Study On The Hepatoprotective Effects Of Morchella Esculenta Fruit Body On Alcoholic Liver Injury

Alcoholic liver disease has a high morbidity and mortality worldwide,and the Morchella esculenta fruit body(ME)may be a therapeutic medicinal fungus for preventing Alcoholic liver disease.The present study aims to investigate the hepatoprotection of ME and underlying mechanisms related to oxidative stress and inflammatory.In this study,we first systematically analyzed the composition of ME.Subsequently,a mouse model of acute alcohol-induced liver injury was established by administering alcohol for two weeks,and serum and liver biochemical indicators were determined by enzyme-linked immunosorbent assay(ELISA).Pathological studies of the liver and kidney of mice using H&E staining techniques.The molecular mechanism of the protection of ME against alcoholic liver injury was determined by Western Blot.To study the hepatoprotective effect of ME on alcoholic liver injury.ME contains 21 types of fatty acid,17 types of amino acid and 12 types of minerals.ME significantly reduced the levels of alanine aminotransferase(ALT)and aspartate aminotransferase(AST),and increased the activity of acetaldehyde dehydrogenase(ALDH)in serum and liver.ME regulated lipid metabolism indicating by reduced the hyper-levels of total cholesterol(TC),high-density lipoprotein(HDL)and triglyceride(TG)in liver.ME reduced the production of inflammatory factors including chemokine(C-X-C motif)ligand 13(CXCL13),chitinase-3 like-1 protein(YKL-40),interleukin-7(IL-7),plasminogen activator inhibitor type 1(PAI-1)and retinol-binding protein 4(RBP4)in serum and/or liver.ME relieved the alcohol-induced imbalance of pro-oxidation and anti-oxidation via nuclear factor-erythroid 2-related factor 2(Nrf2)signal indicating by up-regulation the expressions of superoxide dismutase-1(SOD-1),superoxide dismutase-2(SOD-2),catalase(CAT),heme oxygenase-1(HO-1)and heme oxygenase-2(HO-2),and down-regulation the expression of Keap-1 in liver of mice with acute alcohol liver damage.Moreover,ME inhibited the phosphorylated levels of nuclear factor kappa-B kinase α/β(P-IKKα/β),inhibitor of nuclear factor kappa-B α(P-IκBα),and nuclear factor kappa-B p65(P-NF-κB p65)in liver.The present study successfully confirmed the hepatocyte protection of ME against alcohol-induced acute liver injury,and found the possible mechanism may be related to its improving the anti-oxidative and anti-inflammatory status via regulating Nrf2/NF-κB signaling.