ArticleFrontiers in pharmacology2025
Wuzi-Yanzong-Wan inhibits testicular mitochondrial apoptosis in rats by downregulating TAp73-Mediated P38 MAPK-ADAM17 pathway.
Article in Frontiers in pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objective: This study investigates the relationship between TAp73 protein overexpression and sperm quality, and evaluates the prophylactic and therapeutic effects of Wuzi-Yanzong-Wan (WZYZW) on oligoasthenospermia (OA) induced by tripterygium glycosides (TGs) and etoposide in rats. Furthermore, it elucidates the underlying mechanism by analyzing the intervention's role in downregulating TAp73 protein expression and modulating the P38 MAPK-ADAM17 signaling pathway, ultimately providing empirical evidence to support its clinical application. Methods: Sprague-Dawley (SD) rats received TGs (40 mg/kg/d for 8 weeks) to induce OA. Intervention groups were treated with either WZYZW (1 or 2 g/kg/d) or Shengjing Capsule (SJJN). Meanwhile, a TAp73-overexpressing Sertoli-germ cell co-culture system was established using etoposide (200 μM for 48 h) and treated with WZYZW-containing serum (2.5%-10%), to explore the mechanisms associated with TAp73. Results: The Conclusion: This study highlights that WZYZW effectively alleviates testicular DNA damage and mitochondrial apoptosis, suggesting that its mechanism may be associated with reduced TAp73 expression. These experimental findings provide a novel therapeutic target for the clinical application of WZYZW in OA treatment.
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