Chang BoYoon, Kim Dae Sung, Kim SungYeon
Institute of Pharmaceutical Research and Development College of Pharmacy, Wonkwang University, Iksan, Jeonbuk, Republic of Korea.
Hanpoong Pharm. Co., Ltd., Jeonju-si, Jeonbuk, Republic of Korea.
Evid Based Complement Alternat Med. 2020 Jul 19;2020:1409376. doi: 10.1155/2020/1409376. eCollection 2020.
Postmenopausal women have an increased risk of developing nonalcoholic fatty liver disease (NAFLD). We formulated a combination of three herb mixtures (HPC03) and observed lipid-lowering efficacy. HepG2 cells were treated with oleic acid to induce an NAFLD model (in vitro). Also, we investigated potential of HPC03 in an ovariectomize- (OVX-) induced NAFLD model (in vivo). We separated the mice into six groups, as follows: SHAM, OVX, OVX + -estradiol, and OVX + HPC03 (50, 100, and 200 mg/kg). Rats were administered with/without HPC03 for 12 weeks. HPC03 dose dependently inhibited the lipid accumulation involved in lipogenesis in HepG2 cells. The body weight, fat mass, and weights of the liver were decreased in the OVX group than that in the other groups. HPC03 had decreased adiposity that was induced by OVX. HPC03 treatment reduced liver lipid deposition and prevented the increase in serum and liver triglyceride export when there was a deficiency in estradiol. HPC03 improves OVX-induced fatty liver and lipid metabolism. These findings suggest that HPC03 from postmenopausal women has a protective effect during NAFLD conditions.
绝经后女性患非酒精性脂肪性肝病(NAFLD)的风险增加。我们配制了三种草药混合物的组合(HPC03)并观察其降脂效果。用油酸处理HepG2细胞以诱导NAFLD模型(体外)。此外,我们研究了HPC03在卵巢切除(OVX)诱导的NAFLD模型(体内)中的潜力。我们将小鼠分为六组,如下:假手术组、OVX组、OVX + 雌二醇组和OVX + HPC03组(50、100和200 mg/kg)。给大鼠施用或不施用HPC03,持续12周。HPC03剂量依赖性地抑制HepG2细胞中参与脂肪生成的脂质积累。OVX组的体重、脂肪量和肝脏重量均低于其他组。HPC03减轻了OVX诱导的肥胖。当雌二醇缺乏时,HPC03治疗减少了肝脏脂质沉积,并防止了血清和肝脏甘油三酯输出的增加。HPC03改善了OVX诱导的脂肪肝和脂质代谢。这些发现表明,绝经后女性的HPC03在NAFLD情况下具有保护作用。