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牛膝草全植物提取物对 N-亚硝基二乙胺和 CCl(4)诱导的瑞士白化大鼠肝癌发生的改善作用。

Amelioration effects against N-nitrosodiethylamine and CCl(4)-induced hepatocarcinogenesis in Swiss albino rats by whole plant extract of Achyranthes aspera.

机构信息

Translational Cancer Research laboratory, Rajiv Gandhi Center for Biotechnology, Thycaud P.O, Poojapura, Thiruvananthapuram - 695 014, Kerala; Pharmacognosy and Ethnopharmacology Division, National Botanical Research Institute, Rana Pratap Marg, Lucknow - 226 001.

出版信息

Indian J Pharmacol. 2010 Dec;42(6):370-5. doi: 10.4103/0253-7613.71921.

DOI:10.4103/0253-7613.71921
PMID:21189908
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2991695/
Abstract

OBJECTIVE

The prevalence of oxidative stress may be implicated in the etiology of many pathological conditions. Protective antioxidant action imparted by many plant extracts and plant products make them a promising therapeutic drug for free-radical-induced pathologies. In this study, we assessed the antioxidant potential and suppressive effects of Achyranthes aspera by evaluating the hepatic diagnostic markers on chemical-induced hepatocarcinogenesis.

MATERIALS AND METHODS

The in vivo model of hepatocarcinogenesis was studied in Swiss albino rats. Experimental rats were divided into five groups: control, positive control (NDEA and CCl(4)), A. aspera treated (100, 200, and 400 mg/kg b.w.). At 20 weeks after the administration of NDEA and CCl(4), treated rats received A. aspera extract (AAE) at a dose of 100, 200, and 400 mg/kg once daily route. At the end of 24 weeks, the liver and relative liver weight and body weight were estimated. Lipid peroxidation (LPO), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and reduced glutathione (GSH) were assayed. The hepatic diagnostic markers namely serum glutamic oxaloacetic transminase (AST), serum glutamic pyruvate transminase (ALT), serum alkaline phosphatase (ALP), gamma glutamyl transpeptidase (GGT), and bilirubin (BL) were also assayed, and the histopathological studies were investigated in control, positive control, and experimental groups.

RESULTS

The extract did not show acute toxicity and the per se effect of the extract showed decrease in LPO, demonstrating antioxidant potential and furthermore no change in the hepatic diagnosis markers was observed. Administration of AAE suppressed hepatic diagnostic and oxidative stress markers as revealed by decrease in NDEA and CCl(4) -induced elevated levels of SGPT, SGOT, SALP, GGT, bilirubin, and LPO. There was also a significant elevation in the levels of SOD, CAT, GPx, GST, and GSH as observed after AAE treatment. The liver and relative liver weight were decreased after treatment with AAE in comparison to positive control group. The architecture of hepatic tissue was normalized upon treatment with extract at different dose graded at 100, 200, and 400 mg/kg. b.w. in comparison to positive control group.

CONCLUSION

These results suggest that A. aspera significantly alleviate hepatic diagnostic and oxidative stress markers which signify its protective effect against NDEA and CCl(4)-induced two-stage hepatocarcinogenesis.

摘要

目的

氧化应激的流行可能与许多病理状况的病因有关。许多植物提取物和植物产品具有保护抗氧化作用,这使它们成为治疗自由基诱导的病理的有前途的治疗药物。在这项研究中,我们通过评估化学诱导的肝癌发生中的肝诊断标志物来评估菾菜的抗氧化潜力和抑制作用。

材料和方法

在瑞士白化大鼠中研究了肝癌的体内模型。实验大鼠分为五组:对照组、阳性对照组(NDEA 和 CCl4)、菾菜处理组(100、200 和 400mg/kg.b.w.)。在给予 NDEA 和 CCl4后 20 周,给予菾菜提取物(AAE)100、200 和 400mg/kg 每日一次。在 24 周结束时,估计肝和相对肝重和体重。测定脂质过氧化(LPO)、超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)、谷胱甘肽-S-转移酶(GST)和还原型谷胱甘肽(GSH)。还测定了肝诊断标志物,即血清谷氨酸草酰乙酸转氨酶(AST)、血清谷氨酸丙酮酸转氨酶(ALT)、血清碱性磷酸酶(ALP)、γ-谷氨酰转肽酶(GGT)和胆红素(BL),并对对照组、阳性对照组和实验组进行了组织病理学研究。

结果

提取物未显示出急性毒性,并且提取物的自身作用显示出 LPO 的降低,表明具有抗氧化潜力,并且没有观察到肝诊断标志物的变化。AAE 的给药抑制了肝诊断和氧化应激标志物,如 NDEA 和 CCl4诱导的 SGPT、SGOT、SALP、GGT、胆红素和 LPO 水平升高。在用 AAE 治疗后,SOD、CAT、GPx、GST 和 GSH 的水平也显著升高。与阳性对照组相比,用 AAE 治疗后,肝和相对肝重降低。与阳性对照组相比,在 100、200 和 400mg/kg.b.w.的不同剂量分级下,用提取物处理后,肝组织的结构得到了正常化。

结论

这些结果表明,菾菜显着减轻肝诊断和氧化应激标志物,这表明其对 NDEA 和 CCl4诱导的两阶段肝癌发生具有保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf7d/2991695/88ec9f519ce4/IJPharm-42-370-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf7d/2991695/88ec9f519ce4/IJPharm-42-370-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cf7d/2991695/88ec9f519ce4/IJPharm-42-370-g001.jpg

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