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叶提取物可抑制丙草胺诱导的大鼠肝脏氧化和凋亡损伤。

leaf extract ebbs propanil-induced oxidative and apoptotic damage in the liver of rats.

机构信息

Department of Biochemistry, Faculty of Basic Medical Sciences, Redeemer's University, Ede, Nigeria.

Department of Biochemistry, Faculty of Basic Medical Sciences, University of Ibadan, Ibadan, Nigeria.

出版信息

Drug Chem Toxicol. 2022 Jul;45(4):1476-1483. doi: 10.1080/01480545.2020.1842884. Epub 2020 Nov 4.

DOI:10.1080/01480545.2020.1842884
PMID:33148076
Abstract

Phytochemicals derived from plant sources are well recognized as sources of pharmacologically potent drugs in the treatment of several oxidative stress-related ailments. Dichloromethane/methanol (1:1) leaf extract of was evaluated for its possible protection against oxidative stress and apoptosis in the liver of male Wistar rats exposed to propanil (PRP). In the experimental design, olive oil served as the vehicle, and rats were grouped into control (2 mL/kg olive oil), PRP (200 mg/kg/day), extract (200 mg/kg/day), and extract (200 mg/kg/day)+PRP (200 mg/kg/day), and treated daily, p.o., for seven days. Oxidative stress parameters, B-cell lymphoma 2 (Bcl-2), Bcl 2-associated X protein (Bax), p53, caspases (9/3), and terminal transferase dUTP nick end labeling (TUNEL) assays were observed in all groups. Propanil significantly elevated superoxide dismutase and lipid peroxidation levels, while concomitantly depleting GSH and p53 levels. Further, PRP enhanced the expressions of caspase-9, caspase-3, Bax, and TUNEL-positive cells in the liver of rats. However, these observed alterations were reversed following treatment with extract. Our studies suggest that extract protected against PRP toxicity by reducing oxidative stress and attenuating critical endpoints in the intrinsic apoptotic pathway.

摘要

植物源的植物化学物质被广泛认为是治疗多种氧化应激相关疾病的药理学有效药物的来源。对 的二氯甲烷/甲醇(1:1)叶提取物进行了评估,以研究其对暴露于丙草胺(PRP)的雄性 Wistar 大鼠肝脏中氧化应激和细胞凋亡的可能保护作用。在实验设计中,橄榄油用作载体,将大鼠分为对照组(2ml/kg 橄榄油)、PRP 组(200mg/kg/天)、 提取物组(200mg/kg/天)和 提取物组(200mg/kg/天)+PRP 组(200mg/kg/天),每天口服给药,连续 7 天。观察所有组的氧化应激参数、B 细胞淋巴瘤 2(Bcl-2)、Bcl-2 相关 X 蛋白(Bax)、p53、半胱天冬酶(9/3)和末端转移酶 dUTP 缺口末端标记(TUNEL)测定。丙草胺显著升高超氧化物歧化酶和脂质过氧化水平,同时耗竭 GSH 和 p53 水平。此外,PRP 增强了大鼠肝脏中 caspase-9、caspase-3、Bax 和 TUNEL 阳性细胞的表达。然而,在用 提取物处理后,这些观察到的变化得到了逆转。我们的研究表明, 提取物通过降低氧化应激和减轻内在凋亡途径中的关键终点来保护大鼠免受 PRP 毒性的影响。

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