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Sinomenine Hydrochloride Attenuates Renal Fibrosis by Inhibiting Excessive Autophagy Induced by Adriamycin: An
Ming-Ming Zhao1, Bin Yang1, Qiu Zhang1
1Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing 100091, China.
Abstract:
The objective of this study is to investigate if sinomenine hydrochloride (SIN-HCl) could be effective against adriamycin-induced renal fibrosis by regulating autophagy in a rat model. Forty male Sprague-Dawley (SD) rats were randomly divided into control group, model group, telmisartan group, and SIN-HCl group; rat model was induced by adriamycin; all rats were given intragastric administration for 6 weeks. Urine was collected from rats in metabolic cages to determine 24 h protein level. This was done after intragastric administration for the first two weeks and then once for every two weeks. Renal pathological changes were examined by the staining of HE, Masson, and PASM. Expressions and distributions of fibronectin (FN), laminin (LN), light chain 3 (LC3), and Beclin-1 were observed by immunohistochemistry. SIN-HCl ameliorates proteinuria, meanwhile attenuating the renal pathological changes in adriamycin-induced rats and also attenuating renal fibrosis and excessive autophagy by reducing the expression of FN, LN, LC3, and Beclin-1. SIN-HCl attenuates renal fibrosis by inhibiting excessive autophagy induced by adriamycin and upregulates the basal autophagy.
Insights
Sinomenine hydrochloride (SIN-HCl) effectively treats adriamycin-induced renal fibrosis in rats by regulating autophagy. This compound reduces proteinuria and kidney damage by modulating fibronectin, laminin, LC3, and Beclin-1 levels.
Area of Science:
- Nephrology
- Pharmacology
- Cell Biology
Background:
- Adriamycin-induced nephropathy is a significant cause of renal fibrosis.
- Autophagy plays a complex role in the progression of kidney disease.
Purpose of the Study:
- To investigate the therapeutic potential of sinomenine hydrochloride (SIN-HCl) against adriamycin-induced renal fibrosis.
- To elucidate the role of autophagy regulation in SIN-HCl's renoprotective effects.
Main Methods:
- A rat model of adriamycin-induced renal fibrosis was established.
- Rats were treated with SIN-HCl or telmisartan.
- Proteinuria, renal pathology (HE, Masson, PASM staining), and expression of fibronectin, laminin, LC3, and Beclin-1 were assessed.
Main Results:
- SIN-HCl treatment ameliorated proteinuria and attenuated renal pathological changes.
- SIN-HCl reduced the expression of fibronectin, laminin, LC3, and Beclin-1, indicating reduced fibrosis and excessive autophagy.
- The drug inhibited adriamycin-induced excessive autophagy while upregulating basal autophagy.
Conclusions:
- Sinomenine hydrochloride demonstrates significant renoprotective effects against adriamycin-induced renal fibrosis.
- Regulation of autophagy is a key mechanism by which SIN-HCl exerts its therapeutic benefits.
- SIN-HCl represents a potential therapeutic agent for managing kidney fibrosis.
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