Isolation and identification of belamcandaoids A−N from Belamcanda chinensis seeds and their inhibition on extracellular matrix in TGF-β1 induced kidney proximal tubular cells

2021 ◽  
pp. 105067
Author(s):  
Ying-Ying Song ◽  
Jian-Bing Jiang ◽  
Yong-Ming Yan ◽  
Yong-Xian Cheng
2021 ◽  
Vol 12 (11) ◽  
Author(s):  
Shaoqun Shu ◽  
Hui Wang ◽  
Jiefu Zhu ◽  
Zhiwen Liu ◽  
Danyi Yang ◽  
...  

AbstractBoth endoplasmic reticulum (ER) stress and autophagy have been implicated in chronic kidney injury and renal fibrosis. However, the relationship and regulatory mechanisms between ER stress and autophagy under this condition remain largely unknown. In this study, we first established a mouse model of ER stress-induced chronic kidney injury by 2 weekly injections of a low dose of tunicamycin (TM), a classical ER stress inducer. This model showed the induction of ER stress, autophagy, fibrosis and apoptosis in kidney tissues. In vitro, TM also induced ER stress, autophagy, fibrosis and apoptosis in HK-2 human kidney proximal tubular cells and BUMPT-306 mouse kidney proximal tubular cells. In these cells, autophagy inhibitor suppressed TM-induced fibrotic changes and apoptosis, suggesting an involvement of autophagy in ER stress-associated chronic kidney injury. PERK inhibitor ameliorated autophagy, fibrotic protein expression and apoptosis in TM-treated cells, indicating a role of the PERK/eIF2α pathway in autophagy activation during ER stress. Similar results were shown in TGF-β1-treated HK-2 cells. Interestingly, in both TM- or TGF-β1-treated kidney proximal tubular cells, inhibition of autophagy exaggerated ER stress, suggesting that autophagy induced by ER stress provides a negative feedback mechanism to reduce the stress. Together, these results unveil a reciprocal regulation between ER stress and autophagy in chronic kidney injury and fibrosis.


2020 ◽  
Vol 6 (8) ◽  
pp. 2110-2119 ◽  
Author(s):  
Xukai Jiang ◽  
Shuo Zhang ◽  
Mohammad A. K. Azad ◽  
Kade D. Roberts ◽  
Lin Wan ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document