The effect of amygdalin on fat accumulation in the liver

Background and Objective :Nonalcoholic fatty liver disease (NAFLD) is one of the greatest challenges in common public health in recent decades. NAFLD is considered an emerging healthcare problem in Asian countries with a prevalence of 15-45%, which is rising. It has become an important cause of the unexplained rise in transaminases, cryptogenic cirrhosis, and cryptogenic hepatocellular carcinoma. Pathogenesis is related to obesity, insulin resistance, oxidative stress, lipotoxicity, and resultant inflammation in the liver progressing to fibrosis. The endoplasmic reticulum (ER) stress response has recently been proposed to play a crucial role in both the development of steatosis and progression to nonalcoholic steatohepatitis. ER stress creates abnormalities in the fat accumulation, insulin resistance, inflammation, and apoptosis, all of which play important roles in the pathogenesis of NAFLD. Previously, amygdalin a cyanide-containing substance was used for angiogenesis inhibition, asthma, bronchitis, emphysema, renal fibrosis, diabetes treatment, atherosclerosis, and pain relief. We designed this study to evaluate the effect of amygdalin on the ER stress-induced hepatic steatosis. Materials and Methods 03 : Inbred male mice were randomly divided into five equal groups. Three groups received normal saline, dimethyl sulfoxide (DMSO) and amygdalin, respectively as control groups. ER stress was induced by tunicamycin (TM) injection in TM group. And Amygdalin was administered 1 h before the TM challenge for Amy + TM group. Mice body and liver weights were measured. Hematoxylin and eosin (H&E) and oil red O staining from liver tissue, were performed. Total cholesterol (TC), triglyceride (TG), alanine aminotransferase (ALT), and aspartate aminotransferase (AST) levels were measured by an autoanalyzer. Findings :Data analysis revealed that the liver index (liver weight/bodyweight x 100) increased significantly in the ER stress group when compared with the control group (P = 0.021). Histological evaluation revealed that amygdalin was unable to decrease the TM induced liver steatosis; however, ALT and AST levels decreased [ALT :( P < 0.001) and AST ( P < 0.001)]. Amygdalin also decreased triglyceride and cholesterol plasma levels in the Amy + TM group [TG: P = 0.006 and TC: P < 0.001]. Conclusion :Our study has shown that amygdalin reduced the lipid plasma levels and liver inflammation, thus confirming the antilipid and anti-inflammatory effects of amygdalin; however, amygdalin could not attenuate the ER stress-induced liver steatosis.

Keywords:

amygdalin , endoplasmic reticulum stress , liver , tunicamycin , steatosis