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.

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

Indexed on: 22 Jul '18Published on: 22 Jul '18Published in: Food & nutrition research


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. To determine the protective mechanism of bitter melon extract (BME), we performed experiments and . 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-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 was 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. 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.