Abstract
Endoplasmic reticulum (ER) stress creates abnormalities in the insulin action, inflammatory responses, lipoprotein B100 degradation, and hepatic lipogenesis. Hepatic steatosis leads to a broad spectrum of hepatic disorders such as nonalcoholic fatty liver disease (NAFLD) and NASH. Amygdalin has beneficial effects on asthma, bronchitis, diabetes, and atherosclerosis. We designed this study to evaluate the effect of amygdalin on the ER stress induced hepatic steatosis. Inbred mice received saline, DMSO and amygdalin, as control groups. ER stress was induced by tunicamycin (TM) injection. Amygdalin was administered 1 h before the TM challenge (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. Alanin aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride and cholesterol levels were measured. Histological evaluation revealed that amygdalin was unable to decrease the TM induced liver steatosis; however, ALT and AST levels decreased [ALT: 35.33(2.15) U/L versus 92.33(6.66) U/L; (57.000, (50.63, 63.36), P < 0.001) and AST: 93(5.09) U/L versus 345(97.3) U/L, (252, (163.37, 340.62), P < 0.001)]. Amygdalin also decreased triglyceride and cholesterol plasma levels in the Amy + TM group [TG: 42.66(2.15) versus 53.33(7.24) mg/dL; (10.67, (3.80, 17.54), P = 0.006) and TC: 9.33(3.55) versus 112.66(4.31) mg/dL, (103.33, (98.25, 108.40) P < 0.001)]. Amygdalin improved the ALT, AST, and lipid serum levels after the TM challenge; however, it could not attenuate hepatic steatosis.
Highlights
In certain circumstances, such as pharmacological stimuli, dietary demands, viral infections, and oxidative stress, the endoplasmic reticulum (ER) homeostasis may disrupt and induce ER stress phenomenon; this may lead to unfolded or misfolded protein accumulation [1]
Histological evaluation revealed that amygdalin was unable to decrease the TM induced liver steatosis; ALT and AST levels decreased [ALT: 35.33(2.15) U/L versus 92.33(6.66) U/L; (57.000, (50.63, 63.36), P < 0.001) and AST: 93(5.09) U/L versus 345(97.3) U/L, (252, (163.37, 340.62), P < 0.001)]
Considering the aforementioned studies, in this study, we aimed to evaluate the effect of amygdalin on ER stress induced hepatic steatosis
Summary
In certain circumstances, such as pharmacological stimuli, dietary demands, viral infections, and oxidative stress, the endoplasmic reticulum (ER) homeostasis may disrupt and induce ER stress phenomenon; this may lead to unfolded or misfolded protein accumulation [1]. ER stress and unfolded or misfolded protein accumulation create abnormalities in the insulin action, inflammatory responses, and hepatic steatosis [2,3,4]. Amygdalin was used for angiogenesis inhibition, asthma, bronchitis, emphysema, renal fibrosis, diabetes treatment, and pain relief [12,13,14,15,16,17]. Endoplasmic reticulum (ER) stress creates abnormalities in the insulin action, inflammatory responses, lipoprotein B100 degradation, and hepatic lipogenesis. Amygdalin has beneficial effects on asthma, bronchitis, diabetes, and atherosclerosis. We designed this study to evaluate the effect of amygdalin on the ER stress induced hepatic steatosis
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
