Abstract

Objective The purpose of present study was to investigate the potential mechanism underlying the protective effect of Shenling Baizhu San (SLBZS) on nonalcoholic fatty liver disease (NAFLD) by microRNA (miRNA) sequencing. Methods Thirty male Wistar rats were randomly divided into a normal control (NC) group, a high-fat diet (HFD) group, and an SLBZS group. After 12 weeks, the biochemical parameters and liver histologies of the rats were assessed. The Illumina HiSeq 2500 sequencing platform was used to analyse the hepatic miRNA expression profiles. Representative differentially expressed miRNAs were further validated by qRT-PCR. The functions of the differentially expressed miRNAs were analysed by bioinformatics. Results Our results identified 102 miRNAs that were differentially expressed in the HFD group compared with the NC group. Among those differentially expressed miRNAs, the expression levels of 28 miRNAs were reversed by SLBZS administration, suggesting the modulation effect of SLBZS on hepatic miRNA expression profiles. The qRT-PCR results confirmed that the expression levels of miR-155-5p, miR-146b-5p, miR-132-3p, and miR-34a-5p were consistent with those detected by sequencing. Bioinformatics analyses indicated that the target genes of the differentially expressed miRNAs reversed by SLBZS were mainly related to metabolic pathways. Conclusion This study provides novel insights into the mechanism of SLBZS in protecting against NAFLD; this mechanism may be partly related to the modulation of hepatic miRNA expression and their target pathways.

Highlights

  • Nonalcoholic fatty liver disease (NAFLD) is defined as the pathological accumulation of fat in the liver without a history of excessive alcohol consumption

  • We found that the abnormal expression of 28 miRNAs in the high-fat diet (HFD) group was reversed by Shenling Baizhu San (SLBZS) administration (Figure 4). e 28 differentially expressed miRNAs are listed in Table 3, and cluster analysis of miRNA expression is shown in Figure 5. ese results indicate that SLBZS systematically modulated hepatic miRNA expression profiles in HFD-fed rats, and these 28 miRNAs may be important factors in the reversion progression of NAFLD by SLBZS

  • We confirmed that SLBZS can improve biochemical parameters in HFD-induced NAFLD rats. e administration of SLBZS plays a protective role in improving the abnormal serum lipid profiles and liver transaminases in HFD-fed rats. erefore, SLBZS may improve metabolic disorders and protect liver function to

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Summary

Introduction

Nonalcoholic fatty liver disease (NAFLD) is defined as the pathological accumulation of fat in the liver without a history of excessive alcohol consumption. It encompasses a wide spectrum of conditions ranging from simple steatosis to nonalcoholic steatohepatitis (NASH) and may progress to advanced liver cirrhosis and hepatocellular carcinoma (HCC) [1, 2]. As a multifactorial disease with a complex pathogenesis, NAFLD is currently considered as the liver manifestation of the metabolic syndrome (MS). Especially central obesity, insulin resistance, oxidative stress, mitochondrial dysfunction, glucose intolerance, dyslipidemia, and other metabolic syndromes are closely related to NAFLD [3,4,5]. Lifestyle modification is still regarded as an important approach to slow the progression of NAFLD, but long-term adherence to lifestyle interventions is often difficult for patients to adhere to [8, 9]. erefore, much effort has been focused on the development of novel prophylactic and therapeutic agents for NAFLD

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