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

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

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。

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 lupus nephritis. Methods Twenty-four 16-week-old female MRL/lpr mice were randomly divided into model control group, EsA group, and EsA +IL-12p35 antibody group. The mice were intraperitoneally injected once a day. After four weeks, all mice were killed to check urine protein / creatinine value, serum creatinine concentration, IL-35, IL-17, iTr35 ratio and renal pathology. 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 creatinine concentration 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 pathological changes of kidney were improved in EsA group and EsA + IL-12p35 antibody group. Conclusion There is abnormal expressions of IL-35 and IL-17 in lupus nephritis. EsA is effective in the treatment of lupus nephritis, and which may be through regulating the expression of IL-35, IL-17 and iTr35.