Bitter melon extract ameliorates palmitate-induced apoptosis via inhibition of endoplasmic reticulum stress in HepG2 cells and high-fat/high-fructose-diet-induced fatty liver
Background: Bitter melon (BM) improves glucose level, lipid homeostasis, and insulin resistance in vivo. However, the preventive mechanism of BM in nonalcoholic fatty liver disease (NAFLD) has not been elucidated yet. Aim & Design: To determine the protective mechanism of bitter melon extract (B...
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Swedish Nutrition Foundation
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doaj-09427701510547708005cf27dbbb37622020-11-24T23:16:59ZengSwedish Nutrition FoundationFood & Nutrition Research1654-661X2018-03-0162011010.29219/fnr.v62.13191319Bitter melon extract ameliorates palmitate-induced apoptosis via inhibition of endoplasmic reticulum stress in HepG2 cells and high-fat/high-fructose-diet-induced fatty liverHwa Joung Lee0Rihua Cui1Sung-E Choi2Ja Young Jeon3Hae Jin Kim4Tae Ho Kim5Yup Kang6Kwan-Woo Lee7Department of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon, Republic of KoreaDepartment of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon, Republic of KoreaDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of KoreaDepartment of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon, Republic of KoreaDepartment of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon, Republic of KoreaDivision of Endocrine and Metabolism, Department of Internal Medicine, Seoul Medical Center, Seoul, Republic of KoreaDepartment of Physiology, Ajou University School of Medicine, Suwon, Republic of KoreaDepartment of Endocrinology and Metabolism, Ajou University School of Medicine, Suwon, Republic of KoreaBackground: Bitter melon (BM) improves glucose level, lipid homeostasis, and insulin resistance in vivo. However, the preventive mechanism of BM in nonalcoholic fatty liver disease (NAFLD) has not been elucidated yet. Aim & Design: To determine the protective mechanism of bitter melon extract (BME), we performed experiments in vitro and in vivo. BME were treated palmitate (PA)-administrated HepG2 cells. C57BL/6J mice were divided into two groups: high-fat/high-fructose (HF/HFr) without or with BME supplementation (100 mg/kg body weight). Endoplasmic reticulum (ER) stress, apoptosis, and biochemical markers were then examined by western blot and real-time PCR analyses. Results: BME significantly decreased expression levels of ER-stress markers (including phospho-eIF2α, CHOP, and phospho-JNK [Jun N-terminal kinases]) in PA-treated HepG2 cells. BME also significantly decreased the activity of cleaved caspase-3 (a well known apoptotic-induced molecule) and DNA fragmentation. The effect of BME on ER stress–mediated apoptosis in vitro was similarly observed in HF/HFr-fed mice in vivo. BME significantly reduced HF/HFr-induced hepatic triglyceride (TG) and serum alanine aminotransferase (ALT) as markers of hepatic damage in mice. In addition, BME ameliorated HF/HFr-induced serum TG and serum-free fatty acids. Conclusion: These data indicate that BME has protective effects against ER stress mediated apoptosis in HepG2 cells as well as in HF/HFr-induced fatty liver of mouse. Therefore, BME might be useful for preventing and treating NAFLD.http://foodandnutritionresearch.net/index.php/fnr/article/view/1319/4691bitter melon extractpalmitatehigh-fat/high-fructose dietnonalcoholic fatty liver diseaseendoplasmic reticulum stressapoptosis |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Hwa Joung Lee Rihua Cui Sung-E Choi Ja Young Jeon Hae Jin Kim Tae Ho Kim Yup Kang Kwan-Woo Lee |
spellingShingle |
Hwa Joung Lee Rihua Cui Sung-E Choi Ja Young Jeon Hae Jin Kim Tae Ho Kim Yup Kang Kwan-Woo Lee Bitter melon extract ameliorates palmitate-induced apoptosis via inhibition of endoplasmic reticulum stress in HepG2 cells and high-fat/high-fructose-diet-induced fatty liver Food & Nutrition Research bitter melon extract palmitate high-fat/high-fructose diet nonalcoholic fatty liver disease endoplasmic reticulum stress apoptosis |
author_facet |
Hwa Joung Lee Rihua Cui Sung-E Choi Ja Young Jeon Hae Jin Kim Tae Ho Kim Yup Kang Kwan-Woo Lee |
author_sort |
Hwa Joung Lee |
title |
Bitter melon extract ameliorates palmitate-induced apoptosis via inhibition of endoplasmic reticulum stress in HepG2 cells and high-fat/high-fructose-diet-induced fatty liver |
title_short |
Bitter melon extract ameliorates palmitate-induced apoptosis via inhibition of endoplasmic reticulum stress in HepG2 cells and high-fat/high-fructose-diet-induced fatty liver |
title_full |
Bitter melon extract ameliorates palmitate-induced apoptosis via inhibition of endoplasmic reticulum stress in HepG2 cells and high-fat/high-fructose-diet-induced fatty liver |
title_fullStr |
Bitter melon extract ameliorates palmitate-induced apoptosis via inhibition of endoplasmic reticulum stress in HepG2 cells and high-fat/high-fructose-diet-induced fatty liver |
title_full_unstemmed |
Bitter melon extract ameliorates palmitate-induced apoptosis via inhibition of endoplasmic reticulum stress in HepG2 cells and high-fat/high-fructose-diet-induced fatty liver |
title_sort |
bitter melon extract ameliorates palmitate-induced apoptosis via inhibition of endoplasmic reticulum stress in hepg2 cells and high-fat/high-fructose-diet-induced fatty liver |
publisher |
Swedish Nutrition Foundation |
series |
Food & Nutrition Research |
issn |
1654-661X |
publishDate |
2018-03-01 |
description |
Background: Bitter melon (BM) improves glucose level, lipid homeostasis, and insulin resistance in vivo. However, the preventive mechanism of BM in nonalcoholic fatty liver disease (NAFLD) has not been elucidated yet. Aim & Design: To determine the protective mechanism of bitter melon extract (BME), we performed experiments in vitro and in vivo. BME were treated palmitate (PA)-administrated HepG2 cells. C57BL/6J mice were divided into two groups: high-fat/high-fructose (HF/HFr) without or with BME supplementation (100 mg/kg body weight). Endoplasmic reticulum (ER) stress, apoptosis, and biochemical markers were then examined by western blot and real-time PCR analyses. Results: BME significantly decreased expression levels of ER-stress markers (including phospho-eIF2α, CHOP, and phospho-JNK [Jun N-terminal kinases]) in PA-treated HepG2 cells. BME also significantly decreased the activity of cleaved caspase-3 (a well known apoptotic-induced molecule) and DNA fragmentation. The effect of BME on ER stress–mediated apoptosis in vitro was similarly observed in HF/HFr-fed mice in vivo. BME significantly reduced HF/HFr-induced hepatic triglyceride (TG) and serum alanine aminotransferase (ALT) as markers of hepatic damage in mice. In addition, BME ameliorated HF/HFr-induced serum TG and serum-free fatty acids. Conclusion: These data indicate that BME has protective effects against ER stress mediated apoptosis in HepG2 cells as well as in HF/HFr-induced fatty liver of mouse. Therefore, BME might be useful for preventing and treating NAFLD. |
topic |
bitter melon extract palmitate high-fat/high-fructose diet nonalcoholic fatty liver disease endoplasmic reticulum stress apoptosis |
url |
http://foodandnutritionresearch.net/index.php/fnr/article/view/1319/4691 |
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