Fan Houmin, Shen Yanyan, Ren Ya, Mou Qiuju, Lin Tao, Zhu Lili, Ren Tingting
Guizhou Medical University, Guiyang, Guizhou, China.
Tongren Maternal and Child Health Care Hospital, Tongren, Guizhou, China.
Nutr Metab (Lond). 2021 May 10;18(1):50. doi: 10.1186/s12986-021-00554-3.
Mitochondrial dysfunction has been implicated as a significant factor in the liver disease process. Blueberry juice and probiotics (BP) synergistically improve liver function in alcoholic fatty liver disease (AFLD), although the mechanism for this effect was unclear. This study aims to investigate the effect and specific mechanisms of BP on AFLD.
C57/BL6 mice were randomly divided into seven groups: CG (control), MG (AFLD model), BJ (MG mice treated with blueberry), BJB (MG mice treated with BP), SI (AFLD mice treated with SIRT1 siRNA), BJSI (SI mice treated with blueberry), and BJBSI (SI mice treated with BP). The mice were fed an alcohol liquid diet for 10 days to establish the AFLD model, and subjected to BP and SIRT1 siRNA intervention for 10 days. Liver pathology was performed on day 11, and biochemical and molecular analyses of liver mitochondria were employed on day 12.
BP significantly ameliorated hepatic mitochondrial injury, mitochondrial swelling, and hepatic necrosis in AFLD. BP alleviated hepatic mitochondrial dysfunction by increasing the expression of succinate dehydrogenase and cytochrome c oxidase, increasing respiratory control rate and the ADP/O ratio, and facilitating the synthesis of energy-related molecules. Besides, BP increased the expression of glutathione and superoxide dismutase, and inhibited malondialdehyde expression and reactive oxygen species activity. BP-induced sirtuin 1 (SIRT1), which activates peroxisome proliferator-activated receptor-gamma coactivator-1α, both of which mediate mitochondrial homeostasis. SIRT1 silencing suppressed the BP-induced changes in liver mitochondria, blunting its efficacy.
The ingredients of BP ameliorate hepatocyte mitochondrial dysfunction in AFLD mice.
线粒体功能障碍被认为是肝脏疾病进程中的一个重要因素。蓝莓汁和益生菌（BP）可协同改善酒精性脂肪性肝病（AFLD）的肝功能，但其作用机制尚不清楚。本研究旨在探讨BP对AFLD的作用及具体机制。
将C57/BL6小鼠随机分为七组：CG（对照组）、MG（AFLD模型组）、BJ（用蓝莓治疗的MG小鼠）、BJB（用BP治疗的MG小鼠）、SI（用SIRT1小干扰RNA治疗的AFLD小鼠）、BJSI（用蓝莓治疗的SI小鼠）和BJBSI（用BP治疗的SI小鼠）。小鼠接受酒精液体饮食10天以建立AFLD模型，并接受BP和SIRT1小干扰RNA干预10天。在第11天进行肝脏病理学检查，在第12天进行肝脏线粒体的生化和分子分析。
BP显著改善了AFLD中的肝线粒体损伤、线粒体肿胀和肝坏死。BP通过增加琥珀酸脱氢酶和细胞色素c氧化酶的表达、提高呼吸控制率和ADP/O比值以及促进能量相关分子的合成来减轻肝线粒体功能障碍。此外，BP增加了谷胱甘肽和超氧化物歧化酶的表达，并抑制了丙二醛的表达和活性氧的活性。BP诱导沉默调节蛋白1（SIRT1），其激活过氧化物酶体增殖物激活受体γ共激活因子1α，二者均介导线粒体稳态。SIRT1沉默抑制了BP诱导的肝线粒体变化，削弱了其疗效。
BP成分改善了AFLD小鼠肝细胞的线粒体功能障碍。
