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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.

ABSTRACT: 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.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.BME significantly decreased expression levels of ER-stress markers (including phospho-eIF2?, 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.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.

SUBMITTER: Lee HJ

PROVIDER: S-EPMC5883859 | biostudies-other | 2018

REPOSITORIES: biostudies-other

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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.

Lee Hwa Joung HJ Cui Rihua R Choi Sung-E SE Jeon Ja Young JY Kim Hae Jin HJ Kim Tae Ho TH Kang Yup Y Lee Kwan-Woo KW

Food & nutrition research 20180322

<h4>Background</h4>Bitter melon (BM) improves glucose level, lipid homeostasis, and insulin resistance <i>in vivo</i>. However, the preventive mechanism of BM in nonalcoholic fatty liver disease (NAFLD) has not been elucidated yet.<h4>Aim & design</h4>To determine the protective mechanism of bitter melon extract (BME), we performed experiments <i>in vitro</i> and <i>in vivo</i>. BME were treated palmitate (PA)-administrated HepG2 cells. C57BL/6J mice were divided into two groups: high-fat/high-f ...[more]

PMID: 30026676

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Project description:Saponins from bitter melon (BMS) are well-known to have various biological activities, especially in the field of fat-lowering. However, many gaps remain in our knowledge of BMS-induced fat reduction and health benefits. Here, we aimed to investigate the precise mechanism of BMS in alleviating fat accumulation in C. elegans and HepG2 cell line. Results indicated that BMS showed strong fat-lowering and lifespan-extension properties. Lipidomic analysis illustrated that BMS could alter the lipid profile, especially represented by phosphatidylethanolamine (PE) increase, which plays an essential role in autophagy. Furthermore, we applied gene-deficient mutants and RNAi technology to confirm that BMS largely depended on daf-16/FoxO1 and hlh-30/TFEB mediated lipophagy to reduce fat deposition. In addition, BMS could ameliorate oil acid (OA)-induced fat accumulation in HepG2 cells by induction of autophagy-related proteins, such as the phosphorylated AMPK and LC3B. In conclusion, our results elucidated the underlying mechanism of bitter melon saponins interfering with lipid metabolism from the autophagy point of view, which provide new insights into a nutraceutical to mitigate obesity. Graphical abstract We aimed to investigate the precise mechanism of saponins from bitter melon (BMS) in alleviating fat accumulation in C. elegans. Results indicated that BMS showed strong fat-lowering and lifespan-extension properties. Lipidomic analysis illustrated that BMS could alter the lipid profile, especially represented by PE increase, which plays an essential role in autophagy. Furthermore, we applied gene-deficient mutants and RNAi technology to confirm that BMS could inhibit fat deposition through daf-16/FoxO1 and hlh-30/TFEB mediated lipophagy. In addition, BMS could ameliorate oil acid (OA)-induced fat accumulation in HepG2 cells by induction of AMPK phosphorylation and LC3B expression, which were involved in autophagy. Thus, we concluded that BMS could ameliorate fat accumulation by inducing autophagy.Image 1 Highlights • Bitter melon saponin (BMS) could inhibit fat accumulation and extended the lifespan of C. elegans.• Lipidomics analysis predicted autophagy may be a key pathway involved in the fat-lowering effects of BMS.• BMS induced daf-16/hlh-30 mediated lipophagy to confer fat-lowering benefit.• BMS regulated autophagy via activating AMPK phosphorylation and LC3B expressions in HepG2 cells.

Dataset Information

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.

Publications

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.

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