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Objective To explore the effects of Sishen Pill and Gegen Qinlian Tablet on cytokines of acute and chronic colitis induced by dextran sulfate sodium (DSS) in mice. Methods Mice freely drank 4%DSS dissolved in drinking water for continuous 5 days to establish acute colitis model. Mice circularly drank 3% DSS for 4 times for the establishment of chronic colitis model. In the acute or chronic colitis experiment, mice were randomly divided into control group, acute and chronic model groups, Sishen Pill group, and Gegen Qinlian Tablet group. Acute model group was administrated one day after DSS drinking for 8 days. Chronic model group was administrated after the second time of circular drinking for 16 days. ELISA was used to detect the contents of IFN-γ, IL-17 and IL-22 in cultural supernatant of mouse colon. Results Contents of IFN-γ, IL-17A and IL-22 in cultural supernatant increased significantly in acute models (P<0.01). Gegen Qinlian Tablet can significantly decrease the contents of IFN-γ and IL-17A of acute models (P<0.05). Sishen Pill can significantly decrease the content of IL-17A (P<0.05). IFN-γand IL-17A in cultural supernatant in chronic model mice significantly increased compared with control group (P<0.01). Sishen Pill and Gegen Qinlian Tablet inhibited the contents of IFN-γ and IL-17A. Compared with control group, Sishen Pill significantly increased the content of IL-22 (P<0.05). Conclusion Sishen Pill and Gegen Qinlian Tablet can treat colitis by decreasing the contents of IFN-γ and IL-17A in acute colitis model mice;Sishen Pill can treat chronic colitis by promoting IL-22 to increase.
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<p><b>BACKGROUND</b>Suppression of myostatin (MSTN) has been associated with skeletal muscle atrophy and insulin resistance (IR). However, few studies link MSTN suppression by ladder-climbing training (LCT) and IR. Therefore, we intended to identify the correlation with IR between LCT and to analyze the signaling pathways through which MSTN suppression by LCT regulates IR.</p><p><b>METHODS</b>The rats were randomly assigned to two types of diet: normal pellet diet (NPD, n = 8) and high-fat diet (HFD, n = 16). After 8 weeks, the HFD rats were randomly re-assigned to two groups (n = 8 for each group): HFD sedentary (HFD-S) and high-fat diet ladder-climbing training (HFD-LCT). HFD-LCT rats were assigned to LCT for 8 weeks. Western blotting, immunohistochemistry and enzyme assays were used to measure expression levels and activities of MSTN, GLUT4, PI3K, Akt and Akt-activated targets (mTOR, FoxO1 and GSK-3β).</p><p><b>RESULTS</b>The LCT significantly improved IR and whole-body insulin sensitivity in HDF-fed rats. MSTN protein levels decreased in matching serum (42%, P = 0.007) and muscle samples (25%, P = 0.035) and its receptor mRNA expression also decreased (16%, P = 0.041) from obese rats after LCT. But the mRNA expression of insulin receptor had no obvious changes in LCT group compared with NPD and HFD-S groups (P = 0.074). The ladder-climbing training significantly enhanced PI3K activity (1.7-fold, P = 0.024) and Akt phosphorylation (83.3%, P = 0.022) in HFD-fed rats, significantly increased GLUT4 protein expression (84.5%, P = 0.036), enhanced phosphorylation of mTOR (4.8-fold, P < 0.001) and inhibited phosphorylation of FoxO1 (57.7%, P = 0.020), but did not affect the phosphorylation of GSK-3β.</p><p><b>CONCLUSIONS</b>The LCT significantly reduced IR in diet-induced obese rats. MSTN may play an important role in regulating IR and fat accumulation by LCT via PI3K/Akt/mTOR and PI3K/Akt/FoxO1 signaling pathway in HFD-fed rats.</p>
Subject(s)
Animals , Male , Rats , Blotting, Western , Diet, High-Fat , Glucose Tolerance Test , Glucose Transporter Type 4 , Metabolism , Immunohistochemistry , Insulin Resistance , Physiology , Myostatin , Metabolism , Obesity , Metabolism , Phosphatidylinositol 3-Kinases , Metabolism , Proto-Oncogene Proteins c-akt , Metabolism , Quadriceps Muscle , Metabolism , Rats, Sprague-DawleyABSTRACT
AIM: To discuss the discrepancy of microRNA (miRNA) in nasopharyngeal carcinoma (NPC) cells CNE-1 and CNE-2 on the basis of validating their different radioresistance.METHODS: Following the effect of X ray on the clones of CNE-1 and CNE-2 cells, the dose-survival curve and biological characteristics of CNE-1 and CNE-2 cells were determined by SigmaPlot software and the linear quadratic model of survival curves analysis. MicroRNAs were detected by Paraflo microfluidic microRNA chip, hybridization images collected using a laser scanner and normalizing the signals using a LOWESS filter. The relationship between the discrepancy of NPC radiosensitivity and the expression of microRNA was predicted according to Targetscan3.1 database (http:www.targetscan.org) after analyzing the data.RESULTS: Compared to CNE-2 cells, 20 microRNAs were gain-of-function and 13 microRNAs loss-of-function in CNE-1 cells among 326 detected microRNAs. 4 miRNAs that one detective value was more than 2000 and 3 folds than the other were hsa-miR-152, hsa-miR-7, hsa-miR-205 and hsa-miR-572. Data showed that radio-sensitivity was relative to the distinct discrepancy of miRNAs. CONCLUSION: The discrepancy of miRNAs is presents in different radioresistant NPC cell lines and related to radiosensitivity.
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Aim To establish experimental colitis model in Balb/c mice by Trinitrobenzene Sulfonic Acid (TNBS) enema. Methods Several doses of TNBS instilled into mice colon induced experimental colitis, then mortality rates of mice were observed. Severity of colitis was evaluated by the Disease Activity Index (DAI),Morphologic and Histologic analysis and Myeloperoxidase (MPO) analysis. We also observed the T cell proliferation of spleen. Results It showed that the mice mortality rate was increased when the mice were given the higher dose of TNBS. Most survived mice showed chronic inflammation in reduction colon. Histological examinations of the colon showed multiple erosive lesions and inflammatory cell infiltration composed of macrophages, lymphocytes, neutrophils in lamina propria and beyond mucosal layer. Some colon showed crypt distortion or reduction and high vascular density. Conclusion A TNBS dose of 1.5mg for each mouse was chosen for an appropriate experimental dose since the group showed less mortality rate and appropriate experimental colitis.
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Objective: To explore cytokine mechanism of Zhongjiling Tablet therapy to experimental autoimmune myasthenia gravis (EAMG). Methods: Lewis rats were immunized with N2-AChR(from Torpedo's electrical organ)in CFA. ELISA were adopted to determine IFN-?,IL-4,TGF-? levels in serum and surpernatant fluids and anti-N2-AChR total IgG,IgG1,IgG2 titers in serum of EAMG on week 7 post immunization and treatment.Results:In serum and surpernatant fluids:IFN-?,IL-4 level in model group were dramatically higher than CEA group ( P
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Objective:To analyze immune mechanisms of total glycoside from Cornus officinalis (TGCO) against rheumatoid arthritis.Methods:Rat immunized by CⅡ in CFA were treated with TGCO ,at different times after immunization,CⅡ-specific antibodies in serum,lymphnode cells(LNC) IFN-? production was studied and cell proliferation response were also detected.Results:Treatment inhibit disease severity to a greater extent. TGCO effectively decreased anti-CⅡantibody titer in serum, considerably reduced IFN-? secretion before the onset arthritis and the acute stage of arthritis and suppressed T cell differentiation or proliferation.Conclusion:The both lead to supprese arthritis.
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Objective; To explore mechanism of Zhongjiling tablet treats experimental autoimmune myasthenia gravis on rats. Methods:Normal mice, immunosuppressive mice and EAMG rats were used to investigate the mechanism. Results:Zhongjiling tablet enhanced T and B cells proliferation of normal mice and immunosuppressive mice induced by ConA or LPS, and increased the production of IL-2. T cell proliferation of EAMG rats was improvement stimulated by AChR and decline by ConA. Zhongjiling tablet inhibited the improvement by AChR and enhanced the decline by ConA, and reduced the expression of IFN-? and IL-4 mRNA. Zhongjiling tablet also induced the apoptosis of CD4 + T lymphocyte stimulated by AChR. Conclusion: Zhongjiling tablet increased immunity of normal mice, immunosuppressive mice and EAMG rats. But it suppressed specific T lymphocyte proliferation induced by AChR and reduced the expression of IFN-? and IL-4 mRNA. It was probably one of mechanisms Zhongjiling tablet induced the apoptosis AChR specific CD4+T lymphocyte.