Complanatuside A Inhibits Seminal Vesicle Cell Apoptosis by Activating SerpinB1a in Type 2 Diabetic Mice

Abstract

Type 2 diabetes mellitus (T2DM) can trigger cell apoptosis of seminal vesicles (SVs) and impair seminal secretory functions. Complanatuside A (CA) is known for its anti‐inflammatory and antioxidant effects, as well as its ability to repair cellular damage. This study aimed to explore the potential molecular mechanisms through which CA mitigates cell apoptosis in the SVs of type 2 diabetic mice. A streptozotocin‐induced type 2 diabetic mice model was utilized, and a 1‐month intervention using CA (70 mg/kg) was administered. We monitored body weight, blood glucose levels, SV volume, and concentration of SV fluid. Hematoxylin and eosin staining was used to assess tissue damage. RNA sequencing was applied to identify differential gene expression, and the expression of target genes (ARG2, PBK, SerpinB1a, E2F2) was verified by qRT‐PCR. Changes in the apoptosis level of SV tissues in mice were detected with TUNEL staining. Compared to the control group, mice with T2DM exhibited decreased SV volume and SV fluid content, which was improved with CA treatment. Elevated expression of SerpinB1a and reduced apoptosis were observed in the T2DM‐CA group compared to T2DM mice. In summary, CA can inhibit cell apoptosis in the SVs, there by improving tissue damage in type 2 diabetic mice. SerpinB1a may be involved in this process. This study provides a new theoretical foundation for the treatment of seminal vesicle secretory dysfunction in type 2 diabetes mellitus.