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百里香酚在药物诱导性胃溃疡模型中的肝保护作用。

Hepatoprotective Role of Thymol in Drug-Induced Gastric Ulcer Model.

机构信息

Department of Biology, Faculty of Science, Ataturk University, Erzurum, TURKEY.

Department of Biochemistry, Faculty of Veterinary, Ataturk University, Erzurum, TURKEY.

出版信息

Ann Hepatol. 2018 Oct 16;17(6):980-991. doi: 10.5604/01.3001.0012.7198.

Abstract

INTRODUCTION AND AIM

Indo is widely one of the non-steroidal anti-inflammatory drugs and one of the common toxic effects of this drug is hepatic failure. Thymol is a monoterpene phenol with many different pharmacological activities. However, up to now its hepatoprotective effects on Indo-induced gastric ulcer model in rats have not been explored yet.

MATERIAL AND METHODS

Thirty five Sprague-Dawley rats were divided into seven groups: control, ulcer control (30 mg/kg Indo), Indo + reference standard (50 mg/kg Rantidine), Indo + Thymol (75, 100, 250 and 500 mg/kg) groups. 10 minutes after the induction of ulcer with Indo; Thymol was orally administered to the rats. Liver function enzymes (AST, ALT and LDH) were measured from serum samples. TOS/TAC, TNF-α and PGE2 levels, eNOS and Caspase-3 activity were assessed from tissue homogenate samples. In addition, histopathologic analysis on liver sections was performed.

RESULTS

Indo significantly increased the levels of hepatic enzymes, TNF-α and eNOS, and caspase-3 activation, while decreased PGE2 levels. Furthermore, it induced oxidative stress as evidenced by elevated TOS and decreased TAC levels. However, Thymol treatment induced a significant improvement in these parameters, especially in 250 mg/kg dose. On the other hand, treatment with Thymol 500 mg/kg dramatically affected the parameters much worse than the Indo treated group.

CONCLUSION

The findings of the current study demonstrated that Thymol administration significantly ameliorated liver injury due to Indo toxicity. This effect of Thymol (250 mg/kg) may be mediated by its anti-oxidative or anti-inflammatory effect, and up-regulation the synthesis of PGE2.

摘要

简介和目的

吲哚美辛是一种广泛使用的非甾体抗炎药,这种药物的常见毒性作用之一是肝衰竭。百里香酚是一种单萜酚类化合物,具有许多不同的药理活性。然而,到目前为止,它对吲哚美辛诱导的大鼠胃溃疡模型的保肝作用尚未得到探索。

材料和方法

35 只 Sprague-Dawley 大鼠分为 7 组:对照组、溃疡对照组(30mg/kg 吲哚美辛)、吲哚美辛+参比标准(50mg/kg 雷尼替丁)、吲哚美辛+百里香酚(75、100、250 和 500mg/kg)组。吲哚美辛诱导溃疡 10 分钟后,将百里香酚灌胃给药。从血清样本中测量肝功能酶(AST、ALT 和 LDH)。从组织匀浆样本中评估 TOS/TAC、TNF-α 和 PGE2 水平、eNOS 和 Caspase-3 活性。此外,对肝切片进行组织病理学分析。

结果

吲哚美辛显著增加了肝酶、TNF-α 和 eNOS 的水平,以及 Caspase-3 的激活,同时降低了 PGE2 水平。此外,它还通过增加 TOS 和降低 TAC 水平引起氧化应激。然而,百里香酚治疗显著改善了这些参数,尤其是在 250mg/kg 剂量下。另一方面,500mg/kg 剂量的百里香酚治疗对这些参数的影响比吲哚美辛治疗组差得多。

结论

本研究结果表明,百里香酚给药可显著改善吲哚美辛毒性引起的肝损伤。百里香酚(250mg/kg)的这种作用可能是通过其抗氧化或抗炎作用介导的,并上调 PGE2 的合成。

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