Indexed on: 25 Sep '08Published on: 25 Sep '08Published in: Clinical and Experimental Medicine
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 microg ml(-1) in the LAB-fed group and 795.15 +/- 203.45 microg 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.