Wu Jing-Tao, Yang Gui-Wen, Qi Cui-Hua, Zhou Lei, Hu Jian-Guo, Wang Mao-Shan
Department of science and technology.
College of life science, Shandong normal university, Jinan 250014, China.
Afr J Tradit Complement Altern Med. 2016 Jul 3;13(4):176-183. doi: 10.21010/ajtcam.v13i4.23. eCollection 2016.
The current study was designed to evaluate the effect of Platycodin D (PD), triterpenoid saponins extracted from the roots of (PG) on alcohol-induced fatty liver (AFL) and investigate the possible mechanism.
A rat model was set up by feeding ethanol and fish oil to experimental rats, which then were treated with PD of 10, 20, 30 mg/kg body weight/day for 4 weeks, respectively, whereafter, liver function enzymes, endotoxin of serum and liver lipid were assayed by biochemical methods, cytokines, histochemistry of hepatic tissue, the protein expression of CD14 and TLR4, the mRNA expression of MD-2, MyD 88 and TRAF-6 were assayed.
Treatment with PD on AFL rats significantly decreased the levels of serum ALT, AST and TBIL, coefficient of liver index and the hepatic tissue contents of TG, additionally and dramatically decreased serum endotoxin levels, down-regulated MD-2 and CD14 levels, as well as the mRNA expression of TLR4, MyD88 and TRAF-6, accordingly suppressed NF-κB: p65 as well as endotoxin-mediated inflammatory factors such as TNF-α and IL-6.
Treatment with PD effectively protects against AFL through anti-inflammatory and anti-endotoxic process, and the confirmed mechanism is that PD treatment ameliorate alcoholic-induced liver injury mainly via TLR4-MyD88-NF-K: B signal path in AFL rat. AFL: alcoholic-induced fatty liver, CD14: cluster of differentiation 14, LPS: lipopolysaccharide, LBP: lipopolysaccharide-binding protein, TLR4: toll-like receptor 4, MD-2: molecule myeloid differential protein-2, MyD 88: myeloid differentiation primary response protein 88, TRAF-6: TNF-receptor associated factor-6, NF-κB: nuclear transcription factor kappa B, IL-6: interleukin-6, TNF-α: tumor necrosis factor-α, PG: , PD: Platycodin D.
本研究旨在评估桔梗皂苷D（PD），即从桔梗（PG）根部提取的三萜皂苷，对酒精性脂肪肝（AFL）的影响，并探究其可能的作用机制。
通过给实验大鼠喂食乙醇和鱼油建立大鼠模型，然后分别用10、20、30mg/kg体重/天的PD对其进行为期4周的治疗，之后采用生化方法检测肝功能酶、血清内毒素和肝脂质，检测细胞因子、肝组织的组织化学、CD14和TLR4的蛋白表达、MD-2、MyD 88和TRAF-6的mRNA表达。
用PD治疗AFL大鼠可显著降低血清谷丙转氨酶（ALT）、谷草转氨酶（AST）和总胆红素（TBIL）水平、肝脏指数系数以及肝组织甘油三酯（TG）含量，此外还能显著降低血清内毒素水平，下调MD-2和CD14水平以及TLR4、MyD88和TRAF-6的mRNA表达，从而抑制核转录因子κB（NF-κB）：p65以及内毒素介导的炎性因子如肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）。
PD治疗通过抗炎和抗内毒素作用有效预防AFL，且已证实的机制是PD治疗主要通过AFL大鼠的TLR4-MyD88-NF-κB信号通路改善酒精性肝损伤。AFL：酒精性脂肪肝，CD14：分化簇14，LPS：脂多糖，LBP：脂多糖结合蛋白，TLR4：Toll样受体4，MD-2：髓样分化蛋白-2，MyD 88：髓样分化初级反应蛋白88，TRAF-6：肿瘤坏死因子受体相关因子-6，NF-κB：核转录因子κB，IL-6：白细胞介素-6，TNF-α：肿瘤坏死因子-α，PG：桔梗，PD：桔梗皂苷D
