Multi-targeting therapeutic mechanisms of the Chinese herbal medicine QHD in the treatment of non-alcoholic fatty liver disease

Abstract

// Qin Feng 1, 2, 3, * , Wensheng Liu 2, 3, * , Susan S. Baker 2, 3 , Hongshan Li 4 , Cheng Chen 1 , Qian Liu 1 , Shijie Tang 5 , Lingyu Guan 5 , Maria Tsompana 6 , Rafal Kozielski 8, 9 , Robert D. Baker 2, 3 , Jinghua Peng 1 , Ping Liu 1 , Ruixin Zhu 5 , Yiyang Hu 1 , Lixin Zhu 2, 3, 7 1 Institute of Liver Disease, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China 2 Digestive Diseases and Nutrition Center, Women and Children’s Hospital of Buffalo, Buffalo, NY, USA 3 Department of Pediatrics, The State University of New York at Buffalo, Buffalo, New York, USA 4 Ningbo No.2 Hospital, Ningbo, Zhejiang Province, China 5 Department of Bioinformatics, Tongji University, Shanghai, China 6 Center of Excellence in Bioinformatics and Life Sciences, The State University of New York at Buffalo, Buffalo, New York, USA 7 Institute of Digestive Diseases, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China 8 Women and Children’s Hospital of Buffalo, Buffalo, NY, USA 9 Department of Pathology, The State University of New York at Buffalo, Buffalo, New York, USA * These authors contributed equally to this work Correspondence to: Lixin Zhu, email: lixinzhu@buffalo.edu Yiyang Hu, email: yyhuliver@163.com Keywords: NAFLD, lipid synthesis, anti-oxidant, gut microbiome, Treg Received: December 28, 2016      Accepted: February 08, 2017      Published: February 18, 2017 ABSTRACT Beneficial effects of the Chinese herbal medicine Qushi Huayu Decoction (QHD) were observed with non-alcoholic fatty liver disease (NAFLD) patients and animal models. The impact of QHD or its active components (geniposide and chlorogenic acid, GC) on NAFLD liver transcriptome and gut microbiota was examined with NAFLD rats. Increased expression for genes required for glutathione production and decreased expression for genes required for lipid synthesis was observed in NAFLD livers treated with QHD and GC. GC treatment decreased serum LPS, which could be explained by reduced mucosal damage in the colon of GC-treated rats. Further, our data suggest an increased abundance of Treg-inducing bacteria that stimulated the Treg activity in GC treated colon, which in turn down-regulated inflammatory signals, improved gut barrier function and consequently reduced hepatic exposure to microbial products. Our study suggests that QHD simultaneously enhanced the hepatic anti-oxidative mechanism, decreased hepatic lipid synthesis, and promoted the regulatory T cell inducing microbiota in the gut.