CAJ | 학술논문

目的观察阻塞性睡眠呼吸暂停综合征(OSA)患者内源性大麻素系统(ECS)合成及降解酶的变化.方法对2009年7月至12月在山西医科大学第二医院睡眠中心就诊的患者行整夜多导睡眠监测(PSG),实时PCR法检测外周血单个核细胞上花生四烯酸乙醇胺(AEA)及2-花生四烯酸甘油(2-AG)的合成及降解酶水平,了解OSA病情严重程度对其的影响.结果与正常对照组相比,OSA组ECS中两种酶N-酰基磷脂酰乙醇胺水解磷脂酶D(NAPE)、单酰基甘油脂肪酶(MAGL)的表达有差异(P＜0.05).MAGL与最长呼吸暂停时间(LA)、最低血氧饱和度(LSaO2)、微觉醒指数(MAI)存在相关(r值为0.34、-0.31和0.24,均P＜0.05).与单纯OSA组相比,合并高血压的OSA患者FAAH表达有差异(P＜0.05).结论 OSA可影响ECS合成酶及降解酶的表达,使内源性大麻素物质升高.
목적 관찰조새성수면호흡잠정종합정(OSA)환자내원성대마소계통(ECS)합성급강해매적변화.방법 대2009년7월지12월재산서의과대학제이의원수면중심취진적환자행정야다도수면감측(PSG),실시PCR법검측외주혈단개핵세포상화생사희산을순알(AEA)급2-화생사희산감유(2-AG)적합성급강해매수평,료해OSA병정엄중정도대기적영향.결과 여정상대조조상비,OSA조ECS중량충매N-선기린지선을순알수해린지매D(NAPE)、단선기감유지방매(MAGL)적표체유차이(P＜0.05).MAGL여최장호흡잠정시간(LA)、최저혈양포화도(LSaO2)、미각성지수(MAI)존재상관(r치위0.34、-0.31화0.24,균P＜0.05).여단순OSA조상비,합병고혈압적OSA환자FAAH표체유차이(P＜0.05).결론 OSA가영향ECS합성매급강해매적표체,사내원성대마소물질승고.
Objective To observe the differences of endogenous cannabinoid system(ECS) synthetic and catabolic enzyme levels between the obstructive sleep apnea syndrome(OSA)patients and the control subjects.Methods Patients with OSA confirmed by PSG in our Sleep Center were randomly recruited from July to December,2009.Peripheral blood was obtained to isolate mononuclear cells and the mRNA levels of anandamide(AEA)synthase N-acylphosphatidylethanolamine hydrolyzing phospholipase D (NAPE),fatty acid amide hydmlase(FAAH)and 2-arachidonoylg lycerol(2-AG)synthase diacylglycerol lipase(DAGL)and hydrolase monoacyiglycerol lipase(MAGL)were measured by real-time polymerase chain reaction.The association between the severity of OSA and the enzyme levels were explored.Results There Was a significant difference in beth the NAPE and MAGL levels between patients with OSA and the control subiects.The level of MAGL Was related to some indices of severity of OSA,including the longest apnea time,lowest blood oxygen saturation and the micro-arousal index(r=0.31,0.24,0.34,respectively.all P＜0.05).Compared with patients with OSA alone,patients with OSA complicated by hypertension showed a different level of FAAH(P＜0.05).Conclusion OSA altered the expression of the ECS synthetic and catabolic enzymes,leading to an increase in endogenous cannabinoid substances.