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目的探究川芎嗪即四甲基吡嗪(TMP)对实验性自身免疫性重症肌无力(EAMG)大鼠的免疫调节机制。方法建立实验性自身免疫性重症肌无力Lewis大鼠模型,实验随机分为空白对照组、EAMG模型组、10 mg/kg TMP处理组和20 mg/kg TMP处理组,每组10只;记录大鼠体质量,并采用Lennon EAMG评分标准评价大鼠肌无力症状;免疫荧光技术检测神经肌肉接头处乙酰胆碱受体(AChR)、Ig G和C3含量;ELISA检测血清中R97-116抗体(Ig G1、Ig G2a和Ig G2b)的水平,以及肿瘤坏死因子α(TNF-α)、γ干扰素(IFN-γ)和白细胞介素10(IL-10)水平。结果 TMP能抑制EMAG大鼠体质量与肌无力评分下降,逆转肌肉接头处AChR含量的下降与Ig G和补体C3含量的上升;降低血清中R97-116抗体(Ig G1、Ig G2a)和TNF-α,增加IL-10含量,Ig G2b和IFN-γ的含量无明显变化。结论 TMP能缓解肌无力的症状,可能是通过调节细胞因子和Ig G1和Ig G2a的水平实现的。
Objective To investigate the immunoregulatory mechanism of tetramethylpyrazine (TMP) in experimental autoimmune myasthenia gravis (EAMG) in rats. Methods To establish an experimental autoimmune myasthenia gravis model in Lewis rats, the experiment was randomly divided into blank control group, EAMG model group, 10 mg / kg TMP treatment group and 20 mg / kg TMP treatment group, The body weight of rats was assessed by the Lennon EAMG score. The levels of acetylcholine receptor (AChR), Ig G and C3 at the neuromuscular junction were detected by immunofluorescence staining. The levels of Ig G1, Ig G2a and Ig G2b), as well as levels of tumor necrosis factor alpha (TNF-alpha), gamma interferon (IFN-gamma) and interleukin 10 (IL-10). Results TMP inhibited the decrease of body weight and muscle weakness score in EMAG rats, reversed the decrease of AChR content in muscle junction and the increase of Ig G and C3 levels, decreased the expression of R97-116 antibody (Ig G1, Ig G2a) and TNF- α, increase IL-10 content, Ig G2b and IFN-γ content did not change significantly. Conclusion TMP can alleviate the symptoms of myasthenia gravis, probably by regulating the levels of cytokines and Ig G1 and Ig G2a.