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Research Paper|Volume 16, Issue 3|pp 2362—2384

Prepared Radix Polygoni Multiflori and emodin alleviate lipid droplet accumulation in nonalcoholic fatty liver disease through MAPK signaling pathway inhibition

Changyudong Huang1,2, Yiqiong Zhang1,2, Yongjie Xu1, Sijia Wei1,2, Tingting Yang1,2, Shuang Wang1,2, Chengcheng Li1, Hairong Lin1, Xing Li3, Shuyun Zhao4, Liying Zhu2, Wei Pan1
  • 1Guizhou Prenatal Diagnosis Center, Affiliated Hospital of Guizhou Medical University, Guiyang 550004, Guizhou, P.R. China
  • 2School of Clinical Laboratory Science, Guizhou Medical University, Guiyang 550004, Guizhou, P.R. China
  • 3School of Basic Medical Sciences, Guizhou University of Traditional Chinese Medicine, Guiyang 550004, Guizhou, P.R. China
  • 4Reproductive Center, Affiliated Hospital of Guizhou Medical University, Guiyang 550004, Guizhou, P.R. China
* Equal contribution
Received: April 17, 2023Accepted: December 6, 2023Published: January 26, 2024

Copyright: © 2024 Huang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

As one of the most common liver diseases, nonalcoholic fatty liver disease (NAFLD) affects almost one-quarter of the world’s population. Although the prevalence of NAFLD is continuously rising, effective medical treatments are still inadequate. Radix Polygoni Multiflori (RPM) is a traditional Chinese herbal medicine. As a processed product of RPM, prepared Radix Polygoni Multiflori (PRPM) has been reported to have antioxidant and anti-inflammatory effects. This study investigated whether PRPM treatment could significantly improve NAFLD. We used recent literature, the Herb database and the SwissADME database to isolate the active compounds of PRPM. The OMIM, DisGeNET and GeneCards databases were used to isolate NAFLD-related target genes, and GO functional enrichment and KEGG pathway enrichment analyses were conducted. Moreover, PRPM treatment in NAFLD model mice was evaluated. The results indicate that the target genes are mainly enriched in the AMPK and de novo lipogenesis signaling pathways and that PRPM treatment improves NAFLD disease in model mice. Here, we found the potential benefits of PRPM against NAFLD and demonstrated in vivo and in vitro that PRPM and its ingredient emodin downregulate phosphorylated P38/P38, phosphorylated ERK1/2 and genes related to de novo adipogenesis signaling pathways and reduce lipid droplet accumulation. In conclusion, our findings revealed a novel therapeutic role for PRPM in the treatment of NAFLD and metabolic inflammation.