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首页> 外文期刊>Clinical and experimental medicine >Lactic acid bacteria prevent alcohol-induced steatohepatitis in rats by acting on the pathways of alcohol metabolism.
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Lactic acid bacteria prevent alcohol-induced steatohepatitis in rats by acting on the pathways of alcohol metabolism.

机译:乳酸菌通过作用于酒精的代谢途径,预防酒精引起的脂肪性肝炎。

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The objective is to study the possible mechanism by which lactic acid bacteria (LAB) prevent alcohol-induced steatohepatitis in rats. A total of 25 Wistar rats were divided into three groups: a LAB-fed group, an alcohol-treated group and a control group. Both the LAB-fed group and the alcohol-treated group received alcohol (10 g kg(-1) per day) orally for up to 5 days (125 h). Before exposure to alcohol, the LAB-fed group were first treated daily with 1.5 ml/100 g of a mixture comprising 4 x 10(10) ml(-1) of Lactobacillus acidophilus and 2.5 x 10(7) ml(-1) of Bifidobacterium longum, while the control group was treated with normal saline only. Biochemical data, alcohol dehydrogenase (ADH) activity and histology of the liver and stomach were evaluated. The ADH activity in the LAB mixture was 3.52 +/- 0.45 mumol mg(-1) protein (10(9) CFU ml(-1)), and was dose-dependent. By 30 min after taking alcohol, serum alcohol concentrations were 514.24 +/- 80.21 mug ml(-1) in the LAB-fed group and 795.15 +/- 203.45 mug ml(-1) in the alcohol-treated group (P < 0.005). Serum alcohol concentrations were reduced by 48% (P < 0.01) in the LAB-fed group, but by only 4% in the alcohol-treated group (P > 0.05) 120 min after oral intake of alcohol. The blood levels of endotoxin, AST and ALT were improved in the LAB-fed group compared to the alcohol-fed group (P < 0.01). All alcohol-treated rats showed moderate to severe steatohepatitis, but the LAB-fed rats showed almost normal histology or very slight lesions only. In conclusion, LAB decreased the alcohol concentration in the blood by increasing the first-pass metabolism in both the stomach and the liver, and effectively protected against alcohol-induced gastric and liver injury. It is interesting to note that the protection was more effective in the liver.
机译:目的是研究乳酸菌(LAB)预防大鼠酒精性脂肪性肝炎的可能机制。将总共​​25只Wistar大鼠分为三组:LAB喂养组,酒精治疗组和对照组。 LAB喂养组和酒精治疗组均口服酒精(每天10 g kg(-1))达5天(125小时)。在暴露于酒精之前,LAB喂养的组首先每天用1.5 ml / 100 g包含4 x 10(10)ml(-1)嗜酸乳杆菌和2.5 x 10(7)ml(-1)的混合物处理。对照组仅用生理盐水处理。评估生化数据,酒精脱氢酶(ADH)活性以及肝和胃的组织学。 LAB混合物中的ADH活性为3.52 +/- 0.45 mumol mg(-1)蛋白(10(9)CFU ml(-1)),且呈剂量依赖性。服用酒精后30分钟,LAB喂养组的血清酒精浓度为514.24 +/- 80.21马克杯(-1),酒精治疗组的血清酒精浓度为795.15 +/- 203.45马克杯(-1)(P <0.005 )。在LAB喂养组中,口服酒精后120分钟血清酒精浓度降低了48%(P <0.01),而在酒精治疗组中血清酒精浓度仅降低了4%(P> 0.05)。与酒精喂养组相比,LAB喂养组的内毒素,AST和ALT的血液水平有所改善(P <0.01)。所有用酒精治疗的大鼠均显示中度至重度脂肪性肝炎,但用LAB喂养的大鼠仅表现出几乎正常的组织学或仅非常轻微的病变。总之,LAB通过增加胃和肝脏中的首过代谢来降低血液中的酒精浓度,并有效防止酒精引起的胃和肝损伤。有趣的是,这种保护在肝脏中更有效。

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