火棘提取物对氯化镉致大鼠急性肾毒性的保护作用

Yixin Ke, Kaihang Yu, Weiliang Zeng, Guojun Lian
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引用次数: 7

摘要

摘要目的:探讨火棘果提取物(PFE)对氯化镉(CdCl2)致大鼠急性肾毒性的保护作用。方法:大鼠经PFE预处理后,连续注射CdCl2 (6.5 mg/kg) 5 d。结果:CdCl2组血Cd浓度、肾质量、丙二醛(MDA)、一氧化氮(NO)生成显著升高,血浆尿酸、尿素、肌酐水平显著升高(P < 0.001)。而CdCl2处理显著降低了体重和谷胱甘肽(GSH)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)和谷胱甘肽过氧化物酶(GR)水平(P < 0.001)。肾组织组织学表现为严重不良改变。此外,CdCl2治疗显著降低b细胞淋巴瘤-2 (Bcl-2)表达,升高Bcl-2相关X蛋白(Bax)、肿瘤坏死因子-α (TNF-α)表达(P < 0.001)。CdCl2处理后Nrf2/Keap 1相关蛋白Keap-1表达显著升高(P < 0.001), Nrf2、HO-1、γ-GCS、GSH-Px和NQO1表达降低(P < 0.05)。这些大鼠用PFE预处理以改善CdCl2治疗引起的变化。结论:PFE对CdCl2急性肾毒性有保护作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Protective roles of Pyracantha fortuneana extract on acute renal toxicity induced by cadmium chloride in rats 1
Abstract Purpose: To investigate the protective roles of pyracantha fortune fruit extract (PFE) on acute renal toxicity induced by cadmium chloride (CdCl2) in rats. Methods: Rats were pretreated with PFE and consecutively injected with CdCl2 (6.5 mg/kg) for 5 days. Results: The concentration of Cd, kidney weight, malondialdehyde (MDA), and nitric oxide (NO) production were remarkably increased in CdCl2 group as well as the levels of plasma uric acid, urea, and creatinine (P < 0.001). However, the body weight and glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione peroxidase (GR) levels were markedly reduced by CdCl2 treatment (P < 0.001). Histological manifestations of renal tissue showed severely adverse changes. Moreover, CdCl2 treatment significantly decreased the B-cell lymphoma-2 (Bcl-2) expression while increased the Bcl-2-Associated X Protein (Bax), tumor necrosis factor-α (TNF-α) expression (P < 0.001). Additionally, the expression of Nrf2/Keap 1 related proteins Keap-1 gained a significant increase (P < 0.001), whereas the Nrf2, HO-1, γ-GCS, GSH-Px and NQO1 expression decreased by CdCl2 treatment (P < 0.05). These rats were pretreated with PFE to improve the changes caused by CdCl2 treatment. Conclusion: PFE could protect the kidney against acute renal toxicity induced by CdCl2.
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