Experimental Study on Danggui Shaoyao San Improving Renal Fibrosis by Promoting Autophagy

Area of Science:

• Nephrology
• Pharmacology
• Cell Biology

Background:

• Renal fibrosis, characterized by extracellular matrix deposition, is a key pathological feature of chronic kidney disease (CKD).
• Traditional Chinese medicine formulas, such as Danggui Shaoyao San (DSS), have shown potential in managing CKD.
• Autophagy plays a crucial role in cellular homeostasis and has been implicated in the pathogenesis of kidney fibrosis.

Purpose of the Study:

• To investigate the effects of Danggui Shaoyao San (DSS) on renal fibrosis and apoptosis in a TGF-β1-induced cell model.
• To elucidate the underlying mechanism of DSS action, particularly its role in regulating autophagy.
• To compare the efficacy of DSS with rapamycin, a known autophagy enhancer.

Main Methods:

• Establishment of a renal fibrosis model using NRK-52E cells stimulated with TGF-β1.
• Treatment of cells with DSS and rapamycin (positive control), with 3-MA used to inhibit autophagy.
• Assessment of fibronectin (FN), caspase-3, and autophagy-related proteins (LC3 II/I, Beclin 1, mTOR, p62) using Western blot and immunofluorescence assays.

Main Results:

• DSS significantly reduced the protein levels of fibronectin and caspase-3 in TGF-β1-induced NRK-52E cells.
• TGF-β1 stimulation decreased autophagy markers (LC3 II/I, Beclin 1) and increased mTOR and p62; DSS reversed these changes.
• DSS promoted autophagy, evidenced by increased LC3 II/I and Beclin 1, and reduced mTOR in cells treated with the autophagy inhibitor 3-MA.

Conclusions:

• Danggui Shaoyao San (DSS) effectively mitigates TGF-β1-induced renal fibrosis and apoptosis in NRK-52E cells.
• The renoprotective effects of DSS are likely mediated through the promotion of autophagy.
• DSS represents a promising therapeutic agent for managing chronic kidney disease by modulating cellular autophagy pathways.