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目的动脉粥样硬化是一个炎性过程,探讨炎性细胞因子白细胞介素1β(IL-1β)和肿瘤坏死因子α(TNF-α)是否通过调节酰基辅酶A:胆固醇酰基转移酶1(ACAT-1)的活性,参与泡沫细胞形成,进一步探讨动脉粥样硬化形成的机制。方法在小鼠主动脉平滑肌细胞及肌源性泡沫细胞中分别加入IL-1β(10μg/L)和TNF-α(20μg/L),孵育24h,用放射性同位素标记的方法检测ACAT-1的活性。结果①与平滑肌细胞相比,泡沫细胞ACAT-1酶活性明显增加[(84.8±16.7)比平滑肌细胞(48.5±12.5)nkat/g,P<0.05]。②TNF-α对平滑肌细胞和平滑肌源性泡沫细胞中ACAT-1酶活性无影响(P>0.05)。③IL-1β干预后,肌源性泡沫细胞中ACAT-1酶活性由(84.8±16.7)提高到(138.3±4.7)nkat/g(P<0.05)。结论IL-1β增加ACAT-1酶活性,促使胆固醇的酯化和胆固醇的沉积,参与动脉粥样硬化的形成和发展。
Atherosclerosis is an inflammatory process that explores whether interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) are regulated by the modulation of acyl-coenzyme A: cholesterol acyltransferase 1 (ACAT- 1) activity, participate in the formation of foam cells, to further explore the mechanism of atherosclerosis. Methods IL-1β (10μg / L) and TNF-α (20μg / L) were respectively added into mouse aortic smooth muscle cells and myogenic foam cells and incubated for 24 hours. The activity of ACAT-1 was detected by radioisotope labeling . Results ① Compared with smooth muscle cells, ACAT-1 activity of foam cells increased significantly ([84.8 ± 16.7] nkat / g, P <0.05] compared with smooth muscle cells (48.5 ± 12.5). ②TNF-α had no effect on the activity of ACAT-1 in smooth muscle cells and smooth muscle-derived foam cells (P> 0.05). ③ The activity of ACAT-1 in myogenic foam cells increased from (84.8 ± 16.7) to (138.3 ± 4.7) nkat / g after IL-1β intervention (P <0.05). Conclusion IL-1β can increase the activity of ACAT-1, promote the esterification of cholesterol and the deposition of cholesterol, and participate in the formation and development of atherosclerosis.