赤雹根总皂苷对佐剂关节炎大鼠血清及足TNF-α,IL-1β,IL-6水平的影响

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目的:观察赤雹根总皂苷对佐剂型关节炎大鼠血清及足跖中肿瘤坏死因子-α、白介素-1β、白介素-6(TNF-α,IL-1β,IL-6)表达水平的影响,探讨赤雹根总皂苷治疗类风湿性关节炎的机制。方法:雄性SD大鼠随机分为正常对照组、模型对照组、赤雹根总皂苷40、80、160 mg/kg剂量组和雷公藤多苷12mg/kg阳性对照组。除正常对照组外,其余各组大鼠均于右后足跖部皮下注射完全弗氏佐剂0.1ml。造模18天后,各给药组均灌胃给予相应药物,连续21天。计算大鼠关节炎指数,酶联免疫法(ELISA)检测大鼠血清TNF-α、IL-1β、IL-6水平,免疫组织化学法测定足跖以上三种因子蛋白表达水平。结果:赤雹根总皂苷剂量40、80、160mg/kg组大鼠关节炎指数分别为6.00±0.40、5.10±0.18、4.20±0.32均显著低于模型对照组7.20±0.32;血清中TNF-α水平分别为0.56±0.05、0.32±0.04、0.18±0.04 ng/ml均显著低于模型对照组0.98±0.08 ng/ml,IL-1β水平分别为0.29±0.02、0.17±0.01、0.13±0.01 ng/ml均显著低于模型对照组0.49±0.01ng/ml,IL-6水平分别为1.13±0.03、0.95±0.01、0.79±0.06 ng/ml均显著低于模型对照组1.58±0.04ng/ml;足跖中TNF-α蛋白表达水平分别为1.09±0.27、0.61±0.13、0.57±0.11 IOD均显著低于模型对照组2.17±0.34,IL-1β蛋白表达水平分别为1.13±0.32、0.65±0.22、0.63±0.24 IOD均显著低于模型对照组2.23±0.46IOD,IL-6蛋白表达水平分别为1.31±0.29、0.59±0.21、0.45±0.17 IOD均显著低于模型对照组2.49±0.38 IOD。结论:抑制TNF-α、IL-1β、IL-6水平及表达是赤雹根总皂苷治疗佐剂型关节炎的机制之一。 AIM: To investigate the effects of total alkaloids from Hail Haemostatus on the expression of TNF-α, IL-1β, IL-6 and IL-6 in serum and plantar mass of adjuvant arthritis rats To investigate the mechanism of the treatment of rheumatoid arthritis with total glucocorticoid Methods: Male Sprague-Dawley rats were randomly divided into normal control group, model control group, 40,80,160 mg / kg total glucocorticoid group and 12 mg / kg tripterygium glycosides positive control group. Except for the normal control group, rats in other groups were subcutaneously injected 0.1 ml of complete Freund’s adjuvant in the right hind foot. After 18 days of modeling, each administration group was given the corresponding drug by gavage for 21 consecutive days. The arthritis index was calculated. The levels of TNF-α, IL-1β and IL-6 in serum of rats were detected by enzyme-linked immunosorbent assay (ELISA). The protein level of the above three factors was measured by immunohistochemistry. Results: The arthritis index of 40, 80 and 160 mg / kg group were 6.00 ± 0.40, 5.10 ± 0.18 and 4.20 ± 0.32, respectively, which were significantly lower than that of model control group (7.20 ± 0.32); TNF- α The levels were 0.56 ± 0.05, 0.32 ± 0.04 and 0.18 ± 0.04 ng / ml, respectively. The levels of IL-1β were 0.29 ± 0.02, 0.17 ± 0.01 and 0.13 ± 0.01 ng / ml were significantly lower than the model control group 0.49 ± 0.01ng / ml, IL-6 levels were 1.13 ± 0.03,0.95 ± 0.01,0.79 ± 0.06 ng / ml were significantly lower than the model control group 1.58 ± 0.04ng / ml; The levels of TNF-α in plantar mass were 1.09 ± 0.27,0.61 ± 0.13,0.57 ± 0.11, respectively, which were significantly lower than those in model control group (2.17 ± 0.34, 1.13 ± 0.32,0.65 ± 0.22, 0.63, respectively) ± 0.24 IOD were significantly lower than the model control group 2.23 ± 0.46IOD, IL-6 protein expression levels were 1.31 ± 0.29,0.59 ± 0.21,0.45 ± 0.17IOD were significantly lower than the model control group 2.49 ± 0.38IOD. Conclusion: Inhibition of TNF-α, IL-1β, IL-6 levels and expression is one of the mechanisms of the treatment of adjuvant arthritis with total glucosinolate of Hail Haemostat.
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