【摘要】 目的探讨分化型胚胎软骨发育基因1(differentiation type embryonic cartilage development genes 1,DEC1)、肝X受体β(Liver X receptorβ,LXRβ)在动脉硬化性脑梗死患者血清中的水平及其临床意义。方法选择2013年3月~2015年12月本院的60例急性脑梗死患者为研究对象,选择2013年3月~2015年12月健康人群60例为对照组,检测入组对象血清DEC1、LXRβ水平。结果脑梗死组血清DEC1水平高于对照组(P<0.01),脑梗死组血清LXRβ水平低于对照组(P<0.01)。随着脑梗死患者病情的加重,血清DEC1水平呈不断升高趋势(P<0.05);随着患者功能障碍程度的加重,血清DEC1水平不断升高(P<0.05)。随着急性脑梗死患者脑梗死病情的加重,血清LXRβ水平不断降低(P<0.05);随着急性脑梗死患者功能障碍程度的加重,血清LXRβ水平不断降低(P<0.05)。急性脑梗死患者血清DEC1水平与LXRβ水平呈负相关(r=-0.331,P=0.009)。结论 DEC1、LXRβ可能参与了急性脑梗死的发病及病情进展,且DEC1可能通过负向调控LXRβ进而在急性脑梗死发病、病情加重、功能障碍程度加重过程中发挥作用。更多还原

【Abstract】 Objective To detect the expression of serum differentiation type embryonic cartilage development genes 1(DEC1)and liver X receptor β(LXRβ)in atherosclerotic cerebral infarction,and explore its clinical significance.Methods 60 patients with acute cerebral infarction from March2011 to December 2015 in our hospital were selected as the research object,and 60 healthy people from March 2013 to December 2015 were selected as control group.The concentration of serum DEC1 and LXRβ in all cases was detected.Results The serum level of DEC1 in acute stroke group was significantly higher than in the control group(P<0.01).The serum level of LXRβ in the acute stroke group was significantly lower than in the control group(P<0.01).With the deterioration of patients’ condition,the serum level of DEC1 was rising(P<0.05).When the patients’ dysfunction was aggravating,the serum level of DEC1 was rising(P<0.05).With the deterioration of patients’ condition,the serum level of LXRβ trended to decrease(P <0.05).As the patients’ dysfunction was aggravating,the serum level of LXRβ trended to decrease(P<0.05).The serum level of DEC1 in patients with acute stroke had a negative correlation with that of LXRβ(r=-0.331,P=0.009).Conclusion DEC1 and LXRβ are involved in the onset of acute cerebral infarction and its progression.DEC1 plays a role in the pathogenesis of acute cerebral infarction,its deteriorating process and the aggravation of patients’ dysfunction through negatively regulating LXRβ.更多还原