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阿魏酸苯乙酯对乙酰水杨酸毒性大鼠肾脏的保护作用。

Caffeic acid phenethyl ester protects kidneys against acetylsalicylic acid toxicity in rats.

机构信息

Faculty of Medicine, Department of Urology, Dicle University, Diyarbakir, Turkey.

出版信息

Ren Fail. 2012;34(9):1150-5. doi: 10.3109/0886022X.2012.717485. Epub 2012 Sep 6.

DOI:10.3109/0886022X.2012.717485
PMID:22950656
Abstract

AIM

The aim of this study was to investigate the protective effect of caffeic acid phenethyl ester (CAPE) on acetylsalicylic acid (ASA)-induced renal damage in rats.

MATERIALS AND METHODS

A total of 40 rats were randomly divided into five groups, with eight rats in each group-group 1: control, not receiving any medication; group 2: ASA (50 mg/kg/day); group 3: ASA (50 mg/kg/day) + CAPE (20 μg/kg/day); group 4: ASA (100 mg/kg/day); and group 5: ASA (100 mg/kg/day) + CAPE (20 μg/kg/day). ASA and CAPE were given via orogastric gavage for 5 days. The total oxidant status (TOS), total antioxidant capacity (TAC), and paraoxonase-1 (PON-1) activity of the blood samples and kidney tissues were determined. Histopathological examinations of the kidneys were performed using light microscopic methods.

RESULTS

The TOS level in the serum of rats and kidney tissues given ASA (groups 2 and 4) significantly increased, but the levels of TAC and PON-1 in these tissues significantly decreased in group 4 when compared with the control rats (p < 0.05). The levels of TAC and PON-1 in the kidney tissues increased and the levels of TOS decreased in the CAPE treatment groups (groups 3 and 5) when compared with the rats in the no CAPE treatment groups (groups 2 and 4). The PON-1, TAC, and TOS values reverted to normal levels in group 5 when compared to group 4 (p < 0.05). These results were supported by histopathological observation.

CONCLUSION

Oxidative stress plays an important role in ASA-induced nephrotoxicity, and CAPE may protect against ASA-induced nephrotoxicity in rats.

摘要

目的

本研究旨在探讨咖啡酸苯乙酯(CAPE)对乙酰水杨酸(ASA)诱导的大鼠肾损伤的保护作用。

材料和方法

将 40 只大鼠随机分为五组,每组 8 只:组 1:对照组,未给予任何药物;组 2:ASA(50mg/kg/天);组 3:ASA(50mg/kg/天)+CAPE(20μg/kg/天);组 4:ASA(100mg/kg/天);组 5:ASA(100mg/kg/天)+CAPE(20μg/kg/天)。ASA 和 CAPE 通过灌胃给予,共 5 天。测定血液样本和肾组织中的总氧化状态(TOS)、总抗氧化能力(TAC)和对氧磷酶-1(PON-1)活性。采用光镜方法对肾脏进行组织病理学检查。

结果

与对照组大鼠相比,给予 ASA(组 2 和 4)的大鼠血清和肾组织中的 TOS 水平显著升高,而 TAC 和 PON-1 水平显著降低(p<0.05)。与未给予 CAPE 治疗的大鼠(组 2 和 4)相比,给予 CAPE 治疗的大鼠(组 3 和 5)肾组织中的 TAC 和 PON-1 水平升高,TOS 水平降低。与组 4 相比,组 5 中的 PON-1、TAC 和 TOS 值恢复正常(p<0.05)。这些结果得到了组织病理学观察的支持。

结论

氧化应激在 ASA 诱导的肾毒性中起重要作用,CAPE 可能对 ASA 诱导的大鼠肾毒性具有保护作用。

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