辣木(Mo11)和Musa sapientum(Ms06)的抗毒作用通过Ki67/P53介导的途径改善氯化镉诱导的大鼠肾脏增生和细胞凋亡

A. Akinlolu, Mubarak Oloduowo Ameen, G. Ebito, N. Asogwa, R. Akindele, B. Fagbohunka, Zainab Arowolo, T. Garuba
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引用次数: 0

摘要

背景:镉(Cd)是一种公认的致癌物质。镉诱导的肾毒性导致氧化应激、排泄肾功能丧失和小鼠肾细胞凋亡。目的:本研究评估了MO11(从辣木叶中分离)和MS06(从Musa sapientum suckers中分离)对氯化镉(CdCl2)诱导的大鼠肾毒性、肾增生和细胞凋亡的肾保护作用。材料和方法:24只成年雄性Wistar大鼠(平均体重155g)随机分为7组(n=4)。第1组接受生理盐水。第2-4组和第6组接受1.5 mg/kg体重CdCl2的单次腹膜内(i.p)给药(第1天)。第3-4组和第6组分别用15 mg/kg体重的MO11、15 mg/kg重量的MO11+7 mg/kg体重的MS06和3.35 mg/kg体重的阿霉素进行后处理(第1-17天)。第5组分别只接受橄榄油剂量(载体)(第1-17天)。评估了1-6组大鼠肾匀浆中增殖(Ki67)和凋亡(p53)生物标志物的肾脏组织病理学(苏木精和伊红技术)和酶联免疫吸附测定浓度。结果:组织病理学分析显示1-6组大鼠肾脏组织学正常。与第2组相比,用MO11、MO11+MS06和阿霉素对CdCl2诱导的肾毒性进行后处理导致第3、4和6组Ki67和p53的下调。结论:MO11和MS06具有肾保护、抗增殖和抗细胞凋亡的作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Antitoxic principles from Moringa oleifera (Mo11) and Musa sapientum (Ms06) ameliorated cadmium chloride-induced renal hyperplasia and apoptosis through Ki67/P53-mediated pathway in rats
Background: Cadmium (Cd) is an established carcinogen. Cd-induced renotoxicity resulted in oxidative stress, loss of excretory kidney functions, and apoptosis of murine kidney cells. Objectives: This study evaluated renoprotective potentials of MO11 (isolated from Moringa oleifera leaves) and MS06 (isolated from Musa sapientum suckers) against Cd chloride (CdCl2)-induced renotoxicity, renal hyperplasia, and apoptosis in rats. Materials and Methods: Twenty-four adult male Wistar rats (average weight of 155 g) were randomly divided into seven groups (n = 4). Group 1 received physiological saline. Groups 2–4 and 6 received single intraperitoneal (i.p) administration of 1.5 mg/kg body weight of CdCl2 (i.p) (Day 1). Groups 3–4 and 6 were posttreated with 15 mg/kg body weight of MO11, 15 mg/kg body weight of MO11 +7 mg/kg body weight of MS06, and 3.35 mg/kg body weight of doxorubicin, respectively (days: 1–17). Group 5 received only olive oil dose (vehicle), respectively (days: 1–17). Kidney histopathology (hematoxylin and eosin technique) and enzyme-linked immunosorbent assay concentrations of biomarkers of proliferation (Ki67) and apoptosis (p53) in kidney homogenates of rats of Groups 1–6 were evaluated. Results: Histopathological analyses showed normal kidney histology in the rats of Groups 1–6. Posttreatments of CdCl2-induced renotoxicity with MO11, MO11+MS06, and doxorubicin resulted in downregulations of Ki67 and p53 in Groups 3, 4, and 6 as compared with Group 2. Conclusion: MO11 and MS06 possess renoprotective, anti-proliferation, and anti-apoptosis potentials.
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