迷迭香提取物對(duì)小鼠急性酒精肝模型保護(hù)作用研究
發(fā)布時(shí)間:2018-01-30 00:54
本文關(guān)鍵詞: 迷迭香提取物 急性酒精肝 氧化損傷 脂代謝 炎癥 出處:《天然產(chǎn)物研究與開(kāi)發(fā)》2017年02期 論文類(lèi)型:期刊論文
【摘要】:研究迷迭香提取物(Rosemary Extract,RE)對(duì)小鼠急性酒精肝損傷的保護(hù)作用,并從酒精代謝、脂代謝、抗氧化和抗炎幾個(gè)方面探討其作用機(jī)制。將小鼠隨機(jī)分為空白對(duì)照組(Control)、模型組(Model)、欣立得組(Metadoxine Capsules,MC,200 mg/kg·d),RE劑量組80、160、400 mg/kg·d,給藥30 d后建立小鼠急性酒精肝損傷模型,檢測(cè)血清ALT、AST、TG、TNF-α、IL-6、IL-10濃度,肝臟MDA、SOD、GSH-Px、ADH活性,qRT-PCR檢測(cè)肝臟脂肪酸合成酶(FAS)、脂肪分化相關(guān)蛋白(ADRP)、細(xì)胞色素P450 2E1(CYP2E1)、過(guò)氧化物酶體增值物激活α受體(PPARα)和半胱氨酸天冬氨酸蛋白酶3(caspase3)mRNA的表達(dá),HE染色觀察肝臟組織病理變化。RE組小鼠血清ADH活性升高,ALT、AST和TG含量降低,醒酒時(shí)間縮短,肝臟組織脂肪變性減輕,細(xì)胞凋亡相關(guān)基因Caspase3表達(dá)降低,保護(hù)機(jī)制研究發(fā)現(xiàn)RE能下調(diào)FAS和ADRP基因表達(dá),減少肝臟脂肪合成;提高抗氧化損傷酶SOD、GSH-Px活性,下調(diào)酒精代謝中ROS合成基因CYP2E1和上調(diào)抗氧化損傷和炎癥基因PPARα表達(dá),使MDA濃度降低,減輕肝臟氧化損傷;降低炎性因子TNF-α和IL-6濃度,提高抗炎因子IL-10濃度。實(shí)驗(yàn)結(jié)果表明RE對(duì)小鼠急性酒精肝損傷具有保護(hù)作用,其作用機(jī)制可能與抗氧化、抗炎和脂肪代謝調(diào)節(jié)有關(guān)。
[Abstract]:To study the protective effect of Rosemary ExtractRE) on acute alcoholic liver injury in mice from alcohol metabolism and lipid metabolism. To explore the mechanism of anti-oxidation and anti-inflammation, mice were randomly divided into blank control group (control group) and model group (model group). Metadoxine Capsulesus, 200 mg/kg 路d, RE group, 80,160,400 mg/kg 路d. A model of acute alcoholic liver injury was established in mice 30 days after administration. The concentration of IL-10 in serum of TGN TNF- 偽 and MDA-SOD in liver was detected. Liver fatty acid synthase (FASP) and adipose differentiation related protein (ADRP) were detected by qRT-PCR. Cytochrome P450 2E1 (CYP2E1). Peroxisome value-added activated the expression of PPAR 偽 and caspase3 mRNA of cysteine aspartate protease 3. The activity of serum ADH was increased and the contents of alt AST and TG were decreased, the time of soaking up was shortened, and the steatosis of liver tissue was reduced in the group of HE staining. The expression of apoptosis-related gene Caspase3 was decreased. The protective mechanism showed that RE could down-regulate the expression of FAS and ADRP genes and reduce hepatic fat synthesis. The activity of GSH-Px was increased, the ROS synthesis gene CYP2E1 and the expression of antioxidant injury and inflammatory gene PPAR 偽 were down-regulated in alcohol metabolism. The concentration of MDA was decreased and the oxidative damage of liver was alleviated. The experimental results showed that RE has protective effect on acute alcoholic liver injury in mice, and its mechanism may be related to antioxidation. Anti-inflammatory and fat metabolism regulation.
【作者單位】: 昆明醫(yī)科大學(xué)生物醫(yī)學(xué)工程研究中心;昆明醫(yī)科大學(xué)藥學(xué)院暨云南省天然藥物藥理重點(diǎn)實(shí)驗(yàn)室;
【基金】:云南省南藥研究協(xié)同創(chuàng)新中心項(xiàng)目(NY2014002)
【分類(lèi)號(hào)】:R285.5;R-332
【正文快照】: 酒精性肝病(alcoholic liver disease,ALD)是由于過(guò)度飲酒導(dǎo)致的肝損傷,也是引發(fā)肝臟疾病的重要原因。人體長(zhǎng)期飲酒或短期大量飲酒會(huì)引起酒精性肝細(xì)胞損傷,導(dǎo)致肝細(xì)胞發(fā)生脂肪變性、炎癥和壞死等[1]病變,其發(fā)病機(jī)制與酒精代謝引發(fā)的氧化應(yīng)激、細(xì)胞因子釋放、線粒體損傷、肝細(xì)
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