Multi-targeting therapeutic mechanisms of the Chinese herbal medicine QHD in the treatment of non-alcoholic fatty liver disease
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Qin Feng1,2,3,*, Wensheng Liu2,3,*, Susan S. Baker2,3, Hongshan Li4, Cheng Chen1, Qian Liu1, Shijie Tang5, Lingyu Guan5, Maria Tsompana6, Rafal Kozielski8,9, Robert D. Baker2,3, Jinghua Peng1, Ping Liu1, Ruixin Zhu5, Yiyang Hu1, Lixin Zhu2,3,7
1Institute of Liver Disease, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China
2Digestive Diseases and Nutrition Center, Women and Children’s Hospital of Buffalo, Buffalo, NY, USA
3Department of Pediatrics, The State University of New York at Buffalo, Buffalo, New York, USA
4Ningbo No.2 Hospital, Ningbo, Zhejiang Province, China
5Department of Bioinformatics, Tongji University, Shanghai, China
6Center of Excellence in Bioinformatics and Life Sciences, The State University of New York at Buffalo, Buffalo, New York, USA
7Institute of Digestive Diseases, Longhua Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China
8Women and Children’s Hospital of Buffalo, Buffalo, NY, USA
9Department of Pathology, The State University of New York at Buffalo, Buffalo, New York, USA
*These authors contributed equally to this work
Lixin Zhu, email: firstname.lastname@example.org
Yiyang Hu, email: email@example.com
Keywords: NAFLD, lipid synthesis, anti-oxidant, gut microbiome, Treg
Received: December 28, 2016 Accepted: February 08, 2017 Published: February 18, 2017
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.
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