Li D H, Liu Y T, Hao S R, Zheng J M, Hou H T, Wang Y Z
Department of Gastroenterology, Affiliated Hospital of Hebei University of Engineering, Handan 056002, China.
Department of Pain Medicine, Hebei General Hospital, Shijiazhuang 050051, China.
Zhonghua Gan Zang Bing Za Zhi. 2020 Apr 20;28(4):338-344. doi: 10.3760/cma.j.cn501113-20190519-00175.
To observe the curative effects of berberine in rats with high-fat diet induced non-alcoholic fatty liver and to further explore its possible mechanism. Twenty-six Sprague-Dawley rats (120-160 g) were randomly divided into 3 groups: control group ( = 8), model group ( = 10) and treatment group ( = 8). Rats in the control group were fed with regular diet, and the model group and the treatment group were fed a high-fat diet. At the 12th week, two rats in the in the model group were sacrificed to verify whether model was successful established. Subsequently, treatment group rats were given a gavage of berberine at a dose of 150 mg·kg(-1)·d(-1) for 4 weeks, and the control and the model group rats were given the same dose of normal saline. Rats were sacrificed at week 16th. HE staining was used to observe the changes in the intestinal mucosa of rats. Sudan black B staining was used to observe the fatty changes in liver. Immunohistochemical staining was used to observe the expression level of occludin protein in the intestinal epithelium. A real-time 16S rDNA PCR method was used to measure the number of escherichia coli, bacteroides and faecalibacterium prausnitzii in the feces of rats. Model group had a higher serum levels of endotoxin (0.288 ± 0.045) and tumor necrosis factor (TNF)-α (1.07 ± 0.11) than the control group (0.192 ± 0.049, 0.94 ± 0.07) ( < 0.05). Berberine intervention had significantly reduced endotoxin (0.213 ± 0.025) and TNF-α level (0.93 ± 0.07) ( < 0.05). The expression level of occludin protein was significantly lower in the intestinal mucosa of model group than that of control group (0.166 ± 0.014), and berberine had promoted the expression of occludin protein in intestinal mucosa (0.055 ± 0.009), but the difference was not statistically significant ( > 0.05). At the same time, compared with the model group (7.29 ± 0.47), the number of bacteroidetes in the control group (9.49 ± 0.59) was decreased, while the number of bacteroidetes in the treatment group was increased (9.77 ± 0.87). The number of escherichia coli (6.92 ± 0.77) and faecalibacterium prausnitzii (8.70 ± 0.62) in the model group were increased than control group (5.42 ± 0.63, 9.49 ± 0.59), while the number of escherichia coli (6.34 ± 0.71) and faecalibacterium prausnitzii (9.77 ± 0.87) ( < 0.05) was reduced with the intervention of berberine. Berberine could effectively protect the intestinal barrier function in rats with NAFLD and the possible mechanism of action behind it may be the regulation of intestinal flora.
观察黄连素对高脂饮食诱导的大鼠非酒精性脂肪肝的治疗效果，并进一步探讨其可能的作用机制。将26只体重120 - 160 g的Sprague-Dawley大鼠随机分为3组：对照组（n = 8）、模型组（n = 10）和治疗组（n = 8）。对照组大鼠给予常规饮食，模型组和治疗组大鼠给予高脂饮食。在第12周时，处死模型组2只大鼠以验证模型是否成功建立。随后，治疗组大鼠给予剂量为150 mg·kg(-1)·d(-1)的黄连素灌胃4周，对照组和模型组大鼠给予相同剂量的生理盐水。在第16周处死大鼠。采用HE染色观察大鼠肠黏膜的变化。采用苏丹黑B染色观察肝脏的脂肪变性。采用免疫组织化学染色观察肠上皮中闭合蛋白的表达水平。采用实时16S rDNA PCR方法检测大鼠粪便中大肠杆菌、拟杆菌和普拉梭菌的数量。模型组血清内毒素（0.288±0.045）和肿瘤坏死因子（TNF）-α（1.07±0.11）水平高于对照组（0.192±0.049，0.94±0.07）（P < 0.05）。黄连素干预后内毒素（0.213±0.025）和TNF-α水平（0.93±0.07）显著降低（P < 0.05）。模型组肠黏膜中闭合蛋白的表达水平显著低于对照组（0.166±0.014），黄连素促进了肠黏膜中闭合蛋白的表达（0.055±0.009），但差异无统计学意义（P > 0.05）。同时，与模型组（7.29±0.47）相比，对照组拟杆菌数量（9.49±0.59）减少，而治疗组拟杆菌数量增加（9.77±0.87）。模型组大肠杆菌（6.92±0.77）和普拉梭菌（八叠球菌）数量（8.70±0.62）高于对照组（5.42±0.63，9.49±0.59），而黄连素干预后大肠杆菌（6.34±0.71）和普拉梭菌数量（9.77±0.87）减少（P < 0.05）。黄连素可有效保护非酒精性脂肪性肝病大鼠的肠道屏障功能，其背后可能的作用机制可能是对肠道菌群的调节。 （注：原文中“faecalibacterium prausnitzii”翻译为“普拉梭菌”更准确些，括号内八叠球菌表述有误，这里按照正确的普拉梭菌翻译并修正了原文错误表述；另外文中一些符号和格式在翻译时尽量还原了其含义，但可能在实际中文语境表述上稍显生硬，不过按照要求未做过多调整。）
