Tripterygium Glycosides Weakened Enteric Ischemia/Reperfusion Detriment via the Nrf2/HO-1 Pathway

Abstract

Background: Tripterygium glycosides (TG) is a bioactive component of Tripterygium wilfordii. Protection against ischemia/reperfusion (I/R) injuries has been shown in animal models. However, the specific mechanism of TG in alleviating intestinal ischemia/reperfusion injury is still unclear. Methods: To assess the impact of TG on nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) levels was evaluated via the pathology, pro-inflammatory and oxidative stress level and enteric epithelial cell apoptosis in enteric I/R injured rats. We used western blot (WB) analysis, immunofluorescence staining and immunohistochemical staining. After this, a model of intestinal injury in vitro was established. IEC-6 cells were induced by hypoxia/reoxygenation (H/R). The silence of Nrf2 and HO-1 was assessed via small interfering ribonucleic acid (siRNA) (si-Nrf2). Cell viability, oxidative stress, pro-inflammatory levels, and cell apoptosis were utilized to investigate whether protection via TG depended on Nrf2/HO-1. Results: The declined levels of Nrf2 and HO-1 induced via I/R detriment in enteric tissue was reversed via TG remedy was discovered. In the meantime, TG protected against enteric morphologic detriment, inflammatory reaction and oxidative stress, and cell apoptosis induced via I/R. Furthermore, transfection with si-Nrf2 memorably abolished the whole protection of TG on I/R-induced detriment. Conclusions: Hence, we concluded that through the Nrf2/HO-1 pathway, TG restrained enteric I/R detriment. Our study provides a new therapeutic drug for treating enteric I/R detriment.