Modulation of Prostaglandin-Endoperoxide Synthase 1 by Caulis Sinomenii: A Novel Approach to Alleviating Diabetic Peripheral Neuropathy Through Apoptosis Inhibition and Anti-inflammatory Effects.

Abstract

Diabetic peripheral neuropathy (DPN) is a common and debilitating complication of diabetes, characterized by neurodegeneration and chronic pain. This study investigates the potential of Caulis Sinomenii (CS), a traditional Chinese medicine, to alleviate DPN through the modulation of prostaglandin-endoperoxide synthase 1 (PTGS1), microglial apoptosis, and inflammation. DPN was induced in mice using streptozotocin (STZ). Pain sensitivity was assessed using the hot plate and mechanical allodynia tests. Inflammatory cytokines (IL-6, TNF-α) were measured by ELISA. Histopathology and TUNEL staining were used to evaluate tissue damage and apoptosis. Network pharmacology and molecular docking identified key targets, including PTGS1. In vitro, BV2 microglial cells were treated with CS to assess cell viability, apoptosis, and inflammation. CS significantly reduced pain sensitivity, inflammatory cytokines, and neuronal apoptosis in DPN mice. Network analysis highlighted PTGS1 as a critical target of CS. In vitro, CS downregulated PTGS1 and reduced apoptosis while suppressing inflammatory responses. CS alleviates DPN by modulating PTGS1 expression, inhibiting apoptosis, and reducing inflammation. These findings suggest CS as a promising therapeutic for DPN.