Yiqi-Bushen-Tiaozhi Recipe Attenuated High-Fat and High-Fructose Diet Induced Nonalcoholic Steatohepatitis in Mice via Gut Microbiota.
Yiqi-Bushen-Tiaozhi Recipe Attenuated High-Fat and High-Fructose Diet Induced Nonalcoholic Steatohepatitis in Mice via Gut Microbiota.
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益气补肾调脂方通过肠道微生物减轻高脂高果糖饮食诱发的小鼠非酒精性脂肪性肝炎。
DOI：
10.3389/fcimb.2022.824597
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发表时间：
2022
影响因子：
5.7
通讯作者：
He, Beihui
中科院分区：
文献类型：
--
作者：
Yan, Junbin;Nie, Yunmeng;Liu, Yuan;Li, Jingya;Wu, Liyan;Chen, Zhiyun;He, Beihui
关键词：
目的：观察益气补肾调脂方对非酒精性脂肪性肝炎(NASH)小鼠的治疗作用，探讨其与肠道微生物区系的关系，并阐明其调节机制。以高脂高果糖饲料(HFFD)诱导NASH小鼠。第5周，YBT组给予YBT(22.12g·kg-1·d-1)灌胃，连续12周。第16周取小鼠新鲜粪便进行16S rDNA分析。用肝脏病理和生化指标反映养肝通络汤对NASH小鼠肝脏炎症和脂代谢的改善作用。用实时定量聚合酶链式反应(qRT-PCR)对PICRUST分析结果进行验证。病理生化指标检测结果表明，养阴补肾汤对NASH小鼠有一定的改善作用。与改善炎症和肝细胞损伤相比，YBT可能更专注于增强小鼠的代谢紊乱，如提高高密度脂蛋白-c水平。HFFD诱导的NASH小鼠肠道微生物区系的多样性和丰富度与正常对照组(NC组)有显著差异。经YBT处理后，小鼠的微生物区系的多样性和丰富度将增加，与类似的NC小鼠相比。类水平变化最显著的是假单胞菌属、乙酸因子、泽泻属、假单胞菌属、乙酸因子和泽泻属。根据16S rDNA结果和参考测序结果进行PICRUST分析以预测基因组功能。YBT治疗NASH的疗效可以通过调节肠道微生物区系的多样性和丰富性来实现。PICRUST分析结果表明，微生物区系结构变异最相关的功能是α-亚麻酸(ALA)代谢。定量RT-PCR结果显示，与ALA代谢相关的脂肪酸脱饱和酶1(FADS1)、脂肪酸脱饱和酶2(FADS2)、酰辅酶A氧化酶1(ACOX1)和酰辅酶A氧化酶2(ACOX2)的表达在不同组间有显著差异。HFFD组小鼠肝脏和小肠组织中上述基因的表达均受到抑制，养阴还五汤治疗后可恢复上述基因的表达。养阴补阳还五汤可通过改善肠道微生物区系的多样性和丰富性，进而改善ALA代谢，从而治疗NASH小鼠。
To investigate the treating effect of Yiqi-Bushen-Tiaozhi (YBT) recipe on nonalcoholic steatohepatitis (NASH) mice, determine whether the outcome was associated with gut microbiota, and clarify the regulating mechanism. NASH mice were induced by high-fat and high-fructose diets (HFFD). In the fifth week, mice in the YBT group were orally administrated YBT (22.12g·kg-1·d-1) daily for 12 weeks. Fresh stool of mice was collected at the 16th week for fecal 16S rDNA analysis. Hepatic pathology and biochemical indicators were used to reflect the improvement of YBT on hepatic inflammation and lipid metabolism in NASH mice. Quantitative real-time PCR (qRT-PCR) was used to verify the results of PICRUSt analysis. Results of the pathological and biochemical index showed that YBT could improve NASH mice. Compared with improving inflammation and hepatocyte damage, YBT may be more focused on enhancing metabolic disorders in mice, such as increasing HDL-c level. The diversity and richness of the gut microbiota of NASH mice induced by HFFD are significantly different from the normal control (NC) group. After YBT treatment, the diversity and richness of the mice microbiota will be increased to similar NC mice. Intestinimonas, Acetatifactor, Alistipes, Intestinimonas, Acetatifactor, and Alistipes have the most significant changes in the class level. PICRUSt analysis was performed to predict genomic functions based on the 16S rDNA results and reference sequencing. The efficacy of YBT in the treatment of NASH can be achieved by regulating the diversity and richness of gut microbiota. PICRUSt analysis results showed that the most relevant function of the microbiota construction variations is α- Linolenic acid (ALA) metabolism. Results of qRT-PCR showed significant differences between groups in the expression of Fatty acid desaturase 1 (FADS1), Fatty acid desaturase 2 (FADS2), Acyl-CoA Oxidase 1 (ACOX1), and Acyl-CoA Oxidase 2 (ACOX2) related to ALA metabolism. The expression of the above genes will be inhibited in the liver and small intestine of the HFFD group mice, and the expression can be restored after YBT treatment. YBT could treat NASH mice by improving the diversity and richness of gut microbiota and further the improvement of ALA metabolism.
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