Department of Medical Physiology, Faculty of Medicine, Assiut University, Assiut, 71526, Egypt.
Laboratory of Physiology, Department of Zoology and Entomology, Faculty of Science, Assiut University, Assiut, Egypt.
BMC Complement Med Ther. 2023 Nov 22;23(1):423. doi: 10.1186/s12906-023-04250-y.
The liver was identified as a primary target organ for the chemo-radiological effects of uranyl acetate (UA). Although the anti-oxidant and anti-apoptotic properties of gallic acid (GA) make it a promising phytochemical to resist its hazards, there is no available data in this area of research.
To address this issue, eighteen rats were randomly and equally divided into three groups. One group was received carboxymethyl cellulose (vehicle of GA) and kept as a control. The UA group was injected intraperitoneally with UA at a single dose of 5 mg/kg body weight. The third group (GA + UA group) was treated with GA orally at a dose of 100 mg/kg body weight for 14 days before UA exposure. UA was injected on the 15th day of the experiment in either the UA group or the GA + UA group. The biochemical, histological, and immunohistochemical findings in the GA + UA group were compared to both control and UA groups.
The results showed that UA exposure led to a range of adverse effects. These included elevated plasma levels of aspartate aminotransferase, lactate dehydrogenase, total protein, globulin, glucose, total cholesterol, triglycerides, low-density lipoprotein cholesterol, and very-low-density lipoprotein and decreased plasma levels of high-density lipoprotein cholesterol. The exposure also disrupted the redox balance, evident through decreased plasma total antioxidant capacity and hepatic nitric oxide, superoxide dismutase, reduced glutathione, glutathione-S-transferase, glutathione reductase, and glutathione peroxidase and increased hepatic oxidized glutathione and malondialdehyde. Plasma levels of albumin and alanine aminotransferase did not significantly change in all groups. Histopathological analysis revealed damage to liver tissue, characterized by deteriorations in tissue structure, excessive collagen accumulation, and depletion of glycogen. Furthermore, UA exposure up-regulated the immuno-expression of cleaved caspase-3 and down-regulated the immuno-expression of nuclear factor-erythroid-2-related factor 2 in hepatic tissues, indicating an induction of apoptosis and oxidative stress response. However, the pre-treatment with GA proved to be effective in mitigating these negative effects induced by UA exposure, except for the disturbances in the lipid profile.
The study suggests that GA has the potential to act as a protective agent against the adverse effects of UA exposure on the liver. Its ability to restore redox balance and inhibit apoptosis makes it a promising candidate for countering the harmful effects of chemo-radiological agents such as UA.
醋酸铀酰被认为是化学辐射对肝脏产生毒副作用的主要靶器官。虽然没食子酸（GA）具有抗氧化和抗凋亡的特性，使其成为一种有前途的植物化学物质，可以抵抗其危害，但在这一研究领域尚无可用数据。
为了解决这个问题，将 18 只大鼠随机均分为三组。一组给予羧甲基纤维素（GA 的载体）作为对照。UA 组一次性腹腔注射 5mg/kg 体重的 UA。第三组（GA+UA 组）在暴露于 UA 之前 14 天每天口服 100mg/kg 体重的 GA。在实验的第 15 天，UA 组或 GA+UA 组注射 UA。将 GA+UA 组的生化、组织学和免疫组织化学结果与对照组和 UA 组进行比较。
结果表明，UA 暴露导致了一系列不良反应。包括天冬氨酸转氨酶、乳酸脱氢酶、总蛋白、球蛋白、葡萄糖、总胆固醇、甘油三酯、低密度脂蛋白胆固醇和极低密度脂蛋白血浆水平升高，而高密度脂蛋白胆固醇血浆水平降低。暴露还破坏了氧化还原平衡，表现为血浆总抗氧化能力和肝一氧化氮、超氧化物歧化酶、还原型谷胱甘肽、谷胱甘肽-S-转移酶、谷胱甘肽还原酶和谷胱甘肽过氧化物酶降低，肝氧化型谷胱甘肽和丙二醛增加。所有组的白蛋白和丙氨酸转氨酶血浆水平均无显著变化。组织病理学分析显示肝组织损伤，表现为组织结构恶化、胶原过度积累和糖原耗竭。此外，UA 暴露上调了肝组织中 cleaved caspase-3 的免疫表达，下调了核因子-红细胞相关因子 2 的免疫表达，提示诱导了细胞凋亡和氧化应激反应。然而，GA 的预处理被证明可以有效减轻 UA 暴露引起的这些负面效应，除了脂质谱的紊乱。
研究表明，GA 具有作为 UA 暴露对肝脏产生的毒副作用的保护剂的潜力。其恢复氧化还原平衡和抑制凋亡的能力使其成为对抗 UA 等化学辐射剂的有害影响的有前途的候选药物。
