Abstract：【Objective】To investigate the effect of astragaloside Ⅳ(AS-Ⅳ) regulating p38 mitogen activated protein kinase (MAPK) pathway on renal tubulointerstitial fibrosis.【Methods】 The animal model of tubulointerstitial fibrosis induced by unilateral ureteral ligation (UUO) was established in C57BL/6 mice and divided into sham operation group (group A), model group (group B) and treatment group (Group C). Group C was gavaged with 20 mg/(kg·d) as-iv for 7 days, and group A and B were gavaged with the same dose of physiological salt water. After 2 weeks, the pathological changes of the kidney were observed (Masson staining), and the transforming growth factor was detected by real-time quantitative TGF-β1 mRNA expression by PCR. According to different cell culture media, NRK-49F cells were divided into negative control group ,TGF-β1 Group (with TGF-β1 10 ng/mL stimulated cells), TGF-β1 + AS-Ⅳ group (before TGF-β1 stimulation, add doses of 50, 100 and 200 μg/mL AS-Ⅳ treatment for 1 h respectively), and the level of p-p38 protein in NRK-49F cells was observed (Western method).【Results】 The relative expression of TGF-β1 mRNA in renal tissue of group A , B and C was 2.65±0.38, 28.71±4.05 and 20.29±3.10, and the group A was at a lower level. Compared with the group A, the renal TGF -β1 mRNA expression in the group B and C was significantly higher than that in the group A (P<0.01), the expression in the group C was significantly lower than that in the group B(P<0.05). The results of in vitro test showed that p-p38 protein level, TGF-β1 GrouP>negative control group (P<0.01), TGF-β1 GrouP>TGF-β1 + AS-Ⅳ group (P<0.01), TGF-β1 + AS-Ⅳ group 200 μg/mL< 100 μg/mL<50 μg/mL(P<0.01). 【Conclusion】AS-Ⅳ can reduce TGF-β1 level, reduce renal tubulointerstitial fibrosis, and its protective effect may be related to the inhibition of p38 MAPK phosphorylation by AS-Ⅳ.
周淑娟, 李伟. 黄芪甲苷调控p38 MAPK信号通路治疗小鼠肾小管间质纤维化的实验研究[J]. 医学临床研究, 2021, 38(10): 1547-1549.
ZHOU Shu-juan, LI Wei. Experimental Study of Astragaloside IV Regulating p38 MAPK Signaling Pathway in the Treatment of Renal Tubulointerstitial Fibrosis. JOURNAL OF CLINICAL RESEARCH, 2021, 38(10): 1547-1549.
[1] 袁倩, 刘友华. 肾脏纤维化的细胞和分子机制研究进展[J].安徽大学学报(自然科学版), 2018, 42(5):120-129. [2] LIA L, HOUB X, XUB R, et al. Research review on the pharmacological effects of astragaloside IV[J].Fundame Clin Pharmacol,2017, 31(1):17-36. [3] 桂定坤, 汪年松. 黄芪甲苷肾保护作用机制[J].中华肾病研究电子杂志, 2013, 2(4):39-41. [4] 罗莹莹,王小琴,邓丹芳,等. 微环境调控在糖尿病肾病肾小管间质纤维化过程中的作用[J].医学综述,2021,27(11):2209-2215. [5] DU Y, YANG Y T, TANG G, et al. Butyrate alleviates diabetic kidney disease by mediating the miR-7a-5p/P311/TGF-beta1 pathway[J].FASEB J,2020,34(8):10462-10475. [6] MENG X M. TGF-β: the master regulator of fibrosis[J].Nat Rev Nephrol,2016,12(6):325-338. [7] WANG D.Inhibition of p38 MAPK attenuates renal atrophy and fibrosis in a murine renal artery stenosis model[J].Am J Physiol,2013, 304(4Pt2):F938-F947. [8] 徐维佳.黄芪甲苷通过调控p38MAPK信号通路改善肾小管间质纤维化[J].中华肾脏病杂志, 2014, 30(10):770-776.
2021, Vol. 38 
