Schisanhenol Alleviates Mycophenolic Acid-Induced Intestinal Epithelial Cell Barrier Damage by Activating the Nrf2/HO-1 Signaling Pathway

五味子酚通过激活Nrf2/HO-1信号通路减轻霉酚酸诱导的肠上皮细胞屏障损伤

阅读:1

Abstract

BACKGROUND: Reactive oxygen species (ROS)-mediated apoptosis of intestinal epithelial cells and tight junction (TJ) protein loss play critical roles in mycophenolic acid (MPA)-induced disruption of intestinal epithelial barrier function, yet no effective therapeutic strategies exist. Schisanhenol (Sal), a major component of the traditional Chinese medicine Wuzhi capsule, exhibits strong antioxidant activity. OBJECTIVES: The present study aimed to investigate the protective efficacy and mechanisms of Sal against MPA-induced damage to the intestinal mechanical barrier. METHODS: Caco-2 cells were exposed to MPA (10 μM), Sal (5, 10, and 25 μM), or ML385 (2 μM) for 24 hours. Cell viability was measured via a Cell Counting Kit-8 (CCK-8) assay. The expression of apoptosis-related and TJ proteins was evaluated through Western blot analysis. Flow cytometry was used to quantify the percentage of apoptotic Caco-2 cells. Immunofluorescence assays were performed to assess the localization of TJ proteins. Intracellular ROS levels were measured using H2DCFDA staining. Oxidative and antioxidative biomarker levels were quantified using specific assay kits. RESULTS: Sal significantly increased the viability of MPA-treated cells. It also upregulated Bcl-2 expression and reduced apoptosis. Furthermore, Sal increased the expression of the TJ proteins ZO-1 and occludin. Additionally, Sal upregulated the MPA-mediated decrease in Nrf2/HO-1 expression, reduced intracellular ROS accumulation, and increased the levels of antioxidants, including SOD, CAT, and GSH. However, ML385 partially abrogated the protective effects of Sal. CONCLUSIONS: Schisanhenol alleviates MPA-induced intestinal mechanical barrier damage via modulation of the Nrf2 signaling pathway, highlighting its antioxidant and antiapoptotic properties.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。