CAJ | 학술논문

目的：研究MAPK信号通路在肺炎衣原体(CP)感染APOE基因敲除(APOE)小鼠促进动脉粥样硬化形成中的作用。方法48只APOE小鼠分为感染-高脂组、高脂组、感染组和对照组，每组12只，喂养20周，采用West-ern blot和Real time-PCR法检测胞外信号调控激酶(p-ERK1/2)、p-P38的蛋白表达和白介素-6(IL-6)、肿瘤坏死因子(TNF-α)的基因的表达。结果感染-高脂组、高脂组、感染组APOE小鼠的主动脉IL-6和TNF-α水平明显高于对照组(P<0.05)。与对照组比较，感染-高脂组、高脂组、感染组p-ERK1/2、p-P38蛋白表达的水平显著降低(P<0.05)。结论 CP感染激发和加重动脉内炎性反应可促进动脉粥样硬化，MAPK信号通路是CP促进动脉粥样硬化的潜在机制。
목적：연구MAPK신호통로재폐염의원체(CP)감염APOE기인고제(APOE)소서촉진동맥죽양경화형성중적작용。방법48지APOE소서분위감염-고지조、고지조、감염조화대조조，매조12지，위양20주，채용West-ern blot화Real time-PCR법검측포외신호조공격매(p-ERK1/2)、p-P38적단백표체화백개소-6(IL-6)、종류배사인자(TNF-α)적기인적표체。결과감염-고지조、고지조、감염조APOE소서적주동맥IL-6화TNF-α수평명현고우대조조(P<0.05)。여대조조비교，감염-고지조、고지조、감염조p-ERK1/2、p-P38단백표체적수평현저강저(P<0.05)。결론 CP감염격발화가중동맥내염성반응가촉진동맥죽양경화，MAPK신호통로시CP촉진동맥죽양경화적잠재궤제。
Objective To investigate the role of MAPK in APOE mice induced atherosclerosis (AS) by chlamydia pneu-moniae (CP) infection. Methods Forty-eight APOE mice were divided into four groups including CP infection and hy-perlipidemia group, hyperlipidemia group, CP infection group and control group, each group had 12 mice. The mice were sacrificed at 20 week of age. Western blot and Real time-PCR were used to detect the p-ERK1/2, p-P38 protein expression and the gene expression of IL-6, TNF-α. Results The levels of IL-6 and TNF-α in CP infection and hy-perlipidemia group, hyperlipidemia group, CP infection group were significantly higher than those in control group, the differences were statistically significant (P< 0.05). Compared with the control group, the levels of p-ERK1/2, p-P38 protein expression in CP infection and hyperlipidemia group, hyperlipidemia group, CP infection group significantly re-duced, with statistically significant differences (P< 0.05). Conclusion Infection with CP may contribute to AS by the initiation and progression of the inflammatory reaction within the artery. MAPK is a potential mechanism of CP induced AS.