For the in vivo experiments, an ALI model was established to detect the number of inflammatory cells and inflammatory factors (IL-1β, TNF-α, and IL-6) in bronchoalveolar lavage fluid (BALF) of mice. The pathological damage in lung tissues was evaluated through H&E staining. Our results showed that CKF can decrease the production of inflammatory mediators, such as NO and PGE2, by inhibiting their synthesis-related enzymes iNOS and COX-2 in LPS-induced PMs. In addition, CKF can downregulate the mRNA levels of IL-1β, TNF-α, and IL-6 to inhibit the production of inflammatory factors. Mechanism studies indicated that CKF possesses a fine anti-inflammatory effect by regulating MyD88/TRIF dependent signaling pathways. Immunocytochemistry staining showed that the CKF extract attenuates the LPS-induced translocation of NF-kB p65 subunit in the nucleus from the cytoplasm. In vivo experiments revealed that the number of inflammatory cells and IL-1β in BALF of mice decrease after CKF treatment. Histopathological observation of lung tissues showed that CKF can remarkably improve alveolar clearance and infiltration of interstitial and alveolar cells after LPS stimulation. In conclusion, our results suggest that CKF inhibits LPS-induced inflammatory response by inhibiting the MyD88/TRIF signaling pathways, thereby protecting mice from LPS-induced ALI.


Subject(s)
Acute Lung Injury , Drug Therapy , Genetics , Metabolism , Adaptor Proteins, Vesicular Transport , Genetics , Metabolism , Animals , Anti-Inflammatory Agents , Chemistry , Cardamine , Chemistry , Cyclooxygenase 2 , Genetics , Metabolism , Female , Flowers , Chemistry , Humans , Lipopolysaccharides , Male , Mice , Myeloid Differentiation Factor 88 , Genetics , Metabolism , NF-kappa B , Genetics , Metabolism , Nitric Oxide Synthase Type II , Genetics , Metabolism , Plant Extracts , Chemistry , Signal Transduction , Tumor Necrosis Factor-alpha , Genetics , Metabolism
17.
Article in Chinese | WPRIM | ID: wpr-776528

ABSTRACT

OBJECTIVE@#To investigate the effects of apple polyphenols on pulmonary vascular remodeling in rats with pulmonary arterial hypertension and its mechanism.@*METHODS@#Rats were randomly divided into 4 groups:control (Con) group, monocrotaline (MCT) group, apple polyphenol (APP) group,monocrotaline + apple polyphenol (MCT+APP) group. In Con group, rats received a subcutaneous injection of physical saline. In APP group, rats received intraperitoneal injection of 20 mg/kg APP, every other day. In MCT group, rats received a single subcutaneous injection of MCT(60 mg/kg). In MCT+APP group, rats received subcutaneous injection of 60 mg/kg MCT followed by an intraperitoneal injection of 20 mg/kg APP every other day. All the disposal lasted 3 weeks. Then the PAH-relevant indicators, such as mean pulmonary artery pressure(mPAP), pulmonary vascular resistance(PVR), right ventricular hypertrophy index (RVHI) ,wall thickness (WT%) and wall area (WA%) were tested. After that, the inflammatory pathway related indicators, such as interleukin1(IL-1),interleukin1(IL-6), tumor necrosis factor α(TNF-α), cyclooxygenase 2(COX-2) and myeloperoxidase(MPO) in pulmonary tissue and free intracellular Ca in pulmonary smooth muscle cell(PASMC), content of eNOS and NO in endothelial cells were determined.@*RESULTS@#Compared with the control group, the levels of mPAP, PVR, RVHI, WA%, WT%, and IL-1, IL-6, TNF-α, COX-2, MPO in tissue and the expression of Ca in PASMC of MCT group were increased significantly, while the contents of eNOS and NO in endothelial cells were decreased significantly (P<0.05). Compared with the MCT group, the apple polyphenol treatment could improve the above mentioned situation, and the COX-2 and Ca indicators of the apple polyphenol treatment group were decreased significantly (P<0.05).@*CONCLUSION@#MCT can increase COX-2 expression and intracellular Ca in pulmonary artery smooth muscle cells, decrease the contents of eNOS and NO in endothelial cells, while apple polyphenols can significantly inhibit these effects.


Subject(s)
Animals , Calcium , Metabolism , Cyclooxygenase 2 , Metabolism , Cytokines , Metabolism , Malus , Chemistry , Monocrotaline , Nitric Oxide , Metabolism , Nitric Oxide Synthase Type III , Metabolism , Polyphenols , Pharmacology , Pulmonary Artery , Pathology , Random Allocation , Rats , Vascular Remodeling
18.
Article in English | WPRIM | ID: wpr-763025

ABSTRACT

We attempted to examine anti-inflammatory and anti-oxidant effects of 4′-O-β-D-glucosyl-5-O-methylvisamminol (GOMV), the first epigenetic inhibitor of histone phosphorylation at Ser10. While GOMV did not affect the viability of murine macrophage RAW 264.7 cells, it significantly suppressed lipopolysaccharide (LPS)-induced generation of prostaglandin E₂ (PGE₂) and nitric oxide (NO) through transcriptional inhibition of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS). GOMV also scavenged free radicals in vitro, increased NF-E2-related factor 2 (NRF2), and activated antioxidant response element (ARE), thereby resulting in the induction of phase II cytoprotective enzymes in human keratinocyte HaCaT cells. Finally, GOMV significantly protected HaCaT cells against 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced oxidative intracellular damages. Together, our results illustrate that GOMV possesses anti-inflammatory and anti-oxidant activity.


Subject(s)
Antioxidant Response Elements , Antioxidants , Cyclooxygenase 2 , Epigenomics , Free Radicals , Histones , Humans , In Vitro Techniques , Keratinocytes , Macrophages , NF-E2-Related Factor 2 , Nitric Oxide , Nitric Oxide Synthase Type II , Phosphorylation
19.
Article in English | WPRIM | ID: wpr-761901

ABSTRACT

BACKGROUND: Preterm labor is a leading risk factor for neonatal death and long-term impairment and linked closely with inflammation. Non-obstetric surgery is occasionally needed during pregnancy and the anesthetic drugs or surgery itself can give rise to inflammation. Here, we examined the influence of propofol pretreatment on the expression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) after lipopolysaccharide (LPS) stimulation. In addition, we evaluated the expression of pro-inflammatory cytokines and nuclear factor kappa B (NF-κB). METHODS: Human amnion-derived WISH cells were used to investigate the effect of propofol on the LPS-induced expression of inflammatory substances involved in preterm labor. For the experiment, WISH cells were pretreated with various concentrations propofol (0.01–10 µg/ml) for 1 h and then treated with LPS (1 µg/ml) for 24 h. Cytotoxicity was evaluated using MTT assay. PGE2 concentration was assessed by ELISA. Protein expressions of COX-2, PGE2 and NF-κB were analyzed by western blotting analysis. RT-PCR was used for analysis of mRNA expression of COX-2, PGE2, interlukin (IL)-1β and tumor necrosis factor (TNF)-α. RESULTS: Propofol showed no cytotoxicity on the WISH cells. LPS-induced PGE2 production and COX-2 and PGE2 expression were decreased after propofol pretreatment. Propofol also attenuated the LPS-induced mRNA expression of IL-1β and TNF-α. Moreover, the activation of NF-jB was inhibited by propofol pretreatment on LPS-stimulated WISH cells. CONCLUSION: We demonstrated that propofol suppresses the expression of inflammatory substances enhanced by LPS stimulation. Furthermore, this inhibitory effect of propofol on the inflammatory substance expression is mediated by suppression of NF-κB activation.


Subject(s)
Amnion , Anesthetics , Blotting, Western , Cyclooxygenase 2 , Cytokines , Dinoprostone , Enzyme-Linked Immunosorbent Assay , Female , Humans , Inflammation , NF-kappa B , Obstetric Labor, Premature , Perinatal Death , Pregnancy , Propofol , Risk Factors , RNA, Messenger , Tumor Necrosis Factor-alpha
20.
Article in English | WPRIM | ID: wpr-761814

ABSTRACT

Macrophage-associated inflammation is crucial for the pathogenesis of diverse diseases including metabolic disorders. Rhodanthpyrone (Rho) is an active component of Gentiana rhodantha, which has been used in traditional Chinese medicine to treat inflammation. Although synthesis procedures of RhoA and RhoB were reported, the biological effects of the specific compounds have never been explored. In this study, the anti-inflammatory activity and mechanisms of action of RhoA and RhoB were studied in lipopolysaccharide (LPS)-stimulated macrophages. Pretreatment with RhoA and RhoB decreased inducible nitric oxide synthase and cyclooxygenase-2 expressions in RAW 264.7 cells and in thioglycollate-elicited mouse peritoneal macrophages. In addition, it downregulated transcript levels of several inflammatory genes in LPS-stimulated RAW 264.7 cells, including inflammatory cytokines/chemokines (Tnfa, Il6, and Ccl2) and inflammatory mediators (Nos2 and Ptgs2). Macrophage chemotaxis was also inhibited by treatment with the compounds. Mechanistic studies revealed that RhoA and RhoB suppressed the nuclear factor (NF)-κB pathway, but not the canonical mitogen activated protein kinase pathway, in LPS-stimulated condition. Moreover, the inhibitory effect of RhoA and RhoB on inflammatory gene expressions was attenuated by treatment with an NF-κB inhibitor. Our findings suggest that RhoA and RhoB play an anti-inflammatory role at least in part by suppressing the NF-κB pathway during macrophage-mediated inflammation.


Subject(s)
Animals , Chemotaxis , Cyclooxygenase 2 , Gene Expression , Gentiana , Inflammation , Interleukin-6 , Macrophages , Macrophages, Peritoneal , Medicine, Chinese Traditional , Mice , Nitric Oxide Synthase Type II , Protein Kinases
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