国际心血管病杂志
國際心血管病雜誌
국제심혈관병잡지
INTERNATIONAL JOURNAL OF CARDIOVASCULAR DISEASE
2014年
2期
120-123
,共4页
阿托伐他汀%衰老%过氧化物酶体增殖物激活物受体β/δ%肿瘤坏死因子-α
阿託伐他汀%衰老%過氧化物酶體增殖物激活物受體β/δ%腫瘤壞死因子-α
아탁벌타정%쇠로%과양화물매체증식물격활물수체β/δ%종류배사인자-α
Atorvastatin%Aging%Peroxisome proliferator activated receptorβ/δ%Tumor necrosis factor-α
目的：观察阿托伐他汀下调老年大鼠心肌肿瘤坏死因子-α（TNF-α）表达的作用及其与过氧化物酶体增殖物激活型受体β/δ（PPARβ/δ）信号通路之间的关系。方法：分离培养24个月龄大鼠的心肌细胞，将心肌细胞分为空白对照组、溶剂对照组、阿托伐他汀组、阿托伐他汀＋PPARβ/δ拮抗剂 GSK0660组。各组细胞分别加入细胞培养液、二甲基亚砜（DMSO）、阿托伐他汀、阿托伐他汀＋ GSK0660处理。用 RT-PCR 方法检测各组大鼠衰老心肌细胞的 TNF-αmRNA 表达水平，用 western blot 方法检测各组 TNF-α蛋白含量。结果：（1）与空白对照组相比，溶剂对照组大鼠衰老心肌细胞的 TNF-αmRNA 和蛋白水平均无显著差异；（2）与空白对照组相比，阿托伐他汀组的 TNF-αmRNA 和蛋白水平含量均显著降低（P ＜0．01）；（3）阿托伐他汀＋GSK0660组的 TNF-αmRNA 表达水平及蛋白含量均显著高于阿托伐他汀组，但仍低于空白对照组（P ＜0．05）。结论：阿托伐他汀可通过激活 PPARβ/δ信号通路下调衰老心肌细胞 TNF-α的表达。
目的：觀察阿託伐他汀下調老年大鼠心肌腫瘤壞死因子-α（TNF-α）錶達的作用及其與過氧化物酶體增殖物激活型受體β/δ（PPARβ/δ）信號通路之間的關繫。方法：分離培養24箇月齡大鼠的心肌細胞，將心肌細胞分為空白對照組、溶劑對照組、阿託伐他汀組、阿託伐他汀＋PPARβ/δ拮抗劑 GSK0660組。各組細胞分彆加入細胞培養液、二甲基亞砜（DMSO）、阿託伐他汀、阿託伐他汀＋ GSK0660處理。用 RT-PCR 方法檢測各組大鼠衰老心肌細胞的 TNF-αmRNA 錶達水平，用 western blot 方法檢測各組 TNF-α蛋白含量。結果：（1）與空白對照組相比，溶劑對照組大鼠衰老心肌細胞的 TNF-αmRNA 和蛋白水平均無顯著差異；（2）與空白對照組相比，阿託伐他汀組的 TNF-αmRNA 和蛋白水平含量均顯著降低（P ＜0．01）；（3）阿託伐他汀＋GSK0660組的 TNF-αmRNA 錶達水平及蛋白含量均顯著高于阿託伐他汀組，但仍低于空白對照組（P ＜0．05）。結論：阿託伐他汀可通過激活 PPARβ/δ信號通路下調衰老心肌細胞 TNF-α的錶達。
목적：관찰아탁벌타정하조노년대서심기종류배사인자-α（TNF-α）표체적작용급기여과양화물매체증식물격활형수체β/δ（PPARβ/δ）신호통로지간적관계。방법：분리배양24개월령대서적심기세포，장심기세포분위공백대조조、용제대조조、아탁벌타정조、아탁벌타정＋PPARβ/δ길항제 GSK0660조。각조세포분별가입세포배양액、이갑기아풍（DMSO）、아탁벌타정、아탁벌타정＋ GSK0660처리。용 RT-PCR 방법검측각조대서쇠로심기세포적 TNF-αmRNA 표체수평，용 western blot 방법검측각조 TNF-α단백함량。결과：（1）여공백대조조상비，용제대조조대서쇠로심기세포적 TNF-αmRNA 화단백수평균무현저차이；（2）여공백대조조상비，아탁벌타정조적 TNF-αmRNA 화단백수평함량균현저강저（P ＜0．01）；（3）아탁벌타정＋GSK0660조적 TNF-αmRNA 표체수평급단백함량균현저고우아탁벌타정조，단잉저우공백대조조（P ＜0．05）。결론：아탁벌타정가통과격활 PPARβ/δ신호통로하조쇠로심기세포 TNF-α적표체。
Objective:To investigate the effects of atorvastatin on tumor necrosis factor-α(TNF-α) expression in aging cardiomyocytes and the role of peroxisome proliferator activated receptor β/δ(PPARβ/δ)signal pathway. Methods:Senescent cardiomyocytes obtained from aging rats of 24 months old were randomly divided into control group,DMSO group,atorvastatin group and atorvastatin +GSK0660 group,which were treated by cell culture medium,DMSO,atorvastatin,atorvastatin +GSK0660,respectively.The mRNA levels of TNF-α were evaluated by RT-PCR,and the protein contents of TNF-αwere detected by western blot. Results:(1)There were no differences in the mRNA and protein levels of TNF-αbetween control group and DMSO group (P >0.05);(2)The mRNA and protein levels of TNF-αin atorvastatin group were significantly lower than those in control group (P <0.01 );(3)Both mRNA and protein expression of TNF-αin atorvastatin + GSK0660 group were higher than those in atorvastatin group (P <0.05 or P <0.01),but were lower than those in control group (P<0.05). Conclusion:Atorvastatin can down-regulate TNF-αexpression in senescent cardiomyocytes by activating PPARβ/δsignal pathway.
