 |
 |
支氣管哮喘大鼠淋巴液中淋巴細(xì)胞線粒體跨膜電位變化及地塞米松對其干預(yù)的影響
【摘要】 目的 探討哮喘大鼠淋巴液中淋巴細(xì)胞線粒體跨膜電位、Fas/FasL變化以及地塞米松干預(yù)的影響。方法 建立哮喘模型，收集激發(fā)后2、6、12、24、48 h淋巴液、血液、肺泡灌洗液(bronchoalveolar lavage fluid，BALF)中淋巴細(xì)胞，流式細(xì)胞儀(FCM)檢測淋巴細(xì)胞線粒體的跨膜電位(△·ψm)，細(xì)胞免疫組化(SABC法)檢測淋巴細(xì)胞表面Fas/FasL蛋白的表達(dá)。結(jié)果哮喘組淋巴液、血液、BALF淋巴細(xì)胞線粒體跨膜電位均較對照組和治療組峰值升高(P<0.05)，而對照組和治療組之間則無顯著性差異(P>0.05);與對照組、治療組相比較，哮喘組淋巴液和BALF中淋巴細(xì)胞表面Fas、FasL蛋白光密度明顯降低(P<0.001)，而治療組和對照組比較無顯著性差異(P>0.05)。結(jié)論 哮喘大鼠淋巴液、血液、BALF中均存在明顯的淋巴細(xì)胞早期凋亡障礙和Fas/FasL表達(dá)降低，尤其是哮喘淋巴液中淋巴細(xì)胞凋亡障礙和Fas/FasL降低程度較其血液、BALF更為明顯;地塞米松可能是通過提高哮喘Fas/FasL蛋白的表達(dá)來加速淋巴細(xì)胞凋亡而發(fā)揮治療作用。
【關(guān)鍵詞】 哮喘;淋巴液;線粒體跨膜電位(△·ψm);Fas/FasL;凋亡
Lymphocyte mitochondrial membrane potential in the lymph of bronchial asthmaticrat and the effect of dexamethasone on it
XING Chaopin1 FENG Xuebin1 SONG Xiaodong2 et al醫(yī).學(xué)全.在.線網(wǎng)站payment-defi.com
1 Depertment of Pediatric,Binzhou Medical University,Binzhou 256603;2 Experimental Conter of Binzhou Medical University
【Abstract】 Objective To observe the levels of lymphocyte mitochondrial membrane potential(△·ψm) and Fas/FasL change in lymph,and the effect of dexamethasone on it.Methods The establishment of asthma model .After the inspired collection 2 h,6 h,12 h,24 h,48 h lymph, blood, bronchoalveolar lavage fluid (BALF) of lymphocytes by flow cytometry (FCM) detection of lymphocyte mitochondria transmembrane potential (△·ψm), cell immunohistochemistry (SABC method) was used to detect cell surface Fas FasL protein expression.Results The peak of mitochondrial transmembrane potential in the asthma lymph, blood, BALF lymphocytes was lower compared with the control group and treatment group (P<0.001). There was no significant difference between the control and treatment groups (P>0.05).The Fas, FasL protein optical density on the surface of lymphocytes in the asthma lymph,BALF was obvious lower than that of the control and treatment group, and there was no significant difference between the control group and treatment group.Conclusion The early lymphocyte apoptosis obstacles and the low of Fas / FasL expression were found in asthma rat in lymph,blood and BALF. Particularly, the degree of T lymphocyte apoptosis obstacles and low of Fas / FasL in lymph were remarkable to the blood and BALF in asthma. Dexamethasone may enhance the cell surface through the Fas / FasL expression to accelerate the apoptosis of lymphocytes in asthma.
【Key words】 asthma, lymph,mitochondrial membrane potential，F(xiàn)as/FasL，apoptosis
支氣管哮喘(簡稱哮喘) 是臨床常見的慢性呼吸道疾病,其發(fā)病機制尚未明確[1]。諸多研究認(rèn)為T細(xì)胞增多是哮喘炎癥持續(xù)存在的關(guān)鍵環(huán)節(jié)[2]。關(guān)于哮喘時T細(xì)胞增多的機制研究目前大多集中于外周血、肺泡灌洗液(BALF)等組織，而關(guān)于哮喘淋巴液免疫狀態(tài)研究尚未見報道。本文通過檢測哮喘大鼠淋巴液中淋巴細(xì)胞線粒體跨膜電位、Fas/FasL變化，并觀察地塞米松干預(yù)的影響，探討淋巴液中淋巴細(xì)胞凋亡與哮喘之間的內(nèi)在關(guān)系。
