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目的观察青藤碱对胶原诱导性大鼠关节炎症的作用特点,初步探讨其作用机制。方法实验采用24只雌性Wistar大鼠,随机分为4组,其中3组胶原诱导成功后,分别给予注射用水、甲氨喋呤、青藤碱。第4组作为正常对照组,分别于第1d、6d、11d、16d、21d记录大鼠右侧后肢关节肿胀程度。21d心脏取血,酶联免疫吸附法测定血清中肿瘤坏死因子-a含量、抗II型胶原抗体含量。处死大鼠,取脾脏分离淋巴细胞,行淋巴细胞转化试验,取右踝关节行钼靶摄片、病理切片观测关节病变情况。结果给药后第6天起甲氨喋呤组关节炎症评分与模型组比较差异有统计学意义(P<0.05)。第11天起青藤碱组与模型组比较差异有统计学意义。青藤碱组及甲氨喋呤组大鼠血清抗II型胶原抗体含量与模型组比较差异有统计学意义(P<0.05),青藤碱与甲氨喋呤对胶原刺激的淋巴细胞增殖有明显抑制作用(P<0.05),钼靶摄片及病理学观察也同样提示青藤碱与甲氨喋呤对关节破坏有抑制作用。而各干预组与模型组比较血清中肿瘤坏死因子-α含量差异无统计学意义(P>0.05)。结论青藤碱能够减少关节局部炎症细胞浸润,缓解关节炎症。通过抑制滑膜中CYR-61表达,进而抑制滑膜炎症细胞黏附浸润为其抗炎机制之一。
Objective To observe the effect of sinomenine on collagen-induced arthritis in rats and to explore its mechanism. METHODS: Twenty-four female Wistar rats were randomly divided into 4 groups. After 3 groups of collagen were successfully induced, they were given water for injection, methotrexate, and sinomenine, respectively. The fourth group was used as a normal control group. The degree of swelling of the right hindlimb joint of the rat was recorded on the 1st, 6th, 11d, 16d, and 21d. Blood was taken from the heart of 21 days and the levels of tumor necrosis factor-α and anti-collagen II antibodies were determined by enzyme-linked immunosorbent assay. The rats were killed and spleens were taken to separate lymphocytes. The lymphocyte transformation test was performed. The right ankle joint was taken with a molybdenum target radiograph and pathological sections to observe the joint lesions. Results The scores of arthritis in the methotrexate group were significantly different from those in the model group on the 6th day after administration (P<0.05). From the 11th day onwards, the difference between the sinomenine group and the model group was statistically significant. Compared with the model group, the serum anti-type II collagen antibody levels in the sinomenine group and the methotrexate group were significantly different (P<0.05). The sinomenine and methotrexate had collagen-stimulated lymphocyte proliferation. Significant inhibition (P<0.05), molybdenum target radiographs and pathological observations also suggested that sinomenine and methotrexate have inhibitory effects on joint destruction. There was no significant difference in serum tumor necrosis factor-α levels between the intervention group and the model group (P>0.05). Conclusion Sinomenine can reduce inflammatory cell infiltration in joints and relieve joint inflammation. By inhibiting the expression of CYR-61 in the synovial membrane, inhibiting the adhesion infiltration of synovial inflammatory cells is one of its anti-inflammatory mechanisms.