二手煙暴露加乘誘發衰老大鼠心肌病變機制

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题名:	二手煙暴露加乘誘發衰老大鼠心肌病變機制 Mechanisms of cardiomyopathy induced by second-hand smoke exposure in the aging rat hearts
作者:	吳嘉平;Jia-Ping Wu
贡献者:	基礎醫學研究所博士班
关键词:	老化;二手煙暴露;左心室肥厚;aging;secondhand smoke exposure;LV hypertrophy
日期:	2015-07-25
上传时间:	2015-11-04 16:59:52 (UTC+8)
出版者:	中國醫藥大學
摘要:	為了要確定衰老大鼠暴露於二手煙暴露醞釀改變左室重構的相關生物分子訊息途徑，是否由於年齡或疾病的變化相關。在本篇研究我們將大鼠分為兩個不同年齡組，包括年輕男性和老年男性大鼠。年輕男性和老年男性大鼠再區分為兩個亞組誘導4週二手煙暴露。分組如下：控制組（C），不暴露於二手煙香煙。吸二手煙組（S），暴露於香煙二手煙。將大鼠放置在整個個體密閉接觸室並暴露於10支香煙。過濾後的空氣被引入到所述密室並以較低的速率引入。大鼠暴露於香煙煙霧中30分鐘，每天兩次，5天/週，持續 1個月。 4週後二手煙暴露，年輕和老年男性大鼠進行形態學研究與免疫組織染色及左室重構相關者印跡蛋白質分析。從心臟超音波結果分析，我們發現EF （％）和FS （％）已於2週二手煙暴露已有減少於老年心臟，在4週的二手煙接觸時，可見二手煙暴露於老年心臟，心臟功能失常增加。同時，比較左心室腔室壁厚度。 LVID，LVPW和IVS分別在收縮期和舒張其直徑增加二手煙暴露。從免疫組織染色結果中得知，在老年和老年暴露二手煙左心室排列紊亂，並具有左心室肌纖維。此外，細胞生存信號傳導路徑（IGF-I -PI3K-Akt ）的下調和細胞凋亡信號傳導路徑表達的上調（FAS -L- FAS- FADD -caspase 8）在老老鼠暴露二手煙被Western blot所檢測。線粒體標的蛋白，t-bid，bid，cytochrome c和bad/bcl 2的比例在老年和老年二手煙暴露均增加。此外，caspase 9和caspase 3在老年和老年的二手煙暴露均與年齡增加。通過Western blot檢測心臟肥大相關蛋白，calcineurin/NFATc4， MEK1/ERK1/2，MEK5/ERK5，和JAK / STAT信號通路蛋白的表達水平。Calcineurin/NFATc4， MEK5/ERK5， MEK1/ERK1/2和JAK/STAT3信號通路是在老年增加，但也可見於二手煙暴露在老年，但在年輕的時候二手煙暴露沒有發現。我們認為，老齡化引起的左心室肥厚是通過calcineurin/NFATc4， MEK5/ERK5， MEK1/ERK1/2和JAK / STAT信號通路。 To determine the aging rat exposure to secondhand smoke exposure engenders changes to left ventricular remodeling due to the age- or disease-dependent alterations. Rats were divided into two age groups, young adult and old male which were divided into two subgroups and treated for 4 weeks secondhand smoke exposure as follows: control (C), not exposed to cigarette SHS. Secondhand smokers (S), exposed to cigarette SHS. The rats were placed in whole-body exposure chambers and exposed to 10 cigarettes. Filtered air was introduced into the chamber at a low rate. Rats were exposed to cigarette smoke for 30 min, twice a day, 5 days/week for 1 month. After 4 weeks secondhand smoke exposure, rats underwent morphological study with trichome stain and left ventricular remodeling related protein analysis by western blot. From echocardiography results, we found EF (%) and FS (%) were decreased in SHS exposure more than in old age heart on 4 weeks, however, in young age exposure to SHS was increased on 4 weeks compared with 2 weeks. LVID, LVPW and IVS were increased in systolic diameters in SHS exposure, but not in diastolic diameters. In addition, downregulation of survival signaling pathway (IGF-I-IGFIR-p-PI3K-p-Akt) and upregulation of apoptosis signaling pathway (TNFα-Fas-L-Fas-FADD-cleaved caspase 8) in SHS exposure were respresented by Western blot. Mitochondrial protein, t-Bid, Bid, cytochrome c and Bad/Bcl 2 ratio were increased in old age and old SHS exposure. Furthermore, caspase 9 and caspase 3 were increased in both young and old exposure to SHS and age rats. Protein expression levels of calcineurin/NFATc4, MEK1/ERK1/2, MEK5/ERK5, and JAK/STAT signaling pathways were detected by Western Blot. Results showed that in old age left ventricular (LV) mass was increased, left ventricular muscle fiber arrangment was disorder. Calcineurin/NFATc4, MEK5/ERK5, MEK1/ERK1/2 and JAK/STAT3 signaling pathways were increased in old age (MOC), but also found in SHS exposure in old age, but not found in young age exposure to SHS. We suggested that ageing induced LV hypertrophy was through calcineurin/NFATc4, MEK5/ERK5, MEK1/ERK1/2 and JAK/STAT signaling pathways.
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