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Lactobacillus rhamnosus GG supplementation attenuates chronic‐alcohol induced liver injury by inhibiting hepatocyte apoptosis
Author(s) -
Wang Chunhong,
Wang Yuhua,
Liu Yanlong,
McClain Craig J,
Feng Wenke
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.848.11
Subject(s) - lactobacillus rhamnosus , apoptosis , tunel assay , reactive oxygen species , oxidative stress , liver injury , probiotic , alcohol , programmed cell death , pharmacology , chemistry , medicine , immunology , biology , biochemistry , lactobacillus , bacteria , genetics , fermentation
Previous studies have demonstrated that chronic alcohol consumption induces liver injury, which is associated with ethanol metabolism‐mediated oxidative stress and apoptotic cell death, in human and experimental animals. As probiotic supplementation is known to reduce the formation of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in the intestine and the liver in the mice chronically fed alcohol, the present study was aimed to investigate whether probiotic supplementation could inhibit alcohol‐induced hepatic apoptosis in mice. C57BJ/6N mice were fed the Lieber deCarli diet containing 5% alcohol with or without Lactobacillus rhamnosus GG (LGG) for 4 weeks. LGG supplementation completely inhibited the chronic alcohol consumption‐increased hepatic apoptosis measured by TUNEL assay along with ROS and RNS production. The anti‐apoptotic effect of LGG on the liver of the alcohol‐treated mice was further confirmed by measuring Caspase 3 activation, and the protein levels of anti‐/pro‐apoptotic proteins, such as Bcl‐2 and Bax, and death signal proteins, such as FasR and FasL. These results indicate that LGG treatment reduces alcohol‐induced hepatic apoptotic cell death by multiple mechanisms, and provides a mechanistic insight for utilization of probiotics for the treatment of ALD.