Abstract

The nonalcoholic fatty liver disease (NAFLD) is a progressive liver disease that affects the health of people in an increasing rate. In the current research, we investigated the beneficial effect of a novel probiotic strain L. paracasei Jlus66 (Jlus66) on rats with high‐fat diet (HFD)‐induced NAFLD. The intestinal flora of rats was analyzed based on V3‐V4 region 16S rDNA sequencing. Moreover, we measured the oxidative stress and inflammation factors in the liver using commercial ELISA kit, and the lipopolysaccharide (LPS) in serum with chromogenic end‐point tachypheus amebocyte lysate. Compared with the HFD‐induced group, Jlus66 treatment significantly decreased the malondialdehyde (MDA) level in the serum (p < 0.05). Additionally, Jlus66 significantly enhanced the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH‐Px) in the liver and serum (p < 0.05). Jlus66 administration also reduced the levels of tumor necrosis factor (TNF‐α) and interleukin‐6 (IL‐6), and inversely increased the interleukin‐10 (IL‐10) level in serum (p < 0.05). Intestinal flora analysis results showed that Jlus66 can improve intestinal flora structure by increasing the abundance of gram‐positive flora such as Firmicutes, and decreasing gram‐negative flora such as Bacteroidetes, Proteobacteria, and Fusobacteria, and then reduced LPS concentration in the serum. So we concluded that Jlus66 can improve NAFLD by modulating the intestinal flora and followed reduction of oxidative stress (OxS) and inflammation.

Highlights

  • nonalcoholic fatty liver disease (NAFLD) is a complicated progressive liver disease that is caused by multiple factors (Bellentani, Scaglioni, Marino, & Bedogni, 2010) and is generally considered by the scientific community as hepatic expression of the metabolic syndrome along with chronic systemic oxidative stress (OxS)

  • Interleukin‐1β (IL‐1β), IL‐6, and TNF‐α are crucial proinflammatory cytokines produced by injured hepatocytes, immune cells, and activated Kupffer cells, which play a vital role in inflammation

  • Our results showed that high‐fat diet (HFD) induction increased the concentration of LPS, accompanied with the increase in TNF‐α and IL‐6 in serum, as well as disordered the intestinal flora by increasing abundance of Gram‐ negative flora (Bacteroidetes, Proteobacteria, and Fusobacteria) and decreasing abundance of gram‐negative flora (Firmicutes)

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Summary

| INTRODUCTION

NAFLD is a complicated progressive liver disease that is caused by multiple factors (Bellentani, Scaglioni, Marino, & Bedogni, 2010) and is generally considered by the scientific community as hepatic expression of the metabolic syndrome along with chronic systemic OxS. Though the mechanism of NAFLD is not fully elucidated, it is believed that oxidative stress plays a key role in the development of hepatocyte injury associated with NAFLD (El Hadi, Vettor, & Rossato, 2018; Masarone et al, 2018), followed by branches of several intracellular events as well as extracellular factors such as dysbiosis of the gut flora (Spahis et al, 2017). Gut microbiota dysbiosis can result in the development of obesity‐related NAFLD It is unclear whether the microbiota have a major impact on the incidence of NAFLD, the relative abundance of certain bacterial groups (Marchesi et al, 2016), the presence of harmful micro‐organisms, the metabolic function of microbes, host genetics, and/or combinations of these factors are important in the pathogenesis of NAFLD. To further investigate the beneficial effects of Jlus on NAFLD, the intestinal flora, oxidative stress, LPS, and inflammatory factors in the serum/liver were evaluated in rats with HFD‐induced NAFLD

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ETHICAL STATEMENT
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