1. Asiatic acid rescues intestinal tissue by suppressing molecular, biochemical, and histopathological changes associated with the development of ulcerative colitis.
- Author
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Lokman MS, Kassab RB, Salem FAM, Elshopakey GE, Hussein A, Aldarmahi AA, Theyab A, Alzahrani KJ, Hassan KE, Alsharif KF, Albrakati A, Tayyeb JZ, El-Khadragy M, Alkhateeb MA, Al-Ghamdy AO, Althagafi HA, Abdel Moneim AE, and El-Hennamy RE
- Subjects
- Animals, Rats, Male, Antioxidants pharmacology, Colon pathology, Colon drug effects, Colon metabolism, Lipid Peroxidation drug effects, Disease Models, Animal, Anti-Inflammatory Agents pharmacology, NF-E2-Related Factor 2 metabolism, Rats, Wistar, Colitis, Ulcerative drug therapy, Colitis, Ulcerative chemically induced, Colitis, Ulcerative pathology, Colitis, Ulcerative metabolism, Pentacyclic Triterpenes pharmacology, Oxidative Stress drug effects, Apoptosis drug effects
- Abstract
Asiatic acid (AA) is a polyphenolic compound with potent antioxidative and anti-inflammatory activities that make it a potential choice to attenuate inflammation and oxidative insults associated with ulcerative colitis (UC). Hence, the present study aimed to evaluate if AA can attenuate molecular, biochemical, and histological alterations in the acetic acid-induced UC model in rats. To perform the study, five groups were applied, including the control, acetic acid-induced UC, UC-treated with 40 mg/kg aminosalicylate (5-ASA), UC-treated with 20 mg/kg AA, and UC-treated with 40 mg/kg AA. Levels of different markers of inflammation, oxidative stress, and apoptosis were studied along with histological approaches. The induction of UC increased the levels of lipid peroxidation (LPO) and nitric oxide (NO). Additionally, the nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream antioxidant proteins [catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), glutathione peroxidase (GPx), and glutathione reductase (GR)] were down-regulated in the colon tissue. Moreover, the inflammatory mediators [myeloperoxidase (MPO), monocyte chemotactic protein 1 (MCP1), prostaglandin E2 (PGE2), nuclear factor-kappa B (NF-κB), tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β)] were increased in the colon tissue after the induction of UC. Notably, an apoptotic response was developed, as demonstrated by the increased caspase-3 and Bax and decreased Bcl2. Interestingly, AA administration at both doses lessened the molecular, biochemical, and histopathological changes following the induction in the colon tissue of UC. In conclusion, AA could improve the antioxidative status and attenuate the inflammatory and apoptotic challenges associated with UC., (© 2024 The Author(s).)
- Published
- 2024
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