Tags

Type your tag names separated by a space and hit enter

Oral administration of heat-killed Lactobacillus brevis SBC8803 ameliorates alcoholic liver disease in ethanol-containing diet-fed C57BL/6N mice.
Int J Food Microbiol 2008; 128(2):371-7IJ

Abstract

We examined the effect of heat-killed Lactobacillus brevis (L. brevis) SBC8803 on the development of alcoholic liver disease using ethanol-containing diet-fed mice. Heat-killed L. brevis was orally administered at a dose of 100 or 500 mg/kg once a day for 35 days. Alcoholic liver injury was examined by measuring the activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in a serum, and the alcoholic fatty liver was assessed from the content of triglyceride (TG) and total cholesterol in the liver. Quantitative RT-PCR was used to examine mRNA expression of tumor necrosis factor (TNF)-alpha, sterol regulatory element-binding protein (SREBP)-1, SREBP-2, and peroxisome proliferator-activated receptor alpha (PPARalpha) in the liver, as well as E-cadherin, Zonula occludens 1 (ZO-1), and heat shock protein (Hsp) 25 in the small intestine. Oral administration of L. brevis significantly inhibited an increase in the level of serum ALT and AST, as well as the content of TG and total cholesterol in the liver caused by ethanol intake. L. brevis supplementation suppressed the overexpression of TNF-alpha, SREBP-1, and SREBP-2 mRNA in the liver induced by ethanol intake and up-regulated the expression of Hsp25 mRNA in the small intestine. These results suggest that L. brevis ameliorated the ethanol-induced liver injury and the fatty liver by suppressing the up-regulation of TNF-alpha and SREBPs in the liver. We speculate that the inhibition of TNF-alpha and SREBPs up-regulation by L. brevis is due to the inhibition of gut-derived endotoxin migration into the liver through the enhancement of intestinal barrier function by the induction of cytoprotective Hsps.

Authors+Show Affiliations

Frontier Laboratories of Value Creation, Sapporo Breweries Ltd., 10 Okatohme, Yaizu, Shizuoka 425-0013, Japan. syuuichi.segawa@sapporobeer.co.jpNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

18976829

Citation

Segawa, Shuichi, et al. "Oral Administration of Heat-killed Lactobacillus Brevis SBC8803 Ameliorates Alcoholic Liver Disease in Ethanol-containing Diet-fed C57BL/6N Mice." International Journal of Food Microbiology, vol. 128, no. 2, 2008, pp. 371-7.
Segawa S, Wakita Y, Hirata H, et al. Oral administration of heat-killed Lactobacillus brevis SBC8803 ameliorates alcoholic liver disease in ethanol-containing diet-fed C57BL/6N mice. Int J Food Microbiol. 2008;128(2):371-7.
Segawa, S., Wakita, Y., Hirata, H., & Watari, J. (2008). Oral administration of heat-killed Lactobacillus brevis SBC8803 ameliorates alcoholic liver disease in ethanol-containing diet-fed C57BL/6N mice. International Journal of Food Microbiology, 128(2), pp. 371-7. doi:10.1016/j.ijfoodmicro.2008.09.023.
Segawa S, et al. Oral Administration of Heat-killed Lactobacillus Brevis SBC8803 Ameliorates Alcoholic Liver Disease in Ethanol-containing Diet-fed C57BL/6N Mice. Int J Food Microbiol. 2008 Dec 10;128(2):371-7. PubMed PMID: 18976829.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oral administration of heat-killed Lactobacillus brevis SBC8803 ameliorates alcoholic liver disease in ethanol-containing diet-fed C57BL/6N mice. AU - Segawa,Shuichi, AU - Wakita,Yoshihisa, AU - Hirata,Hiroshi, AU - Watari,Junji, Y1 - 2008/10/08/ PY - 2008/03/06/received PY - 2008/09/12/revised PY - 2008/09/22/accepted PY - 2008/11/4/pubmed PY - 2009/1/30/medline PY - 2008/11/4/entrez SP - 371 EP - 7 JF - International journal of food microbiology JO - Int. J. Food Microbiol. VL - 128 IS - 2 N2 - We examined the effect of heat-killed Lactobacillus brevis (L. brevis) SBC8803 on the development of alcoholic liver disease using ethanol-containing diet-fed mice. Heat-killed L. brevis was orally administered at a dose of 100 or 500 mg/kg once a day for 35 days. Alcoholic liver injury was examined by measuring the activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in a serum, and the alcoholic fatty liver was assessed from the content of triglyceride (TG) and total cholesterol in the liver. Quantitative RT-PCR was used to examine mRNA expression of tumor necrosis factor (TNF)-alpha, sterol regulatory element-binding protein (SREBP)-1, SREBP-2, and peroxisome proliferator-activated receptor alpha (PPARalpha) in the liver, as well as E-cadherin, Zonula occludens 1 (ZO-1), and heat shock protein (Hsp) 25 in the small intestine. Oral administration of L. brevis significantly inhibited an increase in the level of serum ALT and AST, as well as the content of TG and total cholesterol in the liver caused by ethanol intake. L. brevis supplementation suppressed the overexpression of TNF-alpha, SREBP-1, and SREBP-2 mRNA in the liver induced by ethanol intake and up-regulated the expression of Hsp25 mRNA in the small intestine. These results suggest that L. brevis ameliorated the ethanol-induced liver injury and the fatty liver by suppressing the up-regulation of TNF-alpha and SREBPs in the liver. We speculate that the inhibition of TNF-alpha and SREBPs up-regulation by L. brevis is due to the inhibition of gut-derived endotoxin migration into the liver through the enhancement of intestinal barrier function by the induction of cytoprotective Hsps. SN - 0168-1605 UR - https://www.unboundmedicine.com/medline/citation/18976829/Oral_administration_of_heat_killed_Lactobacillus_brevis_SBC8803_ameliorates_alcoholic_liver_disease_in_ethanol_containing_diet_fed_C57BL/6N_mice_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0168-1605(08)00521-7 DB - PRIME DP - Unbound Medicine ER -