Department of Nutrition Science, Graduate School of Life and Environmental Sciences, Kyoto Prefectural University, 1-5 Shimogamo-hangi-cho, Sakyo, Kyoto 606-8522, Japan.
Nutr Res. 2012 Jul;32(7):522-9. doi: 10.1016/j.nutres.2012.06.007. Epub 2012 Jul 18.
Branched-chain amino acids (BCAA) can function as pharmacologic nutrients for patients with decompensated cirrhosis. However, the effects of BCAA at the early stage of chronic liver disease are not clear. We hypothesized that early BCAA supplementation would attenuate the progression of chronic liver disease. The present study examined the effects of BCAA supplementation on the progression of chronic liver disease in rats caused by injected carbon tetrachloride (CCl₄). Sprague-Dawley rats were fed with a casein diet (control group) or the same diet supplemented with BCAA (BCAA group) for 11 weeks, and all rats were repeatedly injected with CCl₄. Food intake did not significantly differ between control and BCAA groups during the experimental period. Plasma alanine aminotransferase activities gradually increased during the experimental period in both groups but peaked later in the BCAA group. Liver fibrosis was more evident in the control group. Levels of connective tissue growth factor messenger RNA were significantly lower in the livers of rats in the BCAA group than in the control group. Terminal deoxynucleotidyl transferase-mediated deoxyuridine 5-triphosphate nick end labeling assays found considerably more hepatic apoptosis in the control group. Liver cytosolic cytochrome c levels and expression of the proapoptotic Bax protein in the mitochondrial fraction were significantly lower in the BCAA group than in the control group. These results suggest that supplementation with BCAA delays the progression of chronic liver disease caused by CCl₄ in rats by attenuating hepatic apoptosis.
支链氨基酸（BCAA）可作为失代偿期肝硬化患者的药物营养素。然而，BCAA 在慢性肝病早期的作用尚不清楚。我们假设早期补充 BCAA 会减缓慢性肝病的进展。本研究探讨了 BCAA 补充对四氯化碳（CCl₄）诱导的大鼠慢性肝病进展的影响。Sprague-Dawley 大鼠分别用酪蛋白饮食（对照组）或添加 BCAA 的相同饮食（BCAA 组）喂养 11 周，并反复注射 CCl₄。在实验期间，对照组和 BCAA 组的大鼠食物摄入量没有明显差异。两组大鼠的血浆丙氨酸氨基转移酶活性在实验期间逐渐升高，但 BCAA 组升高较晚。对照组肝纤维化更明显。BCAA 组大鼠肝脏中结缔组织生长因子信使 RNA 的水平明显低于对照组。末端脱氧核苷酸转移酶介导的脱氧尿苷 5-三磷酸末端标记试验发现对照组肝凋亡明显更多。BCAA 组大鼠肝胞质细胞色素 c 水平和线粒体部分促凋亡 Bax 蛋白的表达均明显低于对照组。这些结果表明，BCAA 补充通过减轻肝凋亡，延缓 CCl₄ 诱导的大鼠慢性肝病的进展。
