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枸杞多糖可保护小鼠肝脏免受四氯化碳诱导的氧化应激和坏死性炎症。

Lycium barbarum polysaccharides protect mice liver from carbon tetrachloride-induced oxidative stress and necroinflammation.

机构信息

Department of Anatomy, The University of Hong Kong, Hong Kong Special Administrative Region.

出版信息

J Ethnopharmacol. 2012 Jan 31;139(2):462-70. doi: 10.1016/j.jep.2011.11.033. Epub 2011 Nov 26.

Abstract

ETHNOPHARMACOLOGICAL RELEVANCE

Lycium barbarum has been used as a traditional Chinese medicine to nourish liver, kidneys and the eyes.

AIM OF THE STUDY

We investigated the protective mechanisms of Wolfberry, Lycium barbarum polysaccharides (LBP) in carbon tetrachloride (CCl(4))-induced acute liver injury.

MATERIALS AND METHODS

Mice were intraperitoneally injected with a 50 μl/kg CCl(4) to induce acute hepatotoxicity (8h) and were orally fed with LBP 2 h before the CCl(4) injection. There were six experimental groups of mice (n=7-8 per group), namely: control mice (vehicle only; 1 mg/kg LBP or 10 mg/kg LBP), CCl(4)-treated mice and CCl(4)+LBP treated mice (1 mg/kg LBP or 10 mg/kg LBP).

RESULTS

Pre-treatment with LBP effectively reduced the hepatic necrosis and the serum ALT level induced by CCl(4) intoxication. LBP remarkably inhibited cytochrome P450 2E1 expression and restored the expression levels of antioxidant enzymes. It also decreased the level of nitric oxide metabolism and lipid peroxidation induced by CCl(4). LBP attenuated hepatic inflammation via down-regulation of proinflammatory mediators and chemokines. Furthermore, LBP promoted liver regeneration after CCl(4) treatment. The protective effects of LBP against hepatotoxicity were partly through the down-regulation of nuclear factor kappa-B activity.

CONCLUSION

LBP is effective in reducing necroinflammation and oxidative stress induced by a chemical toxin, thus it has a great potential use as a food supplement in the prevention of hepatic diseases.

摘要

民族药理学相关性

枸杞已被用作中药来滋养肝脏、肾脏和眼睛。

研究目的

我们研究了枸杞多糖(LBP)在四氯化碳(CCl4)诱导的急性肝损伤中的保护机制。

材料与方法

通过腹腔注射 50μl/kg 的 CCl4 诱导急性肝毒性(8 小时),并在 CCl4 注射前 2 小时给予 LBP 口服。有 6 组实验小鼠(每组 n=7-8),即:对照组(仅给予载体;1mg/kg LBP 或 10mg/kg LBP)、CCl4 处理组和 CCl4+LBP 处理组(1mg/kg LBP 或 10mg/kg LBP)。

结果

LBP 预处理可有效减少 CCl4 中毒引起的肝坏死和血清 ALT 水平升高。LBP 显著抑制细胞色素 P450 2E1 的表达,并恢复抗氧化酶的表达水平。它还降低了 CCl4 诱导的一氧化氮代谢和脂质过氧化水平。LBP 通过下调促炎介质和趋化因子来减轻肝炎症。此外,LBP 促进 CCl4 处理后的肝再生。LBP 对肝毒性的保护作用部分是通过下调核因子 kappa-B 活性实现的。

结论

LBP 可有效减轻化学毒素引起的坏死性炎症和氧化应激,因此它具有作为预防肝脏疾病的膳食补充剂的巨大潜力。

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