The protective effects of a fermented substance from Saccharomyces cerevisiae on carbon tetrachloride-induced liver damage in rats.
OBJECTIVE
The aim of this study was to investigate the effect of a fermented substance from Saccharomyces cerevisiae (FSSC) on the liver fibrosis induced by chronic carbon tetrachloride (CCl(4)) administration in rats.


METHODS
Rats were divided randomly into four groups: control, CCl(4), and two FSSC groups. Except for rats in the control group, all rats were orally administered CCl(4) twice a week for 8 weeks. Rats in the FSSC groups were treated daily with FSSC (0.5 or 1.5 g/kg) through gastrogavage for the entire experimental period.


RESULTS
CCl(4) caused liver damage, as characterized by increases in levels of plasma transaminase, hepatic malondialdehyde, and hydroxyproline, in addition to increases in spleen and liver weights and decreases in plasma albumin levels. Compared with CCl(4) group, FSSC (1.5 g/kg) treatment significantly decreased the spleen (P<0.01) and liver (P<0.01) weights, the activities of transaminase (P<0.05), and levels of hepatic malondialdehyde (P<0.05) and hydroxyproline (P<0.01); however, the treatment increased plasma albumin level (P<0.05). The pathological results also showed that FSSC (1.5 g/kg) suppressed hepatic inflammation, steatosis and necrosis. Data for hepatic fibrosis were expressed as the mean percentage of the total hepatic area in the tissue sections. FSSC (1.5 g/kg) treatment significantly decreased the hepatic fibrosis (12.8+/-1.2 and 6.4+/-0.7 in CCl(4) and FSSC group, respectively, P<0.001). RT-PCR analysis showed that FSSC (1.5 g/kg) treatment decreased the expression of methionine adenosyltransferase 2A (P<0.01), collagen (alpha1)(I) (3.15+/-0.05 and 1.52+/-0.04 in CCl(4) and FSSC groups, respectively, P<0.001), and transforming growth factor-beta1 (2.50+/-0.05 and 1.21+/-0.04 in CCl(4) and FSSC groups, respectively, P<0.001), apart from increasing the expression of methionine adenosyltransferase 1A (P<0.05).


CONCLUSIONS
These results showed that FSSC protects the liver against CCl(4) damage in rats.
Lai
Jinn-Tsyy
JT
Bioresource Collection and Research Center, Food Industry Research and Development Institute, Hsinchu, Taiwan, ROC.
Hsieh
Wen-Tsong
WT
Fang
Hsun-Lang
HL
Lin
Wen-Chuan
WC
D000818:Animals; D002251:Carbon Tetrachloride / Q000633:toxicity; D024042:Collagen Type I / Q000235:genetics / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005285:Fermentation; D006909:Hydroxyproline / Q000378:metabolism; D008106:Liver Cirrhosis, Experimental / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008716:Methionine Adenosyltransferase / Q000235:genetics / Q000378:metabolism; D009929:Organ Size; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012441:Saccharomyces cerevisiae / Q000378:metabolism*; D012709:Serum Albumin / Q000378:metabolism; D000637:Transaminases / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000235:genetics / Q000378:metabolism
D024042:Collagen Type I; D012333:RNA, Messenger; D012709:Serum Albumin; D053773:Transforming Growth Factor beta1; D008315:Malondialdehyde; D002251:Carbon Tetrachloride; D008716:Methionine Adenosyltransferase; D000637:Transaminases; D006909:Hydroxyproline