本文選題：細(xì)胞凋亡 + 缺氧��； 參考：《重慶醫(yī)學(xué)》2017年26期

【摘要】：目的探討色素上皮衍生因子(PEDF)對H9C2心肌細(xì)胞在低氧無血清條件下的保護作用及其可能的機制。方法體外培養(yǎng)H9C2細(xì)胞進行低氧無血清處理,將細(xì)胞分為對照組(H9C2)、缺氧組(缺氧+H9C2)、PEDF組(缺氧+H9C2+PEDF)、殘粒體分裂抑制劑(Medivi-1)組(缺氧+H9C2+Mdivi-1)。TUNEL染色檢測H9C2心肌細(xì)胞凋亡率;Western blot檢測動力相關(guān)蛋白1(Drp1)、活化半胱天冬酶-3(Cleaved-Caspase3)的蛋白水平;電鏡及MitoTracker Red檢測線粒體形態(tài);采用線粒體膜電位檢測試劑盒(JC-1)檢測線粒體膜電位,MitoSOXTM檢測線粒體活性氧簇(ROS)水平。結(jié)果缺氧誘導(dǎo)H9C2細(xì)胞線粒體分裂,缺氧組(6h)與對照組比較差異有統(tǒng)計學(xué)意義(P0.05),PEDF減少缺氧條件下線粒體分裂,PEDF組與缺氧組(6h)比較差異有統(tǒng)計學(xué)意義(P0.05),PEDF和Mdivi-1可以減少缺氧條件下(24h)細(xì)胞凋亡,與缺氧組(24h)比較差異有統(tǒng)計學(xué)意義(P0.05)。結(jié)論 PEDF通過抑制缺氧條件下H9C2細(xì)胞線粒體分裂減少細(xì)胞凋亡。
[Abstract]:Objective to investigate the protective effect of pigment epithelium-derived factor (PEDF) on H9C2 cardiomyocytes under hypoxic and serum-free conditions and its possible mechanism. Methods H9C2 cells cultured in vitro were treated with hypoxia and serum free. The cells were divided into two groups: control group (H9C2P), hypoxia group (hypoxia H9C2P2PEDF group) group (hypoxia H9C2 PEDF group, residual granulocyte mitosis inhibitor medivi-1 group) group (H9C2 cardiomyocyte apoptosis rate was detected by anoxic H9C2 Mdivi-1).TUNEL staining and H9C2 cardiomyocyte apoptosis rate was detected by Western blot to detect the protein level of dynamic-associated protein 1, activated cysteone asparagase -3Cvelead-Caspase3). The mitochondrial morphology was detected by electron microscope and MitoTracker Red, and the mitochondrial membrane potential (MitoSOXTM) was detected by using mitochondrial membrane potential detection kit (JC-1), and the mitochondrial reactive oxygen species (Ros) level was detected by mitochondrial membrane potential detection kit (JC-1). Results hypoxia induced mitochondrial division in H9C2 cells. There was significant difference between the hypoxia group and the control group at 6 h) the difference was statistically significant (P 0.05) PEDF could reduce the apoptosis of mitochondria mitosis in the hypoxia group and the hypoxia group at 6 h) the P0.05 Mdivi-1 and PEDF could reduce the apoptosis of the cells under hypoxia for 24 h. Compared with hypoxia group for 24 h, the difference was statistically significant (P 0.05). Conclusion PEDF reduces apoptosis by inhibiting mitochondrial mitosis in H9C2 cells under hypoxia.
【作者單位】： 徐州醫(yī)科大學(xué)附屬醫(yī)院心胸外科;徐州醫(yī)科大學(xué)生物化學(xué)與分子生物學(xué)研究中心;徐州醫(yī)科大學(xué)形態(tài)學(xué)科研實驗中心;
【基金】：國家自然科學(xué)基金資助項目(81270173) 江蘇省衛(wèi)生廳科技計劃項目青年基金(Q201407)
【分類號】：R54

【相似文獻】

相關(guān)期刊論文 前3條

1 魏峰濤;楊維巍;楊黃恬;方寧遠(yuǎn);;小分子干擾RNA抑制大鼠心肌H9C2細(xì)胞血管緊張素轉(zhuǎn)換酶2的表達[J];中華高血壓雜志;2007年07期

2 盧曉梅;金玉楠;于艷秋;;醛固酮對H9C2細(xì)胞膠原表達的影響[J];中國現(xiàn)代醫(yī)學(xué)雜志;2011年14期

3 李寶善;馬厚勛;王艷嬌;吳平;;體外轉(zhuǎn)染Klotho基因?qū)9c2(2-1)大鼠心肌細(xì)胞缺血再灌注的影響[J];中國老年學(xué)雜志;2012年05期

相關(guān)博士學(xué)位論文 前1條

1 石瑤;血紅素加氧酶-1介導(dǎo)姜黃素對抗H9c2心肌細(xì)胞氧化應(yīng)激損傷的實驗研究[D];華中科技大學(xué);2012年

相關(guān)碩士學(xué)位論文 前2條

1 張洪生;Fractalkine誘導(dǎo)H9C2心肌細(xì)胞凋亡及黃芪甲苷的干預(yù)作用[D];山東大學(xué);2017年

2 姬婷婷;卡維地洛對TLR4信號通路介導(dǎo)的H9C2心肌細(xì)胞凋亡的影響[D];安徽醫(yī)科大學(xué);2014年

，

本文編號：1965456