商陆皂苷甲对MRL/lpr小鼠iTr35细胞及其相关细胞因子表达的影响

摘要：目的 观察商陆皂苷甲（EsA）对MRL/lpr小鼠的治疗作用和体内iTr35（CD4+Foxp3-IL-12p35+IL-27EBI3+）细胞、白细胞介素（IL）-35及IL-17表达的影响，探讨EsA治疗狼疮性肾炎的可能机制。方法 将24只16周龄、雌性MRL/lpr小鼠随机分为模型对照组、EsA组和EsA+IL-12p35抗体组，分别腹腔注射给药，每日1次，4周后处死小鼠，进行尿蛋白/肌酐值、血肌酐浓度、IL-35、IL-17、iTr35细胞比例、肾脏病理的检测。结果 3组小鼠尿蛋白/肌酐值、血肌酐浓度、IL-35、IL-17、iTr35差异有统计学意义（P＜0.05），其中模型对照组尿蛋白/肌酐值、血肌酐浓度、IL-17含量最高，其次为EsA+IL-12p35抗体组，EsA组最低；相反，EsA组中IL-35、iTr35水平最高，其次为EsA+IL-12p35抗体组，模型对照组最低；与模型对照组相比，EsA组和EsA+IL-12p35抗体组小鼠肾脏病理表现有一定改善。结论 狼疮性肾炎小鼠血清中存在IL-35、IL-17的表达异常，EsA对狼疮性肾炎有效，其机制可能是通过调节IL-35、IL-17及iTr35的表达而发挥作用的。

Effects of esculentoside A on the expression of iTr35 cells and relatedcytokines in MRL/lpr mice

Abstract: Objective To observe the effect of esculentoside A (EsA) on iTr35 (CD4+Foxp3-IL-12p35+IL-27EBI3+)cells and related cytokines in MRL / lpr mice, and to explore the possible mechanism of EsA in the treatment of lupusnephritis. Methods Twenty-four 16-week-old female MRL/lpr mice were randomly divided into model control group, EsAgroup, and EsA +IL-12p35 antibody group. The mice were intraperitoneally injected once a day. After four weeks, all micewere killed to check urine protein / creatinine value, serum creatinine concentration, IL-35, IL-17, iTr35 ratio and renalpathology. Results There were significantly differences in urine protein / creatinine value, serum creatinine concentration,IL-35, IL-17 and iTr35 ratio between the three groups (P＜0.05). The urinary protein / creatinine value, serum creatinineconcentration and IL-17 levels were the highest in the model control group, followed by the EsA+IL-12p35 antibody group,and the lowest was in the EsA group. The levels of IL-35 and iTr35 were the highest in EsA group, followed by EsA + IL-12p35 antibody group, and the lowest was in the model group. Compared with the model control group, the pathologicalchanges of kidney were improved in EsA group and EsA + IL-12p35 antibody group. Conclusion There is abnormalexpressions of IL-35 and IL-17 in lupus nephritis. EsA is effective in the treatment of lupus nephritis, and which may bethrough regulating the expression of IL-35, IL-17 and iTr35.