Kim Hyeong-Geug, Lee Sung-Bae, Lee Jin-Seok, Kim Won-Young, Choi Seung-Hoon, Son Chang-Gue
Liver and Immunology Research Center, Daejeon Oriental Hospital of Oriental Medical College of Daejeon University, 176-9 Daeheung-ro, Jung-gu, Daejeon 301-724, Republic of Korea.
Department of Medical Consilience, Dankook University, 152 Jukjeon-ro, Suji-gu, Yongin-si, Gyeonggi-do 16890, Republic of Korea.
Evid Based Complement Alternat Med. 2017;2017:4390636. doi: 10.1155/2017/4390636. Epub 2017 Oct 17.
The combination of and radix is frequently prescribed for liver diseases in TKM. However, the synergic effects of the two herbs on nonalcoholic steatohepatitis (NASH) have not yet been studied. Therefore, we investigated the anti-NASH effects of the water extract of (AI), radix (CL), and combination of the two herbs (ACE). Hepatic steatosis and NASH were induced in HepG2 cells by treatment with palmitic acid (PA, for 6 h) with/without pretreatment of ACE (25 or 50 g/mL), AI (50 or 100 g/mL), CL (50 or 100 g/mL), curcumin (5 g/mL), or scopoletin (5 g/mL). The PA treatment (200 M) drastically altered intracellular triglyceride levels, total cholesterol, and expression levels of genes related to lipid metabolism (CD36, SREBP1c, PPAR-, and PPAR-), whereas pretreatment with ACE significantly attenuated these alterations. ACE also protected HepG2 cells from PA- (300 M-) induced endoplasmic reticulum (ER) stress and apoptosis and attenuated the related key molecules including GRP78, eIF2, and CHOP, respectively. In conclusion, we found synergic effects of and on NASH, supporting the clinical potential for fatty liver disorders. In addition, modulation of ER stress-relative molecules would be involved in its underlying mechanism.
在传统中医中,[药物名称1]和[药物名称2]的组合常用于治疗肝脏疾病。然而,这两种草药对非酒精性脂肪性肝炎(NASH)的协同作用尚未得到研究。因此,我们研究了[药物名称1]水提取物(AI)、[药物名称2](CL)以及两种草药的组合(ACE)对NASH的抗NASH作用。通过用棕榈酸(PA,处理6小时)处理HepG2细胞来诱导肝脂肪变性和NASH,同时分别用ACE(25或50μg/mL)、AI(50或100μg/mL)、CL(50或100μg/mL)、姜黄素(5μg/mL)或东莨菪素(5μg/mL)进行预处理。PA处理(200μM)显著改变了细胞内甘油三酯水平、总胆固醇以及与脂质代谢相关基因(CD36、SREBP1c、PPAR-α和PPAR-γ)的表达水平,而ACE预处理显著减弱了这些改变。ACE还保护HepG2细胞免受PA(300μM)诱导的内质网(ER)应激和凋亡,并分别减弱了包括GRP78、eIF2和CHOP在内的相关关键分子。总之,我们发现[药物名称1]和[药物名称2]对NASH具有协同作用,支持其在脂肪肝疾病方面的临床应用潜力。此外,内质网应激相关分子的调节可能参与其潜在机制。