Study on mechanism of Vaccarin improving EMT in renal fibrosis model mice through regulating STAT3
- VernacularTitle:王不留行黄酮苷调控STAT3改善肾纤维化模型小鼠EMT的机制研究
- Author:
Meng-jiao CUI
1
;
Qi-ming XU
;
Yu CAO
;
Ye-nan FAN
;
Yi-qing YANG
;
Guang-bo GE
;
Wen-rui LIU
;
Jian-rao LU
;
Jing HU
Author Information
- Publication Type:Journal Article
- Keywords: Vaccarin; renal fibrosis; STAT3; inflamma-tory; EMT; HK2 cells
- From: Chinese Pharmacological Bulletin 2025;41(4):745-752
- CountryChina
- Language:Chinese
- Abstract: Aim To investigate the protective effect of Vaccarin(Va)on epithelial-mesenchymal transition(EMT)in renal fibrosis model mice through regulating STAT3,and the underlying mechanism.Methods Left ureter ligation was used to establish a mouse model of unilateral ureteral obstruction(UUO);human kid-ney tubular epithelial(HK2)cells were induced to differentiate by transforming growth factor-β(TGF-β)in vitro.HE and Masson staining were used to observe the morphological changes of renal tissue;kits were used to detect the levels of BUN,Cr,IL-1β and IL-7 in mouse serum;CCK-8 was used to detect the effect of Va on the viability of HK2 cells;RT-PCR was used to detect the levels of inflammatory factors in HK2 cells;Western blot was used to detect the expression of STAT3,p-STAT3,E-cadherin,and α-SMA proteins in renal tissue and HK2 cells;to further investigate the regulation of Va on STAT3,JAK/STAT3 pathway acti-vator RO8191 was used to treat TGF-β-induced HK2 cells,and functional loss was detected.Results Va improved the pathological damage in UUO mice,inhibi-ted the levels of BUN,Cr and inflammatory factors;Va inhibited the phosphorylation of STAT3,upregulated E-cadherin,and downregulated α-SMA protein expres-sion;RO8191 counteracted the inhibitory effect of Va on the phosphorylation of STAT3.Conclusions Va inhibits the phosphorylation of STAT3 and the release of inflammatory factors,improves EMT,thus exerting an anti-renal fibrosis effect.
