CAJ | 학술논문

目的：探讨竹节参多糖对脂肪变性肝细胞的保护作用。方法制备竹节参多糖不同浓度(30%、60%及90%)乙醇洗脱部位,应用棕榈酸(PA)诱导HepG2脂肪变性的细胞模型,筛选药物的干预活性,采用MTT法观察细胞存活状况,油红O染色观察细胞脂肪变性情况,提取细胞总RNA检测相关因子的表达水平。结果 MTT法检测结果显示,30%醇沉组细胞存活率较模型组明显升高；油红 O 染色其细胞内泡状脂滴数目较模型组明显减少；RT-PCR检测结果显示,内质网应激相关基因葡萄糖调节蛋白、CCAAT/增强子结合蛋白同源蛋白及炎性因子的表达较模型组明显降低。结论竹节参多糖30%乙醇洗脱部位能明显降低PA诱导的HepG2细胞脂肪变性,其机制可能是通过干预内质网应激反应实现。
목적：탐토죽절삼다당대지방변성간세포적보호작용。방법제비죽절삼다당불동농도(30%、60%급90%)을순세탈부위,응용종려산(PA)유도HepG2지방변성적세포모형,사선약물적간예활성,채용MTT법관찰세포존활상황,유홍O염색관찰세포지방변성정황,제취세포총RNA검측상관인자적표체수평。결과 MTT법검측결과현시,30%순침조세포존활솔교모형조명현승고；유홍 O 염색기세포내포상지적수목교모형조명현감소；RT-PCR검측결과현시,내질망응격상관기인포도당조절단백、CCAAT/증강자결합단백동원단백급염성인자적표체교모형조명현강저。결론죽절삼다당30%을순세탈부위능명현강저PA유도적HepG2세포지방변성,기궤제가능시통과간예내질망응격반응실현。
Objective To explore the protective effects of polysaccharide from Panax japonicus on free fatty acid in different parts of hepatic cell injury. Methods Polysaccharide of Panax japonicus was prepared through different concentrations of ethanol precipitation and was named as 30%polysaccharide component (pc), 60% pc and 90% pc. Palmitic acid (PA) was used to induce a cellular model of steatosis in HepG2 cells in order to screen the intervention viability of polysaccharide of Panax japonicus. MTT method was used to detect cell viability, and Oil Red O staining was used to demonstrate steatosis. Total RNA was extracted to detect the expression level of the relevant genes. Results MTT results showed that the 30% pc significantly increased cell viability compared with the model group;Oil Red O staining showed that the number of intracellular lipid droplets was significantly reduced in the 30% pc compared with the model group;RT-PCR results showed that expressions of the endoplasmic reticulum stress-related gene glucoese-regulated protein, CCAAT enhancer binding protein homologous protein and TNF-αwere significantly lower in the 30% pc compared with the model group, and there was no significant difference compared with normal control group. Conclusion The 30%ethanol precipitation fraction of polysaccharide from Panax japonicus significantly reduced PA-induced steatosis in HepG2 cells. Its mechanism was possibly realized through intervention in endoplasmic reticulum stress-related response.