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醫(yī)學(xué)免費(fèi)論文:基質(zhì)金屬蛋白酶9在哮喘大鼠中性粒細(xì)胞中的表達(dá)

來(lái)源:本站原創(chuàng) 更新:2013-10-9 論文投稿平臺(tái)

醫(yī)學(xué)免費(fèi)論文:基質(zhì)金屬蛋白酶9在哮喘大鼠中性粒細(xì)胞中的表達(dá)

【摘要】  目的:觀察基質(zhì)金屬蛋白酶9(MMP-9)在哮喘大鼠血中性粒細(xì)胞(PMN)中的表達(dá),探討PMN能否通過(guò)合成MMP-9參與哮喘的發(fā)病。方法:健康雄性SD大鼠30只,隨機(jī)分成哮喘組(A組)、布地奈德治療組(B組)和正常對(duì)照組(C組),用卵蛋白(OVA)致敏和激發(fā)的方法建立哮喘模型。分離純化血PMN,免疫細(xì)胞化學(xué)法檢測(cè)MMP-9的表達(dá)水平,ELISA法檢測(cè)血清基質(zhì)金屬蛋白酶抑制劑-1(TIMP-1)的濃度。結(jié)果:A組(0.196±0.011,OD值)PMN MMP-9的表達(dá)水平顯著高于C組(0.100±0.010,OD值)(P <0.01),B組(0.135±0.008,OD值)PMN MMP-9的表達(dá)水平顯著低于A組但高于C組(均P <0.01)。A組血清TIMP-1為(34.96±4.54 )ng/mL,表達(dá)水平顯著高于C組的(26.14±3.43) ng/mL(P <0.01),B組血清TIMP-1的表達(dá)水平顯著低于A組但高于C組(P <0.05或P <0.01)。MMP-9與TIMP-1的表達(dá)水平呈顯著正相關(guān)(n =29,r=0.713,P <0.01)。結(jié)論:哮喘大鼠PMN合成MMP-9的功能增加,PMN可能部分通過(guò)增加合成MMP-9參與哮喘的發(fā)病,這種功能可以部分被布地奈德所抑制。

【關(guān)鍵詞】  哮喘;MMP-9;TIMP-1;PMN;大鼠

Expressions of matrix metalloproteinase-9 in blood polymorphonuclear leucocyte of asthmatic rats  JING Wei-ying^,YE Hui,TONG  Xia-sheng,WANG En-zhi,GUO Hai-yuan,RUAN Zheng-ying,JING Xiao-hong.^Department of Pediatrics,Taizhou Integrated Traditional and Western Medicine Hospital,Taizhou, 317523醫(yī).學(xué)全.在.線m.payment-defi.com

Abstract:  Objective: To observe the expressions of matrix metalloproteinase-9 (MMP-9) in blood polymorphonuclear leukocyte (PMN) of asthmatic rats. And to approach whether PMN could participate in asthma pathogenesis through synthesizing MMP-9. Methods :Thirty rats were randomly divided into three groups on average, including asthmatic group (group A), budesonide treated group (group B) and control group (group C). Blood PMN were isolated and purified. The expressions of MMP-9 were detected with immunocytochemical method in blood PMN. The concentration of matrix metallo-proteinase inhibitor-1 (TIMP-1) was detected with ELISA. Results :The level of MMP-9 in group A (0.196±0.011,Optical density) were significantly higher than those in group C (0.100±0.010)(P <0.01). Levels of MMP-9 in group B (0.135±0.008) were significantly lower than those in group A, but higher than those in group C (all P <0.01). Levels of TIMP-1 in group A (34.96±4.54 ng/mL) were significantly higher than those in group C(26.14±3.43 ng/mL)(P <0.01). Levels of TIMP-1 in group B (29.58±2.41 ng/mL) were significantly lower than those in group A, but higher than those in group C (P <0.05 or P <0.01). There was significant positive correlation between the level of MMP-9 and TIMP-1(n =29,r =0.713,P <0.01). Conclusion:Levels of MMP-9 synthesized by PMN increase in asthma rats. PMN may be implicated with asthma pathogenesis via increasing synthesis of MMP-9,but this function of PMN can be partly inhibited by budesonide.

Key words:  asthma;matrix metalloproteinase-9;TIMP-1;polymorphonuclear leukocyte;rat

支氣管哮喘是一種由多種炎性細(xì)胞和細(xì)胞組分參與的氣道慢性炎癥,氣道重構(gòu)和氣道高反應(yīng)性是其特征性病理改變。基質(zhì)金屬蛋白酶9(matrix metalloproteinase-9,MMP-9)及其抑制劑——基質(zhì)金屬蛋白酶抑制劑-1(TIMP-1),在哮喘的氣道炎癥和氣道重構(gòu)中起著重要作用[1]。最近研究發(fā)現(xiàn),中性粒細(xì)胞(PMN)能釋放多種酶、炎癥遞質(zhì)和細(xì)胞因子參與哮喘的炎癥過(guò)程[2],但PMN能否通過(guò)MMPs/TIMPs體系參與哮喘的發(fā)病,目前知之甚少。本實(shí)驗(yàn)通過(guò)檢測(cè)哮喘大鼠血PMN MMP-9和血清TIMP-1的表達(dá)水平,探討它們?cè)谙械目赡茏饔脵C(jī)制。


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