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芹菜素在对乙酰氨基酚诱导的肝毒性大鼠模型中的抗氧化和保护作用

Antioxidative and Protective Actions of Apigenin in a Paracetamol-Induced Hepatotoxicity Rat Model.

作者信息

Rašković Aleksandar, Gigov Slobodan, Čapo Ivan, Paut Kusturica Milica, Milijašević Boris, Kojić-Damjanov Sunčica, Martić Nikola

机构信息

Faculty of Medicine, Novi Sad, Serbia.

出版信息

Eur J Drug Metab Pharmacokinet. 2017 Oct;42(5):849-856. doi: 10.1007/s13318-017-0407-0.

DOI:10.1007/s13318-017-0407-0
PMID:28255865
Abstract

BACKGROUND AND OBJECTIVES

Apigenin is known to have various pharmacological properties without causing significant toxicity; however, hepatoprotective effect of apigenin is not often reported. The aim of our study was to investigate if the alterations in lipid peroxidation and antioxidant status are in favor to prove the efficacy of apigenin against paracetamol-induced hepatotoxicity.

METHODS

The effect of apigenin on paracetamol-induced hepatotoxicity in rats was examined by determining biochemical parameters, histological assessment and oxidative status in liver homogenates.

RESULTS

The treatment of animals with both apigenin and paracetamol attenuates the parameters of hepatotoxicity, especially for ALT and ALP activity which was significantly lower compared to groups of animals treated with saline and paracetamol. Hepatotoxicity induced by toxic dose of paracetamol was revealed also by notable histopathological alterations, which were not observed in the group treated with paracetamol together with apigenin. Apigenin also prevented paracetamol-induced increase in malondialdehyde (MDA) level. The activities of both CAT (catalase) and GR (glutathione reductase) enzymes after the toxic dose of paracetamol were significantly increased in the liver homogenates, compared to control group. Apigenin reversed these parameters near to values of control group.

CONCLUSIONS

The result of our study indicates that apigenin inhibits the level of lipid peroxidation and significantly increases the enzyme antioxidant defense mechanisms in paracetamol-induced hepatotoxicity in rats.

摘要

背景与目的

已知芹菜素具有多种药理特性且无明显毒性;然而,芹菜素的肝脏保护作用报道较少。我们研究的目的是调查脂质过氧化和抗氧化状态的改变是否有助于证明芹菜素对扑热息痛诱导的肝毒性的疗效。

方法

通过测定生化参数、组织学评估和肝脏匀浆中的氧化状态,研究芹菜素对大鼠扑热息痛诱导的肝毒性的影响。

结果

用芹菜素和扑热息痛治疗动物可减轻肝毒性参数,尤其是谷丙转氨酶(ALT)和碱性磷酸酶(ALP)活性,与用生理盐水和扑热息痛治疗的动物组相比显著降低。扑热息痛毒性剂量诱导的肝毒性还表现为明显的组织病理学改变,而在扑热息痛与芹菜素联合治疗组中未观察到。芹菜素还可防止扑热息痛诱导的丙二醛(MDA)水平升高。与对照组相比,扑热息痛毒性剂量后肝脏匀浆中过氧化氢酶(CAT)和谷胱甘肽还原酶(GR)的活性均显著增加。芹菜素使这些参数恢复到接近对照组的值。

结论

我们的研究结果表明,芹菜素可抑制脂质过氧化水平,并显著增强大鼠扑热息痛诱导的肝毒性中酶抗氧化防御机制。

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