Qinling liquid ameliorates renal immune inflammatory damage via activating autophagy through AMPK/Stat3 pathway in uric acid nephropathy

被引：5

作者：

Wang, Jie ^{[1
]}

Bu, Xiangwei ^{[2
]}

Qiu, Xinping ^{[3
]}

Zhang, Xiuyuan ^{[1
]}

Gui, Jianhua ^{[1
]}

Zhang, Honghong ^{[4
]}

Wang, Yun ^{[5
]}

Wang, Chen ^{[3
]}

Meng, Fengxian ^{[6
,7
]}

机构：

[1] Beijing Tradit Chinese Med Hosp, Shunyi Hosp, Dept Endocrinol, Beijing 101300, Peoples R China

[2] China Acad Chinese Med Sci, Guanganmen Hosp, Dept Endocrinol, Beijing 100053, Peoples R China

[3] Beijing Tradit Chinese Med Hosp, Shunyi Hosp, Sci Res Dept, Beijing 101300, Peoples R China

[4] Beijing Tradit Chinese Med Hosp, Shunyi Hosp, Dept Rheumatol, Beijing 101300, Peoples R China

[5] Beijing Tradit Chinese Med Hosp, Shunyi Hosp, Dept Cardiol, Beijing 101300, Peoples R China

[6] Beijing Univ Chinese Med, Dongfang Hosp, Dept Rheumatol, Beijing 100078, Peoples R China

[7] Beijing Univ Chinese Med, Dongfang Hosp, 6,Zone 1,Fangxing Garden, Beijing 100078, Peoples R China

来源：

CYTOKINE | 2023年 / 163卷

基金：

中国国家自然科学基金;

关键词：

Qinling liquid; Uric acid nephropathy; Autophagy; AMPK; Stat3; pathway; SIGNALING PATHWAY; UP-REGULATION; HYPERURICEMIA; INHIBITION; INJURY; STAT3;

D O I：

10.1016/j.cyto.2022.156120

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Background: Excessive deposition of uric acid (UA) is one of the risk factors for kidney damage. Qinling liquid (QL) has a certain therapeutic effect on uric acid nephropathy (UAN), but its regulation mechanism is still unclear.Methods: UAN rat models and UA induced rat renal tubular epithelial cells (NRK-52E) were constructed to evaluate the functional roles of QL. We firstly evaluated the kidney function and the degree of kidney damage in rats after QL treatment. Then, effects of QL on autophagy and NLRP3 inflammasome activation were assessed. Moreover, the regulation of QL in AMPK and Stat3 phosphorylation levels and the relationship among autophagy, AMPK/Stat3 pathway and NLRP3 inflammasomes were determined. Results: QL could alleviate the inflammatory damage in UAN rats and promote the activation of autophagy. In addition, QL suppressed UA-induced activation of NLRP3 inflammasomes in rat renal tubular epithelial cells, which was partially reversed by autophagy inhibitor. Further, AMPK/Stat3 axis-mediated autophagy participated in the regulation of UA-induced NLRP3 inflammasome activation in NRK-52E cells. Finally, we confirmed that inhibiting AMPK/Stat3 pathway partly deteriorated the ameliorating effect of QL on renal immune inflammatory injury in UAN rats.Conclusion: Through in vivo and in vitro experiments, we found that QL promotes autophagy by activating theAMPK/Stat3 pathway, thereby improving renal immune inflammatory injury in UAN.

引用

页数：10

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