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二甲基亚砜对四氯化碳致大鼠肝损伤的影响。

Effects of dimethyl sulphoxide against liver injury caused by carbon tetrachloride in rats.

机构信息

Department of Biology, The Chinese University of Hong Kong, Shatin, N. T., Hong Kong.

出版信息

Toxicol Mech Methods. 2004;14(3):167-76. doi: 10.1080/15376520490429364.

Abstract

A single oral dose of 1.25 ml kg(-1) of carbon tetrachloride (CCl(4)) was sufficient to induce significantly elevated levels of serum glutamic pyruvic transaminase (SGPT) and serum glutamic oxaloacetic transaminase (SGOT) together with signs of acute centrilobular necrosis and fatty accumulation in liver tissue. Dimethyl sulfoxide (DMSO) in different dosages (2750 mg kg(-1), 5500 mg kg(-1) and 8250 mg kg(-1); dissolved in saline) were screened for their potential activity against CCl(4)-induced liver injury in Sprague-Dawley rats. The results showed that post-administration of high dosages (5500 mg kg(-1) and 8250 mg kg(-1)) of DMSO-saline solution significantly reduced CCl(4)-induced acute elevation in the levels of SGPT and SGOT. The same result was observed in histopathological study of liver tissue. DMSO, in high doses, probably prevented CCl(4)-induced liver injury through its antioxidant, anti-inflammatory or microsomal enzyme arresting properties.

摘要

一毫升/千克体重的四氯化碳(CCl(4))口服足以引起显著的血清谷氨酸丙酮酸转氨酶(SGPT)和血清谷氨酸草酰乙酸转氨酶(SGOT)升高,同时伴有肝组织急性中央坏死和脂肪堆积的迹象。二甲基亚砜(DMSO)以不同剂量(2750mg/kg(-1)、5500mg/kg(-1)和 8250mg/kg(-1);溶于生理盐水)筛选对 Sprague-Dawley 大鼠 CCl(4)诱导肝损伤的潜在活性。结果表明,高剂量(5500mg/kg(-1)和 8250mg/kg(-1))的 DMSO 生理盐水溶液给药后,显著降低了 CCl(4)诱导的 SGPT 和 SGOT 的急性升高。肝组织的组织病理学研究也观察到了同样的结果。DMSO 可能通过其抗氧化、抗炎或微粒体酶抑制特性来预防 CCl(4)诱导的肝损伤。

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