Lai Jinn-Tsyy, Hsieh Wen-Tsong, Fang Hsun-Lang, Lin Wen-Chuan
Bioresource Collection and Research Center, Food Industry Research and Development Institute, Hsinchu, Taiwan, ROC.
Clin Nutr. 2009 Jun;28(3):338-45. doi: 10.1016/j.clnu.2009.01.011. Epub 2009 Feb 23.
BACKGROUND & AIMS: 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.
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.
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).
These results showed that FSSC protects the liver against CCl(4) damage in rats.
本研究旨在探讨酿酒酵母发酵物(FSSC)对大鼠慢性四氯化碳(CCl₄)诱导的肝纤维化的影响。
将大鼠随机分为四组:对照组、CCl₄组和两个FSSC组。除对照组大鼠外,所有大鼠每周口服CCl₄两次,共8周。在整个实验期间,FSSC组大鼠每天通过灌胃给予FSSC(0.5或1.5 g/kg)。
CCl₄导致肝脏损伤,表现为血浆转氨酶、肝丙二醛和羟脯氨酸水平升高,同时脾脏和肝脏重量增加,血浆白蛋白水平降低。与CCl₄组相比,FSSC(1.5 g/kg)治疗显著降低了脾脏(P<0.01)和肝脏(P<0.01)重量、转氨酶活性(P<0.05)、肝丙二醛水平(P<0.05)和羟脯氨酸水平(P<0.01);然而,该治疗增加了血浆白蛋白水平(P<0.05)。病理结果还显示,FSSC(1.5 g/kg)抑制了肝脏炎症、脂肪变性和坏死。肝纤维化数据以组织切片中肝总面积的平均百分比表示。FSSC(1.5 g/kg)治疗显著降低了肝纤维化(CCl₄组和FSSC组分别为12.8±1.2和6.4±0.7,P<0.001)。RT-PCR分析表明,FSSC(1.5 g/kg)治疗降低了蛋氨酸腺苷转移酶2A的表达(P<0.01)、胶原蛋白(α1)(I)的表达(CCl₄组和FSSC组分别为3.15±0.05和1.52±0.04,P<0.001)以及转化生长因子-β1的表达(CCl₄组和FSSC组分别为2.50±0.05和1.21±0.04,P<0.001),同时增加了蛋氨酸腺苷转移酶1A的表达(P<0.05)。
这些结果表明,FSSC可保护大鼠肝脏免受CCl₄损伤。