CAJ | 학술논문

目的：检测哮喘大鼠海马组织褪黑素受体1(melatonin receptor 1,MT1)的表达及血清褪黑素的水平,并探讨其在哮喘发生、发展过程中的作用机制。方法60只健康SD大鼠按随机原则分为对照组(20只)、哮喘组(40只)。通过卵清蛋白( OVA)致敏、激发建立哮喘大鼠模型,采用免疫组织化学、逆转录PCR及蛋白免疫印迹技术,检测不同时期哮喘组及对照组大鼠海马组织MT1的表达,并通过ELISA方法检测血清褪黑素水平的变化。结果与对照组比较,哮喘组大鼠海马组织MT1基因和蛋白表达水平均增加(P<0.05),而血清褪黑素水平降低,差异有统计学意义( P<0.05)。在哮喘组中,与哮喘d 5及d 10比较,d 17大鼠海马组织MT1表达增加(P<0.05),而哮喘组d 5与d 10间差异无显著性(P>0.05)。结论褪黑素及MT1可能参与哮喘的发病机制。在哮喘的发生、发展中,大鼠海马组织MT1的表达上调呈时间依赖性,可能是机体应对血清褪黑素水平降低的一种适应性代偿,在哮喘炎症反应和免疫应激过程中发挥神经保护和神经免疫调节作用。
목적：검측효천대서해마조직퇴흑소수체1(melatonin receptor 1,MT1)적표체급혈청퇴흑소적수평,병탐토기재효천발생、발전과정중적작용궤제。방법60지건강SD대서안수궤원칙분위대조조(20지)、효천조(40지)。통과란청단백( OVA)치민、격발건립효천대서모형,채용면역조직화학、역전록PCR급단백면역인적기술,검측불동시기효천조급대조조대서해마조직MT1적표체,병통과ELISA방법검측혈청퇴흑소수평적변화。결과여대조조비교,효천조대서해마조직MT1기인화단백표체수평균증가(P<0.05),이혈청퇴흑소수평강저,차이유통계학의의( P<0.05)。재효천조중,여효천d 5급d 10비교,d 17대서해마조직MT1표체증가(P<0.05),이효천조d 5여d 10간차이무현저성(P>0.05)。결론퇴흑소급MT1가능삼여효천적발병궤제。재효천적발생、발전중,대서해마조직MT1적표체상조정시간의뢰성,가능시궤체응대혈청퇴흑소수평강저적일충괄응성대상,재효천염증반응화면역응격과정중발휘신경보호화신경면역조절작용。
Aim ToinvestigatetheexpressionofMT1 in the hippocampus and serum melatonin in the asth-matic rats, and explore the mechanism in the develop-mentofasthma.Methods SixtyadultSDratswere randomly divided into two groups: control group ( n=20 ) and asthma group ( n=40 ) . Asthma rat model was established by sensitization and stimulation with ovalbumin ( OVA ) . Immunohistochemistry, Western blot, and reverse transcription PCR ( RT-PCR ) were used to evaluate the expression of MT1 in hippocam-pus. Enzyme linked immunosorbent assay ( ELISA ) was used to detect serum melatonin level. Results TheexpressionofMT1inhippocampusatgeneand protein levels were significantly elevated in asthmatic group ( P <0. 05 ) compared with the control group,whereas serum melatonin was obviously reduced ( P<0. 05 ) . Compared with day 5 and day 10 in the asth-matic group, there was a significant increase of MT1 in hippocampus on day 17 ( P<0. 05 ) , while there was no significant difference between day 5 and day 10 ( P>0.05).Conclusions MelatoninandMT1maybe involved in the pathogenesis of asthma. The up-regula-tion of MT1 in hippocampus with time-dependent pat-tern may be a compensatory response to decreased pe-ripheral melatonin levels for augmenting melatoninˊs neuroprotective and neuroimmunomodulatory effects a-gainst inflammatory reaction and stress in asthma.