Shen Qi Wan attenuates renal interstitial fibrosis through upregulating AQP1.
10.1016/S1875-5364(23)60453-4
- Author:
Yiyou LIN
1
;
Jiale WEI
1
;
Yehui ZHANG
1
;
Junhao HUANG
1
;
Sichen WANG
1
;
Qihan LUO
1
;
Hongxia YU
1
;
Liting JI
2
;
Xiaojie ZHOU
3
;
Changyu LI
4
,
5
Author Information
1. School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, China.
2. School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, China. Electronic address: jltzcmu@sina.com.
3. Academy of Chinese Medical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, China. Electronic address: 18768155681@163.com.
4. School of Pharmaceutical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, China
5. Academy of Chinese Medical Sciences, Zhejiang Chinese Medical University, Hangzhou 310053, China. Electronic address: lcyzcmu@sina.com.
- Publication Type:Journal Article
- Keywords:
Aquaporin 1;
Chronic kidney disease;
Epithelial to mesenchymal transition;
Renal interstitial fibrosis;
Shen Qi Wan
- MeSH:
Drugs, Chinese Herbal/pharmacology*;
Humans;
Animals;
Mice;
Male;
Cell Line;
Rats;
Kidney/physiology*;
Fibrosis/drug therapy*;
Renal Insufficiency, Chronic/drug therapy*;
Adenine;
Epithelial-Mesenchymal Transition;
Aquaporin 1/metabolism*
- From:
Chinese Journal of Natural Medicines (English Ed.)
2023;21(5):359-370
- CountryChina
- Language:English
-
Abstract:
Renal interstitial fibrosis (RIF) is the crucial pathway in chronic kidney disease (CKD) leading to the end-stage renal failure. However, the underlying mechanism of Shen Qi Wan (SQW) on RIF is not fully understood. In the current study, we investigated the role of Aquaporin 1 (AQP1) in SQW on tubular epithelial-to-mesenchymal transition (EMT). A RIF mouse model induced by adenine and a TGF-β1-stimulated HK-2 cell model were etablished to explore the involvement of AQP 1 in the protective effect of SQW on EMT in vitro and in vivo. Subsequently, the molecular mechanism of SQW on EMT was explored in HK-2 cells with AQP1 knockdown. The results indicated that SQW alleviated kidney injury and renal collagen deposition in the kidneys of mice induced by adenine, increased the protein expression of E-cadherin and AQP1 expression, and decreased the expression of vimentin and α-smooth muscle actin (α-SMA). Similarly, treatmement with SQW-containing serum significantly halted EMT process in TGF-β1 stimulated HK-2 cells. The expression of snail and slug was significantly upregulated in HK-2 cells after knockdown of AQP1. AQP1 knockdown also increased the mRNA expression of vimentin and α-SMA, and decreased the expression of E-cadherin. The protein expression of vimentin increased, while the expression of E-cadherin and CK-18 significantly decreased after AQP1 knockdown in HK-2 cells. These results revealed that AQP1 knockdown promoted EMT. Furthermore, AQP1 knockdown abolished the protective effect of SQW-containing serum on EMT in HK-2 cells. In sum, SQW attentuates EMT process in RIF through upregulation of the expression of AQP1.
