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Schisandrin A alleviates renal fibrosis by inhibiting PKCβ and oxidative stress
Hui-Ling Liu1, Zhou Huang2, Qing-Zhen Li2
1State Key Laboratory of Natural Medicines, Department of TCMs Pharmaceuticals, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, China.
Background:
Renal fibrosis is a common pathway that drives the advancement of numerous kidney maladies towards end-stage kidney disease (ESKD). Suppressing renal fibrosis holds paramount clinical importance in forestalling or retarding the transition of chronic kidney diseases (CKD) to renal failure. Schisandrin A (Sch A) possesses renoprotective effect in acute kidney injury (AKI), but its effects on renal fibrosis and underlying mechanism(s) have not been studied.
Study Design:
Serum biochemical analysis, histological staining, and expression levels of related proteins were used to assess the effect of PKCβ knockdown on renal fibrosis progression. Untargeted metabolomics was used to assess the effect of PKCβ knockdown on serum metabolites. Unilateral Ureteral Obstruction (UUO) model and TGF-β induced HK-2 cells and NIH-3T3 cells were used to evaluate the effect of Schisandrin A (Sch A) on renal fibrosis. PKCβ overexpressed NIH-3T3 cells were used to verify the possible mechanism of Sch A.
Results:
PKCβ was upregulated in the UUO model. Knockdown of PKCβ mitigated the progression of renal fibrosis by ameliorating perturbations in serum metabolites and curbing oxidative stress. Sch A alleviated renal fibrosis by downregulating the expression of PKCβ in kidney. Treatment with Sch A significantly attenuated the upregulated proteins levels of FN, COL-I, PKCβ, Vimentin and α-SMA in UUO mice. Moreover, Sch A exhibited a beneficial impact on markers associated with oxidative stress, including MDA, SOD, and GSH-Px. Overexpression of PKCβ was found to counteract the renoprotective efficacy of Sch A in vitro.
Conclusion:
Sch A alleviates renal fibrosis by inhibiting PKCβ and attenuating oxidative stress.
Insights
Schisandrin A (Sch A) alleviates kidney fibrosis by inhibiting PKC-beta and reducing oxidative stress. This study investigated Sch A
Area of Science:
- Nephrology
- Pharmacology
- Biochemistry
Background:
- Renal fibrosis is a critical factor in the progression of kidney diseases to end-stage kidney disease (ESKD).
- Inhibiting renal fibrosis is crucial for managing chronic kidney diseases (CKD).
- Schisandrin A (Sch A) shows promise for kidney protection, but its role in fibrosis is unknown.
Purpose of the Study:
- To investigate the antifibrotic effects of Schisandrin A (Sch A) in kidney injury.
- To elucidate the underlying mechanisms of Sch A's renoprotective action, focusing on PKCβ and oxidative stress.
Main Methods:
- Utilized a Unilateral Ureteral Obstruction (UUO) mouse model and TGF-β-induced cell lines (HK-2, NIH-3T3).
- Assessed renal fibrosis progression via serum biochemistry, histology, and protein expression analysis.
- Employed untargeted metabolomics and PKCβ knockdown/overexpression to explore mechanisms.
Main Results:
- PKCβ was upregulated in the UUO model; its knockdown ameliorated fibrosis and oxidative stress.
- Sch A treatment downregulated PKCβ expression and attenuated fibrotic markers (FN, COL-I, Vimentin, α-SMA) in vivo.
- Sch A improved oxidative stress markers (MDA, SOD, GSH-Px) and its efficacy was counteracted by PKCβ overexpression in vitro.
Conclusions:
- Schisandrin A (Sch A) demonstrates significant renoprotective effects against renal fibrosis.
- Sch A alleviates renal fibrosis by inhibiting PKCβ expression and reducing oxidative stress.
- These findings highlight Sch A as a potential therapeutic agent for kidney fibrosis.
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