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Abstract 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.

Abstract Source:

Food Nutr Res. 2018 ;62. Epub 2018 Mar 22. PMID: 30026676

Abstract Author(s):

Hwa Joung Lee, Rihua Cui, Sung-E Choi, Ja Young Jeon, Hae Jin Kim, Tae Ho Kim, Yup Kang, Kwan-Woo Lee

Article Affiliation:

Hwa Joung Lee


Background: Bitter melon (BM) improves glucose level, lipid homeostasis, and insulin resistance. 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 experimentsand. 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 apoptosiswas similarly observed in HF/HFr-fed mice. 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.

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