Therapeutic Effects of Vernonia amygdalina on Oxidative Stress and Histopathological Damage in Pancreatic Toxicity Induced by 1,2-dimethylhydrazine in Wistar Rats

IF 1.9 Q2 Biochemistry, Genetics and Molecular Biology
Augustine O Okpiabhele, D Abu Osahon, E Akpovona Ambrose
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Abstract

Background: 1,2-Dimethylhydrazine (DMH) induces pancreatic oxidative stress via reactive oxygen species overproduction and antioxidant depletion. Given the rich phytochemical and antioxidant properties of Vernonia amygdalina, this study investigated its therapeutic effects in inhibiting oxidative stress and histopathological damage induced by DMH in Wistar rats.

Methods: Adult male Wistar rats were divided into different groups and exposed to DMH via the intraperitoneal route. Animals received oral administration of V. amygdalina ethanol extract at low (200 mg/kg) and high (400 mg/kg) doses, both before and after DMH exposure. The pancreatic tissues were then subjected to biochemical analysis and histopathological examination using standardized protocols.

Results: The administration of V. amygdalina significantly attenuated body weight loss in both the pre- and post-treatment groups. Furthermore, it significantly improved (p < 0.05) the levels of total protein, amylase, nitric oxide, catalase, superoxide dismutase, malondialdehyde, glutathione peroxidase, glutathione (GSH), and glutathione reductase and reduced GSH percentages compared to the DMH group. The pancreatic tissues from DMH-induced rats treated with V. amygdalina showed a significant reduction (p < 0.05) in organ weight compared to the DMH group. Histological studies revealed the protective and regenerative effects of V. amygdalina on pancreatic tissues.

Conclusion: This study indicates that V. amygdalina can effectively suppress irregularities in pancreatic function and oxidative stress induced by DMH toxicity due to its antioxidant properties. This observation implies that V. amygdalina holds promise as a novel therapeutic strategy for improving DMH systemic toxicity in animal models and could serve as a benchmark for future clinical trials.

苦杏仁果对1,2-二甲基肼致胰腺毒性大鼠氧化应激及组织病理损伤的治疗作用
背景:1,2-二甲基肼(DMH)通过活性氧过剩和抗氧化剂消耗诱导胰腺氧化应激。鉴于苦杏仁果丰富的植物化学和抗氧化特性,本研究探讨了苦杏仁果对DMH诱导的Wistar大鼠氧化应激和组织病理学损伤的抑制作用。方法:将成年雄性Wistar大鼠分为不同组,经腹腔注射给药。动物在DMH暴露前后分别口服低剂量(200 mg/kg)和高剂量(400 mg/kg)的苦杏仁花乙醇提取物。然后采用标准化方案对胰腺组织进行生化分析和组织病理学检查。结果:给药后和给药前组小鼠的体重下降明显减轻。与DMH组相比,总蛋白、淀粉酶、一氧化氮、过氧化氢酶、超氧化物歧化酶、丙二醛、谷胱甘肽过氧化物酶、谷胱甘肽(GSH)、谷胱甘肽还原酶水平显著提高(p < 0.05), GSH百分比显著降低。DMH诱导的大鼠胰腺组织与DMH组相比,其脏器重量显著降低(p < 0.05)。组织学研究显示苦杏仁对胰腺组织具有保护和再生作用。结论:苦杏仁苷具有抗氧化作用,可有效抑制DMH毒性引起的胰腺功能紊乱和氧化应激。这一观察结果表明,苦杏仁曲霉有望作为一种新的治疗策略,在动物模型中改善DMH的全身毒性,并可作为未来临床试验的基准。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Iranian Biomedical Journal
Iranian Biomedical Journal Biochemistry, Genetics and Molecular Biology-Biochemistry, Genetics and Molecular Biology (all)
CiteScore
3.20
自引率
0.00%
发文量
42
审稿时长
8 weeks
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