军事医学
軍事醫學
군사의학
Military Medical Sciences
2015年
10期
759-764
,共6页
崔海洋%孙文武%王忠华%曹建平%马壮
崔海洋%孫文武%王忠華%曹建平%馬壯
최해양%손문무%왕충화%조건평%마장
冷空气%TRPA1%炎性因子%肺脏%大鼠
冷空氣%TRPA1%炎性因子%肺髒%大鼠
랭공기%TRPA1%염성인자%폐장%대서
cold air%TRPA1%inflammatory cytokine%lung%rat
目的:探讨短时间内反复冷空气吸入刺激对活体动物肺内瞬时受体电位锚蛋白1( TRPA1)相关炎性因子的影响。方法雄性Wistar大鼠20只,随机分为对照组、冷空气吸入组、暖空气吸入组和激动剂刺激组,每组5只。冷空气吸入组在麻醉后经口气管插管,接气体温度可控吸入装置,吸入(2±1)℃冷空气;暖空气吸入组予以相同处置下吸入(36±1)℃暖空气,每组均处置3次,1 h/次,两次间隔12 h;激动剂刺激组为室温(24±2)℃情况下雾化吸入60 mmol/L丙烯醛,分3次,1 h/次,两次间隔12 h。在最后一次处置结束后活杀大鼠,提取气管及左上肺组织的总RNA,采用PCR方法明确肺TRPA1的表达后,观察反复短时间冷空气吸入刺激对大鼠肺内TRPA1通道相关炎症细胞炎性因子白介素1β(IL-1β)、白介素5(IL-5)、中性粒细胞趋化因子(CXCL-1/KC)mRNA表达的影响。结果 TRPA1在大鼠肺组织中有表达,短时程冷空气刺激组大鼠肺组织的IL-1β、IL-5、CXCL-1/KC mRNA的表达量均较暖空气吸入组及正常对照组升高,TRPA1通道阳性激动剂丙烯醛吸入组也出现相似结果。结论在活体动物层次上,当肺部受到短时有害低温(低于17℃)刺激后,通过TRPA1活化途径使肺内一些炎性因子表达增加。
目的:探討短時間內反複冷空氣吸入刺激對活體動物肺內瞬時受體電位錨蛋白1( TRPA1)相關炎性因子的影響。方法雄性Wistar大鼠20隻,隨機分為對照組、冷空氣吸入組、暖空氣吸入組和激動劑刺激組,每組5隻。冷空氣吸入組在痳醉後經口氣管插管,接氣體溫度可控吸入裝置,吸入(2±1)℃冷空氣;暖空氣吸入組予以相同處置下吸入(36±1)℃暖空氣,每組均處置3次,1 h/次,兩次間隔12 h;激動劑刺激組為室溫(24±2)℃情況下霧化吸入60 mmol/L丙烯醛,分3次,1 h/次,兩次間隔12 h。在最後一次處置結束後活殺大鼠,提取氣管及左上肺組織的總RNA,採用PCR方法明確肺TRPA1的錶達後,觀察反複短時間冷空氣吸入刺激對大鼠肺內TRPA1通道相關炎癥細胞炎性因子白介素1β(IL-1β)、白介素5(IL-5)、中性粒細胞趨化因子(CXCL-1/KC)mRNA錶達的影響。結果 TRPA1在大鼠肺組織中有錶達,短時程冷空氣刺激組大鼠肺組織的IL-1β、IL-5、CXCL-1/KC mRNA的錶達量均較暖空氣吸入組及正常對照組升高,TRPA1通道暘性激動劑丙烯醛吸入組也齣現相似結果。結論在活體動物層次上,噹肺部受到短時有害低溫(低于17℃)刺激後,通過TRPA1活化途徑使肺內一些炎性因子錶達增加。
목적:탐토단시간내반복랭공기흡입자격대활체동물폐내순시수체전위묘단백1( TRPA1)상관염성인자적영향。방법웅성Wistar대서20지,수궤분위대조조、랭공기흡입조、난공기흡입조화격동제자격조,매조5지。랭공기흡입조재마취후경구기관삽관,접기체온도가공흡입장치,흡입(2±1)℃랭공기;난공기흡입조여이상동처치하흡입(36±1)℃난공기,매조균처치3차,1 h/차,량차간격12 h;격동제자격조위실온(24±2)℃정황하무화흡입60 mmol/L병희철,분3차,1 h/차,량차간격12 h。재최후일차처치결속후활살대서,제취기관급좌상폐조직적총RNA,채용PCR방법명학폐TRPA1적표체후,관찰반복단시간랭공기흡입자격대대서폐내TRPA1통도상관염증세포염성인자백개소1β(IL-1β)、백개소5(IL-5)、중성립세포추화인자(CXCL-1/KC)mRNA표체적영향。결과 TRPA1재대서폐조직중유표체,단시정랭공기자격조대서폐조직적IL-1β、IL-5、CXCL-1/KC mRNA적표체량균교난공기흡입조급정상대조조승고,TRPA1통도양성격동제병희철흡입조야출현상사결과。결론재활체동물층차상,당폐부수도단시유해저온(저우17℃)자격후,통과TRPA1활화도경사폐내일사염성인자표체증가。
Objective To investigate the effect of rapid repeated cold air inhalation stimulation on cold-sensitive chan-nel transient receptor potential ankyrin 1(TRPA1) associated inflammatory cytokines in living lungs .Methods A total of 20 male Wistar rats were randomly and evenly divided into 4 groups:cold air inhalation group , warm air inhalation group , TRPA1 channel agonist inhalation group and normal group , respectively . Tracheal intubation was carried out after anesthesia in rats of cold air inhalation group , and the tubes were linked to the air temperature controlled device with the temperature controlled at ( 2 ±1 )℃.The rats of warm air inhalation group were treated in the same way as cold air inhalation group except for the temperature at (36 ±1)℃.The rats of both groups were treated for 3 times, 1 hour each time.There were 12 hour intervals between treatments .The rats of TRPA1 channel agonist inhalation group were treated with atomizing inhalation of 60 mmol/L acrolein at room temperature (24 ±2)℃for 3 times, 1 hour each time.There were 12 hour intervals between two treatments .The rats were sacrificed after the last treatment .The tracheas and left lung tissues of all rats were taken and total RNA was extracted .The mRNA expressions of TRPA1, interleukin 1 beta ( IL-1β), interleukin 5(IL-5),and neutrophil chemoattractant chemokine (CXCL-1/KC)in the rat lungs were detected by real-time quantitative PCR .Results TRPA1 was expressed in rat lung tissues .In the short term cold air inhalation group , the expressions of IL-1β,IL-5 and CXCL-1/KC mRNA in the rat lungs were higher than those of the warm air inhalation or the normal groups .Similar results were also found in the specific TRPA 1 channel positive agonist ( acrolein ) inhalation group . Conclusion In living animals, the TRPA1 channels of the lungs can be activated by short-term cold air(<17℃),which results in the increasing expression of some inflammatory cytokines in lungs .