CAJ | 학술논문

目的研究过氧化物酶体增殖物激活受体-α(PPAR-α)配体非诺贝特对于游离脂肪酸(FFA)介导的胰岛微血管内皮细胞(IMEC)损害的干预作用.方法采用MTT法和流式法分析非诺贝特对FFA诱导IMEC细胞株MS-1细胞损害的影响,应用紫外分光光度法检测细胞培养液中一氧化氮(NO)、超氧化物歧化酶(SOD)、丙二醛(MDA)水平.结果对照组、FFA组以及非诺贝特干预组MS-1细胞增殖率分别为(100.0±0.7)%、(16.2±0.8)%、(26.8±0.8)%,差异具有统计学意义(P＜0.001);三组MS-1细胞凋亡率分别为(4.80±2.07)%、(26.31±1.78)%、(19.20±1.90)%,差异有统计学意义(P＜0.001);细胞培养液NO含量分别为(6.61±0.65)、(2.48±0.62)、(4.11±0.33)μmol/L,差异有统计学意义(P＜0.001);SOD含量分别为(20.29±1.10)、(15.10±0.40)、(16.46±0.73)U/ml,差异有统计学意义(P＜0.001);MDA水平分别为(4.44±0.98)、(8.26±0.85)、(5.56±0.91)μmoL/L,差异有统计学意义(P＜0.001).结论 FFA可以诱导胰岛微血管内皮细胞发生明显脂性凋亡和氧化应激损伤,PPAR-α配体具有保护该细胞免于FFA氧化应激损伤的作用.
목적 연구과양화물매체증식물격활수체-α(PPAR-α)배체비낙패특대우유리지방산(FFA)개도적이도미혈관내피세포(IMEC)손해적간예작용.방법 채용MTT법화류식법분석비낙패특대FFA유도IMEC세포주MS-1세포손해적영향,응용자외분광광도법검측세포배양액중일양화담(NO)、초양화물기화매(SOD)、병이철(MDA)수평.결과 대조조、FFA조이급비낙패특간예조MS-1세포증식솔분별위(100.0±0.7)%、(16.2±0.8)%、(26.8±0.8)%,차이구유통계학의의(P＜0.001);삼조MS-1세포조망솔분별위(4.80±2.07)%、(26.31±1.78)%、(19.20±1.90)%,차이유통계학의의(P＜0.001);세포배양액NO함량분별위(6.61±0.65)、(2.48±0.62)、(4.11±0.33)μmol/L,차이유통계학의의(P＜0.001);SOD함량분별위(20.29±1.10)、(15.10±0.40)、(16.46±0.73)U/ml,차이유통계학의의(P＜0.001);MDA수평분별위(4.44±0.98)、(8.26±0.85)、(5.56±0.91)μmoL/L,차이유통계학의의(P＜0.001).결론 FFA가이유도이도미혈관내피세포발생명현지성조망화양화응격손상,PPAR-α배체구유보호해세포면우FFA양화응격손상적작용.
Objective To investigate the effect of peroxisome proliferators-activated receptor α ligand (fenofibrate) on free fatty acid-induced impairment in islet microvascular endothelial cells.Methods Islet microvascular endothelial cell line,MS-1 cells,was co-incubated with PPAR-α ligand fenofibrate and palmitate.MTT viability assay and flow cytometry were used to analyze the effect of fenofibrate on FFA induced impairment of islet microvascular endothelial cells.The concentrations for NO,SOD and MDA in the culture solution were tested by ultraviolet spectrophotometry.Results MS-1 growth rates of the control group,FFA group and fenofibrate intervention group were (100.0±0.7)%,(16.2±0.8)% and (26.8±0.8)% respectively,and the difference was statistically significant (P ＜ 0.001);MS-1 apoptotic rates of the three groups were (4.80±2.07) %,(26.31±1.78) % and (19.20±1.90) % respectively,and the difference was statistically significant (P＜0.001);NO concentrations were (6.61±0.65),(2.48±0.62),(4.11±0.33) μmol/L respectively,and the difference was statistically significant (P ＜0.001);SOD level of each group was (20.29±1.10),(15.10±0.40) and (16.46±0.73) U/ml respectively,and the difference was statistically significant (P＜0.001);MDA levels were (4.44±0.98),(8.26±0.85) and (5.56±0.91)μmol/L respectively,and the difference was statistically significant (P ＜0.001).Conclusions FFA can mediate/distinctive lipotoxcity and oxidative stress to islet microvascular endothelial cells,and application of PPAR-α ligands may be valuable in protecting islet microvascular endothelial cells from FFA cytotoxicity.