Zhang Dong, Hao Xiuxian, Xu Lili, Cui Jing, Xue Li, Tian Zibin
Medical College, Qingdao University, Qingdao, Shandong 266042, P.R. China.
Department of Gastroenterology, Qingdao Center Hospital, Qingdao, Shandong 266042, P.R. China.
Oncol Lett. 2017 Oct;14(4):4511-4516. doi: 10.3892/ol.2017.6762. Epub 2017 Aug 17.
Intestinal flora performs a crucial role in human health and its imbalance may cause numerous pathological changes. The liver can also affect the intestinal function through bile secretion via the enterohepatic cycle. The pathophysiological association between the gut and the liver is described as the gut-liver axis. The present study investigated the role of intestinal flora in alcohol-induced liver fibrosis. A total of 36 C57 mice were randomly and equally divided into 3 different dietary regimes: Group I (alcohol injury; received alcohol); group II (alcohol injury with flora imbalance; received alcohol plus lincomycin hydrochloride) and group III (alcohol injury with corrected flora imbalance; received alcohol, lincomycin hydrochloride and extra probiotics). The present study then investigated several indicators of liver damage. Alkaline phosphatase (ALP) levels, aspartate aminotransferase (AST) levels and alanine aminotransferase (ALT) levels in mice serum were studied. Masson staining and Annexin V-fluorescein isothiocyanate/propidium iodide double staining was also performed, and the expression of mothers against decapentaplegic homolog (smad) 3 and smad4 proteins in hepatic stellate cells (HSCs) of the mice was examined using western blot analysis. The levels of serum ALP, AST and ALT were the highest in group II mice, and all 3 levels decreased in group III mice compared with those from group II. The degree of liver fibrosis was aggravated in group II mice compared with group I mice. The apoptosis of HSCs was significantly inhibited in group II mice, but was increased in group III mice. The HSCs in group II mice exhibited higher expression of smad3 and smad4, whilst group III mice (with corrected intestinal flora imbalance) exhibited downregulated expression of smad3 and smad4. The present data indicates that the intestinal flora perform a significant role in maintaining liver homeostasis. Furthermore, an imbalance of intestinal flora can exacerbate alcohol-induced liver fibrosis in mice through the transforming growth factor β/SMA/MAD homology signaling pathway, which subsequently leads to more serious liver damage.
肠道菌群在人类健康中发挥着关键作用,其失衡可能导致众多病理变化。肝脏也可通过肠肝循环分泌胆汁来影响肠道功能。肠道与肝脏之间的病理生理联系被描述为肠-肝轴。本研究调查了肠道菌群在酒精性肝纤维化中的作用。总共36只C57小鼠被随机且等分为3种不同饮食方案:第一组(酒精损伤组;给予酒精);第二组(菌群失衡的酒精损伤组;给予酒精加盐酸林可霉素)和第三组(菌群失衡纠正后的酒精损伤组;给予酒精、盐酸林可霉素和额外的益生菌)。本研究随后调查了肝脏损伤的几个指标。研究了小鼠血清中的碱性磷酸酶(ALP)水平、天冬氨酸转氨酶(AST)水平和丙氨酸转氨酶(ALT)水平。还进行了Masson染色和膜联蛋白V-异硫氰酸荧光素/碘化丙啶双重染色,并使用蛋白质印迹分析检测了小鼠肝星状细胞(HSC)中母亲对果蝇节段极性基因同源物(smad)3和smad4蛋白的表达。第二组小鼠血清ALP、AST和ALT水平最高,与第二组相比,第三组小鼠所有这3种水平均降低。与第一组小鼠相比,第二组小鼠肝纤维化程度加重。第二组小鼠肝星状细胞的凋亡明显受到抑制,但在第三组小鼠中增加。第二组小鼠的肝星状细胞表现出smad3和smad4的较高表达,而第三组小鼠(肠道菌群失衡得到纠正)表现出smad3和smad4表达下调。目前的数据表明,肠道菌群在维持肝脏稳态中发挥着重要作用。此外,肠道菌群失衡可通过转化生长因子β/平滑肌肌动蛋白/母源-合子同源信号通路加重小鼠酒精性肝纤维化,进而导致更严重的肝损伤。