Protective effect of Letinous edodes foot peptides against ethanol‑induced liver injury in L02 cells

Ma,Lin; Huo,Chun‑Yan; Zhang,Xiao‑Yu; Qin,Chen‑Qiang; Ren,Di‑Feng; Lu,Jun

doi:10.3892/mmr.2018.9093

Protective effect of Letinous edodes foot peptides against ethanol‑induced liver injury in L02 cells

Authors:
- Lin Ma
- Chun‑Yan Huo
- Xiao‑Yu Zhang
- Chen‑Qiang Qin
- Di‑Feng Ren
- Jun Lu
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Affiliations: Beijing Key Laboratory of Forest Food Processing and Safety, College of Biological Sciences and Biotechnology, Beijing Forestry University, Beijing 100083, P.R. China, Beijing Engineering Research Center of Protein and Functional Peptides, China National Research Institute of Food and Fermentation Industries, Beijing 100015, P.R. China
Published online on: May 29, 2018 https://doi.org/10.3892/mmr.2018.9093
Pages: 1858-1866

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Abstract

The aim of the present study was to evaluate the protective effect and mechanism of Letinous edodes foot peptides on ethanol‑induced L02 cells. A cell model of ethanol‑induced damage was established in vitro to study the effects of the Letinous edodes foot peptides on human L02 hepatocytes. The expression and activity of superoxide dismutase (SOD), malondialdehyde (MDA), aspartate aminotransferase (AST), alanine aminotransferase (ALT), alcohol dehydrogenase (ADH) and acetaldehyde dehydrogenase (ALDH), following treatment were examined to determine the anti‑alcoholism and hepatoprotective functions of Letinous edodes foot peptides. Taking Letinous edodes foot peptides prior to ethanol exposure was more beneficial, which significantly increased SOD activity and the mRNA expression of ADH and ALDH suppressed by ethanol. In addition, the intracellular MDA content, and AST and ALT activity decreased in ethanol‑induced L02 cells pretreated with the peptides, when compared with the control. Furthermore, Letinous edodes foot peptides inhibited the ethanol‑induced activation of the proinflammatory cytokines, interleukin‑6 and tumor necrosis factor‑α, and promoted the metabolic regulation factors, AMP‑activated protein kinase‑α2 and peroxisome proliferator‑activated receptor‑α.

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