Abstract
Abstract
Ulcerative colitis (UC) is a chronic inflammatory bowel disease associated with intestinal inflammation, mucosal injury, and impaired mitochondrial homeostasis. Modulation of mitophagy may help preserve mitochondrial quality and limit tissue damage during intestinal inflammation. This study investigated the protective effects of a p62-mediated mitophagy inducer (PMI) in dextran sulfate sodium (DSS)-induced colitis in mice, focusing on mitochondrial quality control, inflammatory responses, and apoptosis. Male mice were randomly divided into five groups: control, DSS, DSS + PMI, DSS + 5-aminosalicylic acid (5-ASA), and DSS + PMI + 5-ASA. Colitis was induced with 2.5% DSS, and PMI was administered at 10 mg per kg per day Disease severity was determined by body weight, disease activity index DAI, colon length and weight, and histopathological examination. Western blotting was performed to determine the colonic expression of p62, VDAC1, cleaved caspase-3, and COX-2. DSS exposure produced evident clinical and pathological features of colitis, including body weight loss, increased DAI, and reduced colon length. PMI treatment attenuated these changes, while combined administration with 5-ASA produced further improvement in several disease parameters. PMI treatment was also associated with reduced COX-2, p62, and cleaved caspase-3 expression and increased VDAC1 expression, indicating modulation of mitochondrial quality control accompanied by reduced inflammatory and apoptotic signaling. Histopathological examination further showed less mucosal damage and inflammatory alteration following PMI treatment. Overall, PMI attenuated DSS-induced colitis and was associated with improved mitochondrial quality control and reduced inflammatory and apoptotic responses
| Has the manuscript been published | not published |
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| Intend to be published in the IJPS ? | Yes |
