Tianjin Medical Journal ›› 2019, Vol. 47 ›› Issue (5): 483-487.doi: 10.11958/20181663

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

WANG Xing, ZENG Hui-lin, ZHANG Xiang-gui△, TANG Jie-yin   

  1. Department of Nephrology, the Fifth Affiliated Hospital of Zunyi Medical University, Zhuhai 519100, China △Corresponding Author E-mail: zxg5220@163.com
  • Received:2018-11-02 Revised:2019-03-31 Published:2019-05-15 Online:2019-05-15
  • Contact: 王幸 E-mail:609183357@qq.com

Abstract: 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 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.

Key words: Phytolaccoside, interleukin-17, lupus nephritis, MRL/lpr mice, iTr35 cell, interleukin-35