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Objective:To investigate the effects of Guchisan combined with orthodontics therapy on serum tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) levels. Methods:Sixty-six patients with chronic periodontitis who received treatment in Zhejiang Xin'an International Hospital between July 2013 and July 2019 were included in this study. They were randomly divided into control group ( n = 33) and treatment group ( n = 33). Both control and treatment groups received conventional interventions. The control group was treated with orthodontics therapy. The treatment group was treated with Guchisan (0.5 g once, twice a day, 2-3 minutes once) based on orthodontics therapy for 1 month. Gingival index, probing depth, attachment loss, plaque index, gingival bleeding index, and latency to symptom improvement were compared between the two groups. Clinical efficacy was compared between the two groups. Serum IL-1β and TNF-α levels were measured in each group. Results:After treatment, gingival index [(0.51 ± 0.06) vs. (1.12 ± 0.15), t = 21.69], probing depth [(2.01 ± 0.22) mm vs. (2.67 ± 0.30) mm, t = 6.50], attachment loss [(1.10 ± 0.13) mm vs. (1.70 ± 0.18) mm, t = 9.90], plaque index [(0.47 ± 0.05) vs. (1.08 ± 0.13), t = 25.57], and gingival bleeding index [(0.58 ± 0.07) vs. (1.09 ± 0.13), t = 19.84] were significantly lower than those in the control group (all P < 0.01). Latency to tooth loosening [(8.81 ± 0.96) days vs. (13.03 ± 1.62) days, t = 15.01], halitosis [(3.04 ± 0.33) days vs. (7.03 ± 0.76) days, t = 27.66], and swollen gums [(2.21 ± 0.24) days vs. (4.55 ± 0.51) days, t = 23.85] were significantly shorter than those in the control group (all P < 0.01). Total response rate in the treatment group was significantly higher than that in the control group (93.94% vs. 69.70%, χ2 = 4.99, P = 0.025). After treatment, serum levels of TNF-α [(4.01 ± 0.44) ng/L vs. (5.31 ± 0.58) ng/L, t = 10.26] and IL-1β [(16.04 ± 1.97) mg/L vs. (18.30 ± 2.55) mg/L, t = 4.03] in the treatment group were significantly lower than those in the control group (both P < 0.01). Conclusion:Based on conventional treatment, Guchisan combined with orthodontics therapy for treatment of chronic periodontitis with syndrome of excessive stomach fire can greatly improve symptoms of periodontal disease and enhance clinical efficacy. Lowering serum TNF-α and IL-1β levels may be one of effective action ways of this combined therapy.
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Aim To discuss the effect of miR-199/ SIRT1/MFN2 signaling pathway on the progression of NASH and its related mechanisms.Methods 45 BALB/e mice were randomly divided into normal group, high fat diet(HFD) group, total saponins of panax japonicas ( TSPJ ) low-dose group ( 15 mg • kg-1) and TSPJ high-dose group (45 mg • kg"1 ).Normal group was given normal diet, while HFD group, TSPJ low-dose and high-dose groups were given high-fat diet.The mice were intragastrioally given 15 and 45 mg 'kg"1 TSPJ (dissolved in saline) daily in TSPJ low-dose and high-dose groups, while those in other groups were intragastric ally given the same a- mount of saline daily.After seven months, they were sacrificed for serum collection and hepatic tissue col¬lection.Results HE staining showed that liver lipido¬sis and inflammation were obvious in HFD group.while liver lipidosis anrl inflammation were alleviated in TSPJ group.MFN2 and SIRT1 levels significantly de¬creased.TNF-a, 1L-1 p , SREBP, ChREBP levels sig¬nificantly increased in HFD group.After treated with TSPJ, SIRT1 and MFN2 levels were significantly up- regulated , while TNF-a, IL-ip, ChREBP and SREBP levels were significantly down-regulated.The Immuno¬fluorescence results showed that the fluorescence inten¬sity of MFN2 and SIR 11 increased in TSPJ low-dose and high-dose groups.At mRNA level, miR-199 had a negative regulatory relationship with SIRT1.Conclu¬sions TSPJ can alleviate NASH induced by high fat diet through miR-199/SIRTl/MFN2 signaling path¬way.
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Aim To explore the effect of aucubin aucubin (AU), one of the effective ingredients of eucommia, plantain, rehmannia and other herbs, on cardiomyocyte apoptosis and cardiac function after acute myocardial infarction (MI) and the possible mechanisms. Methods In this study, the mouse models of MI were established by ligation of the anterior descending branch of the left coronary artery. Left ventricular function and the infarct size were detected using echocardiography and Masson staining. A Tumor necrosis factor-a (TNF-ot)/cycloheximide (C H X) model of cardiomyocyte injury was established, and the effects AU on myocardial injury were examined using IncuCyte live cell imaging, Western blot and TUNEL staining. Results AU administration dramatically improved cardiac function recovery and decreased infarct size after MI. AU inhibited the apoptosis of cardiomyocytes, reduced the expressions of caspase-3, and significantly increased the ratio of Bcl-2/Bax induced by TNF-ot/ CHX. Meanwhile, the estrogen receptor ß (ERß) protein level was elevated by AU, and the antiapoptotic effect of AU was blocked by ERß inhibitor. Conclusions AU can alleviate MI injury and improve cardiac function via inhibiting the apoptosis of cardiomyocytes, and its mechanism is the activation of ERß pathway.
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BACKGROUND: Currently, studies have focused on the role and mechanism of nuclear factor-kappa B pathway in the pathological process of acute lung injury in burned rats, such as the targeting inhibition of kB kinase by miR-155, which further weakens the activity of nuclear factor-KB and plays a role in acute lung injury in burned rats. However, there are still some pathological mechanisms to be studied and confirmed. OBJECTIVE: To investigate the effect of miR-155 on acute lung injury in burned rats through nuclear factor-KB pathway. METHODS: The rat models of acute lung injury were established by warm water bath simulating bum injury. The burned rats were divided into acute lung injury, miR-155-mimics and miR-155-inhibitor groups. After fluid resuscitation, the rats in the miR-155-mimics and miR-155-inhibitor groups were injected into the tail vein of 5 |_iL of miR-155-mimics and miR-155-inhibitions, respectively. The expression levels of tumor necrosis factor-a and interleukin-1 p in bronchoalveolar lavage fluid were detected by ELISA. The lung morphology in the three groups was observed by hematoxylin-eosin staining. The protein expression levels of nuclear factor-KB and cyclooxygenase 2 were evaluated by western blot assay. The nuclear factor-KB protein in lung tissues was detected by immunohistochemistry. RESULTS AND CONCLUSION: (1) The results of hematoxylin-eosin staining showed that the severity of lung injury in the miR-155-inhibitor group, acute lung injury group and the miR-155-mimics group was increased gradually (P < 0.05). (2) ELISA results showed that compared with the acute lung injury group, the expression levels of tumor necrosis factor-a and interleukin-1 p were increased in the miR-155-mimics group (P < 0.05), and decreased in the miR-155-inhibitor group (P < 0.05). (3) Western blot assay results showed that compared with the acute lung injury group, the expression levels of nuclear factor-KB and cyclooxygenase 2 proteins were increased in the miR-155-mimics group (P < 0.05), and decreased in the miR-155-inhibitor group (P < 0.05). (4) Immunohistochemical results showed that the expression level of nuclear factor-KB was increased in the miR-155-inhibitor group, which was dark brown. The expression of nuclear factor-KB in cytoplasm and nucleus of neutrophils, mononuclear macrophages, alveolar epithelial cells was the most obvious. (5) These results indicate that in lung tissue cells, decreased miR-155 can down-regulate nuclear factor-KB activity, which reduces the inflammatory response of the lung between the damaged tissue. The study was approved by the Laboratory Animal Ethics Committee of the First People’s Hospital of Neijiang, approval No. 1801270.
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Objective: To explore the protective effect of glutamine (GLN) on the hyperoxia lung injury in the neonatal rats, and to elucidate its mechanism. Methods: A total of 90 male and female Wistar rats were selected and randomly divided into control group (FiO2: = 21%). hyperoxia group ( FiO2: > 85%) and hyperioxia + glutamine (GLN) group (FiO2: > 85%) (n=30). The rats in hyperioxia group and hyperioxia + GLN groups were used to establish the models of hyperoxia lung injury (HALI). The rats in hyperoxia+ GLN group were intraperitoneally injected with 0. 75 g • kg-1 • d-1 GLN from the first day of experiment, and the rats in other two groups were abdominally injected with the same volume of normal saline. The body weights, water contents in the lung tissue of the neonatal rats in various groups on the 3rd. 7th. and 14th days of the experiment were measured. I IF staining was used to determine the morphology of lung tissue of the rats in various groups; ELISA was used to detect the levels of interleukin-6 (IL-6)∗ interleukin-1|ß (IL-lf3) and tumor necrosis factor-a (TNF-a) in the lung tissue homogenate of the rats in various groups. Results: Compared with control group at the same time, the weights of the neonatal rats in hyperoxia group were significantly decreased on the 3rd. 7th and 14th days ( P∗CO. 05); the body weights of neonatal rats in hyperoxia + GLN group were significantly higher than those in hyperoxia group at the same time (P<0. 05). On the 3rd. 7th. and 14th days, the water contents of lung tissue of the rats in hyperoxia group were higher than those in control group at the same time ( P< 0. 05). and the difference was gradually increased with the prolongation of time; the water contents of lung tissue of the rats in hyperoxia • GLN group were significantly lower than those in hyperoxia group ( P
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Objective: To investigate the effects of Jiawei Danshen Yin on the cardiac function and serum inflammatory factors interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-α) in the rats with chronic heart failure, and to elucidate the mechanism of Jiawei Danshen Yin in the treatment of chronic heart failure. Methods: The SD rats were randomly divided into blank control group, heart failure model group, captopril group, and Low medium, and high doses of Jiawei Danshen Yin groups. The rat models of chronic heart failure were prepared by intraperitoneal injection of adriamycin solution for 4 weeks. The left ventricular ejection fraction (LVEF) of the rats was measured by echocardiography. The heart rate (HR), cardiac output (CO), systolic blood pressure (SBP), carotid artery diastolic pressure (DBF), left ventricular end diastolic pressure (LVEDP), left ventricular systolic pressure (LVSP) left ventricular pressure change maximum increase/decrease rate (±dp/dtmax) and other related hemodynamic parameters were measured by ventilator in each group to assess the rat heart function. The levels of inflammatory cytokines IL-6 and TNF-α were detected by enzyme-linked immunosorbent assay (ELISA). Results: Compared with blank control group, the LVEF of the rats in model group, captopril groups and low, medium, and high doses of Jiawei Danshen Yin groups were decreased (P<0. 05). Compared with model group, the LVEF of the rats in captopril group and low, medium, and high doses of Jiawei Danshen Yin groups were increased (P<0. 05). The HR, SBF, DBF, CO, LVSPt and ±dp/dtmax of the rats in model group were lower than those in blank control group (P<0. 05), while the LVEDP was increased ( P
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Objective: In this study, we investigated the changes in peripheral blood inflammatory factors and intestinal flora in acquired immune deficiency syndrome (AIDS) and human immunodeficiency virus (HIV)-positive individuals (AIDS/HIV patients), and explored the relationships among intestinal flora, peripheral blood inflammatory factors, and CD4+ T lymphocytes. Methods: Thirty blood and stool samples from an AIDS group and a control group were collected. The levels of tumor necrosis factor-a (TNF-a) and interleukin-6 (IL-6) were determined by enzyme-linked immunosorbent assay (ELISA), and the number of CD4+ T lymphocytes by a FACSCount automated instrument. Quantitative real-time polymerase chain reaction (qRT-PCR) was used to determine the messenger RNA (mRNA) levels of Bifidobacterium, Lactobacillus, Escherichia coli, Enterococcus faecalis, and Enterococcus faecium. Correlations among intestinal flora, inflammatory factor levels, and CD4+ T lymphocyte values were evaluated using the Spearman correlation coefficient. Results: The levels of TNF-a and IL-6 in the AIDS group were higher than those in the control group, while the number of CD4+ T lymphocytes was lower. The amounts of Bifidobacterium and Lactobacillus in the AIDS group were significantly lower than those in control group, while the amounts of E. coli, E. faecalis, and E. faecium were much higher. The amounts of Bifidobacterium and Lactobacillus were negatively correlated with the content of TNF-a and IL-6 and the CD4+ T lymphocyte count, while those correlations were reversed for E. coli, E. faecalis, and E. faecium. Conclusions: The intestinal microbiota of AIDS/HIV patients were disordered, and there was a correlation between the amount of intestinal flora and the number of CD4+ T lymphocytes and the levels of TNF-a and IL-6.
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Objective:To investigate the effect of Manchu medicine north-Schisandra chinensis polysaccharide (NSCP) on the human neutrophils treated by lipopolysaccharide (LPS) cultivated in vitro,and to elucidate its anti inflammatory mechanism.Methods:The neutrophilic inflammatory cell model was established with LPS.The experiment included control group,LPS group (1.0 mg · L-1) and NSCP group (1.25,2.50 and 5.00 g · L-1),the cells in NSCP group were first treated with LPS for 60 min,and then treated with different concentrations of NSCP.The levels of TNF-α in neutrophils were measured with ELISA and the apoptotic rates were detected by flow cytometry.Results:The level of TNF-a in LPS group was increased compared with control group (P＜0.05).The level of TNF-α in NSCP group was decreased compared with LPS group (P＜0.05).The apoptotic rate in LPS group was decreased compared with control group (P＜0.05);the apoptotic rates in NSCP group were increased with the increasing of time and dose,and the best effect was found 16 h after treatment with 5 g · L-1NSCP:the apoptotic rate in NSCP group was significantly increased compared with LPS group (P＜0.05).Conclusion:NSCP can perform the anti-inflammation effect through the suppression of LPS-induced TNF-α secretion in neutrophils and the promotion of neutrophils apoptosis.
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Objective:To investigate the effect of Manchu medicine north-Schisandra chinensis polysaccharide (NSCP) on the human neutrophils treated by lipopolysaccharide (LPS) cultivated in vitro,and to elucidate its anti inflammatory mechanism.Methods:The neutrophilic inflammatory cell model was established with LPS.The experiment included control group,LPS group (1.0 mg · L-1) and NSCP group (1.25,2.50 and 5.00 g · L-1),the cells in NSCP group were first treated with LPS for 60 min,and then treated with different concentrations of NSCP.The levels of TNF-α in neutrophils were measured with ELISA and the apoptotic rates were detected by flow cytometry.Results:The level of TNF-a in LPS group was increased compared with control group (P＜0.05).The level of TNF-α in NSCP group was decreased compared with LPS group (P＜0.05).The apoptotic rate in LPS group was decreased compared with control group (P＜0.05);the apoptotic rates in NSCP group were increased with the increasing of time and dose,and the best effect was found 16 h after treatment with 5 g · L-1NSCP:the apoptotic rate in NSCP group was significantly increased compared with LPS group (P＜0.05).Conclusion:NSCP can perform the anti-inflammation effect through the suppression of LPS-induced TNF-α secretion in neutrophils and the promotion of neutrophils apoptosis.
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OBJECTIVE@#To simulate the expression of TNF-α and PGE2 of periodontal tissues in rat periodontitis model.@*METHODS@#40 Wistar rats were randomly divided into the periodontitis group and the control group (n=20). After the successful establishment of periodontitis rat model, raising for six weeks before the animals were sacrificed. The periodontal tissues were obtained and made into slices. Observed the histopathological changes of the periodontal tissues and measured TNF-α, PGE2 levels change by immunohistochemistry, Western blot analysis and ELISA.@*RESULTS@#TNF-α, PGE2 expression of the periodontitis group was significantly higher than that in the control group, the difference was significant (P<0.05).@*CONCLUSIONS@#The TNF-α, PGE2 expression of the rat periodontal tissue in the periodontitis group was significantly higher than the control group.
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Animales , Masculino , Ratas , Dinoprostona , Metabolismo , Modelos Animales de Enfermedad , Inmunohistoquímica , Periodontitis , Metabolismo , Periodoncio , Química , Metabolismo , Ratas Wistar , Factor de Necrosis Tumoral alfa , MetabolismoRESUMEN
Objective To observe the effect oflipopolysaccharide (LPS) on the cell form of BV-2 cells and the expressions of interleukin-6 (IL-6) and tumor necrosis factor-a (TNF-a) so as to detect the role of silence information regulator 1 (SIRT1) in regulation of LPS-induced proinflammatory cytokines production in activated BV-2 cells.Methods BV-2 cells were divided into control group (normal culture medium) and treatment groups; BV-2 cells in the treatment groups were subdivided into LPS treatment groups,Resveratrol+LPS treatment groups and Sirtinol+LPS treatment groups (cultured with different concentrations of LPS,SIRT1 activator Resveratrol or SIRT1 inhibitor Sirtinol,respectively).MTT assay was employed to identify the cell survival after the inducement.Based on the above MTT results,the cells were then grouped into the control group,LPS treatment group,Resveratrol+LPS treatment group and Sirtinol+LPS treatment group having suitable concentrations of LPS,Resveratrol and Sirtinol; then,the levels of IL-6 and TNF-a were measured with enzyme-linked immuno sorbent assay (ELISA) at 12 and 24 h after the inducement; and the expression of SIRT1 at 24 hafter the inducement was detected by Western blotting.Results As compared with those in the control group,the BV-2 cells in the LPS treatment group had increased cell number,hypertrophic cell body,and shorten cell processes.The cell survival rate increased with increased concentrations of LPS.As compared with those in the control group,the levels of IL-6 and TNF-a in LPS treatment group increased and level of SIRT 1 decreased with significant differences (P＜0.05).Significantly increased levels of IL-6and TNF-a and obviously decreased expression of SIRT1 in the Resveratrol+LPS treatment group were noted as compared with those in the LPS treatment group (P＜0.05); conversely,significantly decreased levels of IL-6 and TNF-a and obviously increased expression of SIRT1 in the Sirtinol+LPS treatment group were noted as compared with those in the LPS treatment group (P＜0.05).Conclusion LPS can change the morphology of BV-2 cells,and induce the levels ofproinflammatory cytokines; impairment of SIRT1 may contribute to such progress obviously.
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Objective To investigate the change of adiponectin (AD),tumor necrosis factor-alpha (TNF-α) and S100 levels in serum elderly patients with rheumatoid arthritis and cerebral infarct in order to evaluate the therapeutic effect of dioscornin.Methods One hundred patients with rheumatoid arthritis and cerebral infarct were selected as our subjects,who were hospitalized in the Department of Neurology of Recovery Changzhi Municipal People's Hospital and the Department of Internal Medicine of the Affiliated Hospital of Shaoxing Medical College,between 2006 September and 2010 September.All subjects (male 55,female 45,average age of 57 years old) were randomly divided into regular and dioscomin groups,50 for per group.Patients in regular group were treated with routine therapy and patients in dioscornin groups were treated with dioscornin 80mg,three daily plus regular treatment drug.Meanwhile 40 middle patients with single rheumatoid arthritis subjects were severed as controls.The changes of BMI,fasting plasma glucose,lipid factors,insulin sensitivity index (ISI),serum adiponectin,TNF-α and serum S100B were determined at treatment before and 6 months after treatments.Results The level of TNF-α,serum S100 in ERA patients were significantly higher andAdiponectin significantly lower than that of the control group,(TNF-α:[(89.0 ± 25.3) ng/L,(88.0 ± 24.2)ng/L vs(74.0 ±21.0) ng/L,F =3.292,P ＜0.05],[S100B:(0.102 ±0.051) μg/L,(0.101 ±0.045) μg/L vs(0.092 ± 0.031) μg/L,F =2.792,P ＜ 0.05],and AD and BMI were lower [AD:(7.2 ± 1.4) μg/L,(7.3 ±1.4) μg/L vs (18.1 ± 3.5) μg/L,F =17.057,P ＜ 0.01],[BMI:(18.9 ± 2.4) kg/m2,(19.0 ± 1.9) kg/m2 vs (21.8 ± 1.8) kg/m2,F =6.147,P ＜ 0.01].There was a negative correlation between adiponect and TNF-α,S100B (r =-0.46,-0.52,P ＜ 0.01) and positive correlation between adiponect and BMI (r =0.44,P ＜0.01).The adiponectin level was significantly increased in patients for six months after dioscornin treatment than that of control group.[AD:(12.2±2.9) μg/L,(7.8 ±1.8) μg/L vs (18.0 ±4.3) μg/L,F=6.480,P＜0.01].The level of TNF-α and S100B significantly decreased than that of the control group,TNF-α:[(72.0 ±21.0) ng/L,(82.0±23.0)ng/L vs (68.0 ±20.0) ng/L,F =3.065,P ＜0.05],[S100B:(0.092 ±0.021)μg/L,(0.099 ±0.031) μg/L vs (0.091 ±0.029) μg/L,F=3.030,P＜0.05].Conclusion Dioscornin could ameliorate the prognosis through decreasing the levels of TNF-α and S100B,and increasing adiponectin level in patients with rheumatoid arthritis and cerebral infarct.
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Objective To observe the dynamic changes of serum inflammatory factors after vertebral artery stenting and to investigate its clinical significance. Methods A total of 48 patients treated with vertebral artery stenting were included, and 48 patients only received cerebral angiography were used as a control group. The levels of soluble intercellular adhesion molecule-1 (sICAM-1), high-sensitivity C-reactive protein (hs-CRP) and tumor-necrosis factor-α (TNF-α) were detected before procedure (angiography), at 24 h, 48 h, 3 d, and 1 and 3 weeks after procedure (angiography). Results The serum levels of hs-CRP (4. 85 ± 0. 53 mg/L vs. 2. 57 ±0. 36 mg/L,P＜0. 05), TNF-α (2.42 ±0. 34 μg/L vs. 1. 08 ±0. 37 μg/L,P ＜0. 05) and sICAM-1 (449.43 ± 47. 16 μg/L vs. 269. 15 ± 37. 46 μg/L, P ＜ 0. 05) at 24 hours after procedure in the stenting group were significantly elevated compared with those before procedure. The Hs-CRP level (6.24 ± 0.59 mg/L) reached the peak at 48 hours after procedure. At week 3 (2. 51 ±0.29 mg/L), it returned to the level before procedure (2. 57 ±0. 36 mg/L); TNF-α level reached the peak at day 3 (2.30 ± 0.25 μg/L), and it remained higher level at week 3 (1. 89 ±0. 13 μg/L); the sICAM-1 level continued to rise at week 3 (296. 95 ± 59. 72 μg/L). The serum hs-CRP, TNF-α and sICAM-1 levels at 24 hours after procedure in the stenting group were significantly higher than those (3. 25 ±0.40 mg/L、J. 18 ±0. 19 μg/L and 336. 57 ± 50. 18μg/L) in the control group (all P＜0.05). Conclusions The serum hs-CRP, TNF-α, sICAM-1 levels were significantly elevated after vertebral artery stenting. It was suggested that the stenting caused a longer duration of inflammatory response.
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Objective: To investigate the effects of edaravone on the functions of major organs and plasma inflammatory cytokine levels following hemorrhagic shock(HS) and resuscitation in rats. Methods: A total of 24 rats were randomly divided into 3 groups: the sham-operated control group (sham), the haemorrhage shock goup (I/R), and the haemorrhage shock plus edaravone injection (I/R-ED) group. Rats in the latter two groups were bled using a femoral artery catheter with MAP maintained within 35-45 mmHg(1 mmHg=0.133 kPa) for 60 min to induce shock, and then resuscitaton was induced by reinjecting 60% autologous blood and 2 times of shed blood Ringer's. At the beginning and ending of resuscitation, I/R group and I/R-ED group were given the same dose (2 ml/kg) of normal saline and edaravone, respectively. The plasma levels of TNF-α, IL-6, ALT, AST, LDH, CK, BUN and Cr were measured at 2 and 24 h after resuscitation. Results: (1)The plasma levels of TNF-α and IL-6 in I/R group were significantly higher than those of the sham group 2 h after hemorrhagic shock and resuscitation (P0.05). The plasma levels of TNF-α and IL-6 in I/R group were also significantly higher than those in the sham group after 24 h(P<0.05), and the levels in I/R-ED group was significantly lower than those in the I/R group(P<0.05). (2) The plasma levels of ALT and AST in I/R group were significantly higher than those in the sham group at 24 h (P<0.05), and the levels in I/R-ED group was significantly lower than that in the I/R group (P<0.05). The plasma levels of BUN and Cr in I/R group were significantly higher than those in the sham group after 2 h(P<0.05), and the levels in I/R-ED group was significantly lower than those in the I/R group(P<0.05). The plasma levels of BUN and Cr in I/R group were also significantly higher than those in the sham group (P<0.05); Cr level in ED group was significantly lower than that in the I/R group(P<0.05); and the BUN level in I/R-ED group was similar to that in I/R group. (3) Great pathological changes were found in the liver, kidney, and lung of rats in I/R Group, and the pathological changes were slight in I/ R-ED Group. Conclusion: Our study suggests that edaravone can decrease the release of inflammatory factors (TNF-α and IL-6) after induction of HS in rats, which can alleviate the pathological damage to major organs after HS.
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The different levels and clinical significance of high sensitivity C reactive protein(hs-CRP) , tumor necrosis factor-a ( TNF-α) , erythrocyte sedimentation rate ( ESR) , and urinary monocyte chemoattractant protein-1 (uMCP-1) in 84 type 2 diabetic patients with different urine albumin excretion (UAE) were observed. The results indicated that the levels of hs-CRP,TNF-α,urinary MCP-1 ,and ESR in diabetic patients were significantly higher than those in control group,and the first three indexes increased with the levels of UAE. The results suggest that diabetic nephropathy seems to be correlated with inflammatory reactions.
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Objective To study the effects of small dosage insulin on intestinal inflammatory responses to endotoxin rats. Method Thirty two male SD rats were randomly divided into 4 groups (n = 8): control group, endotoxin (LPS,6 mg/kg i.p.)group, regular insulin(RI,0.5 IU/kg hypodermic) group and LPS(6 mg/kg i.p) + RI (0.5 IU/kg hypodermic)group. Six hours after LPS or saline injection,all rats were laparotomized to observe the congestion in intestinal mucosa with naked-eyes and photography.Then a segment of intestine was stained with HE to observe the pathological changes. The expressions of IL-6 and TNF-α were detected by RT-PCR.The systemic inflammatory response,blood sugar and food taken in rats were observed simultaneously. Software SPSS 13.0 was used to perform ANOVA and Chi-square test for statistical analysis. Results Compared with LPS group, the differences in hyperemia and inflammatory cell infiltration in intestinal tissue were not noticeable in LPS + RI group. The expression of IL-6 and TNF-α were significantly attenuated in RI + LPS group (P < 0.01). All rats in LPS group manifested systemic inflammatory response syndrome (SIRS) four or five hours after LPS treatment, while there was none in LPS + RI group. Rats in LPS group took less food than rats of other groups while the blood sugar had litter difference in all groups (P > 0.05). Conclusions Small dosage of insulin could reduce intestinal inflammation caused by endotoxemia. Early administration of insulin ould prevent the presence of SIRS while it has no obvious influence on blood sugar.
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Objective To investigate the effects of Ligustrazine on TNF-α-induced TGF-β and CTGF expression in human peritoneal mesothelial cells (HPMCs). Methods HPMCs were isolated from human omenta by trypsin di-gestion. Then, the subcultured HPMCs were divided into control group, TNF-α-induced (1 μg/L) group and TNF-α-induced plus low-, medium-and high-dose Ligustrazine (10, 20 and 40 mg/L Ligustrazine respectively) groups. The viability of HPMCs was measured by MTT assay. RT-PCR was used to detect the expressions of TGF-β1 and CTGF mRNAs in HPMCs. TGF-β1 and CTGF in supernatants were measured by ELISA. Cell protein concentration was measured by trace bicinchoninic acid (BCA) method to validate the ELISA assay results. Results Ligustrazine significantly decreases TNF-α-induced TGF-β1 and CTGF expression in a dose-dependent manner at both protein and gene levels ( P < 0. 05 ). In addition, medium-and high-dose Ligustrazine injection significantly ameliorates the viability of HPMCs inhibited by TNF-α ( P < 0. 05 ). Conclusion Ligustrazine inhibits expressions of TGF-β and CTGF of HPMCs in an inflammatory conditions.
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OBJETIVO: Pesquisas recentes têm implicado fatores imunes na patogênese de diversos transtornos neuropsiquiátricos. O objetivo do presente trabalho é revisar os trabalhos que investigaram a associação entre transtorno bipolar e alterações em parâmetros imunes. MÉTODOS: Artigos que incluíam as palavras-chave: "bipolar disorder", "mania", "immunology", "cytokines", "chemokines", "interleukins", "interferon" e "tumor necrosis factor" foram selecionados em uma revisão sistemática da literatura. As bases de dados avaliadas foram MedLine e Scopus, entre os anos de 1980 e 2008. RESULTADOS: Foram identificados 28 trabalhos que estudaram alterações imunes em pacientes com transtorno bipolar. Seis artigos investigaram genes relacionados à resposta imune; cinco, autoanticorpos; quatro, populações leucocitárias; 13, citocinas e/ou moléculas relacionadas à resposta imune e seis, leucócitos de pacientes in vitro. CONCLUSÕES: Embora haja evidências na literatura correlacionando o transtorno bipolar a alterações imunes, os dados não são conclusivos. O transtorno bipolar parece estar associado a níveis mais elevados de autoanticorpos circulantes, assim como à tendência à ativação imune com produção de citocinas pró-inflamatórias e redução de parâmetros anti-inflamatórios.
OBJECTIVE: Emerging research has implicated immune factors in the pathogenesis of a variety of neuropsychiatric disorders. The objective of the present paper is to review the studies that investigated the association between bipolar disorder and immune parameters. METHODS: Papers that included the keywords "bipolar to disorder", "mania", "immunology", "cytokines", "chemokines", "interleukins", "interferon" and "tumor necrosis factor" were selected in a systematic review of the literature. The evaluated databases were MedLine and Scopus in the period between 1980 and 2008. RESULTS: Twenty eight works were found. Six studies investigated immune response-related genes; five, auto-antibodies; four, leukocyte population; 13, cytokines and/or immune-related molecules; six, leukocytes in vitro. CONCLUSIONS: Although there is evidence in the literature correlating affective disorders with immune parameters, the results are still inconclusive. Bipolar disorder seems to be associated with increased levels of auto-antibodies as well as with a trend for increased immune activation with production of pro-inflammatory cytokines and reduction of the anti-inflammatory parameters.
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Citocinas , Trastorno Bipolar/inmunología , Trastorno Bipolar/terapia , Bases de Datos como Asunto , Literatura de Revisión como AsuntoRESUMEN
Objective To investigate the effects of ulinastatin on the expressions of tumor necrosis factor-a (TNF-a) and interleukon-6 (IL-6) in the brain tissue of rats with sepsis. Methods Filly SD rats were randomly divided into control (n=5), sepsis (n=15), ulinastatin pretreatment (n=15) and ulinastatin treatment (n=15) groups. Sepsis was induced in the latter 3 groups by cecal ligation and puncture (CLP), and in the ulinastatin pretreatment and treatment groups, ulinastatin was administered at the dose 25 000 U/kg 2 h before the operation and at 50 000 U/kg 2 h after the operation, respectively. The rats were sacrificed at 3, 6 and 12 h after CLP, and the brain tissues from the left hemisphere was collected for measurement of TNF-a and IL-6 levels by radioimmunity, and those from the right hemisphere was used for pathological examination. Results Compared with control group, the rats in the sepsis group showed obviously increased TNF-a and IL-6 levels in the brain tissues 6 and 12 h after CLP (P<0.05). Ulinastatin treatment before and after the CLP both resulted in significant reduction in TNF-a levels 6 h after CLP in comparison with the levels in the sepsis group (P<0.05), and significant reduction of IL-6 levels occurred till 12 h after CLP (P<0.05). No significant differences in TNF-a and IL-6 levels were noted between ulinastatin pretreatment and treatment groups (P>0.05). Conclusion The inflammatory response caused by elevated TNF-a and IL-6 levels in the brain of septic rats may be an important mechanism of septic encephalopathy. Ulinastatin can reduce TNF-a and IL-6 levels in the brain of septic rats to alleviate sepsis-induced brain injuries, and its therapeutic and prophylactic (at half dose) administration produces similar effects.
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Clinical manifestations of tuberculosis are closely associated with the initial responses of macrophages to mycobacteria. In this study, we investigated the signal transduction pathways for the secretion of cytokines and chemokines [tumor necrosis factor (TNF)-alpha, interleukin (IL)-10, IL-8, and monocyte chemotactic protein-1 (MCP-1)] in human blood monocytes infected with Mycobacterium tuberculosis H37Rv. M. tuberculosis H37Rv infection induced the secretion of significant amounts of TNF-alpha, IL-10, IL-8, and MCP-1 from human blood monocytes. Analysis of mitogen-activated protein kinase (MAPK) activation [extracellular signal-regulated kinase 1/2 (ERK) and p38 kinase] showed rapid phosphorylation of both subfamilies in response to M. tuberculosis H37Rv. Using highly specific inhibitors of p38 (SB203580) and of MEK-1 (U0126 and PD98059), we found that both p38 and ERK were essential for M. tuberculosis H37Rv-induced TNF-alpha production, whereas activation of the p38 pathway, but not that of ERK, was essential for M. tuberculosis H37Rv-induced IL-10 production. Interestingly, the ERK pathway, but not that of p38, was critical for MCP-1 secretion from human blood monocytes infected with M. tuberculosis H37Rv. However, IL-8 secretion was regulated neither by ERK1/2 nor p38 MAPK. Collectively, these results suggest that induction of the MAPK pathway is required for the expression of TNF-alpha. IL-10, and MCP-1 by human blood monocytes during M. tuberculosis H37Rv infection.