摘要
目的研究bcl-2、bax凋亡相关基因在低氧处理大鼠肺动脉中的表达,探讨低氧肺动脉高压的发病机制及防治措施。方法36只Wistar大鼠随机分为3组,分别为正常对照组、低氧肺动脉高压组、低浓度一氧化碳(CO)组,每组12只,采用原位细胞凋亡、原位杂交、免疫组化等方法检测肺动脉的凋亡状况。结果①原位凋亡检测示,正常对照组、低氧肺动脉高压组、低浓度CO组的凋亡率分别为8.1%,37.6%,76.5%,三者间差异显著;②原位杂交显示,正常对照组bax、bcl-2杂交呈弱阳性表达。低氧肺动脉高压组bax杂交呈弱阳性表达,低浓度CO组呈强阳性表达,但bcl-2杂交可见低氧肺动脉高压组呈强阳性表达,低浓度CO组呈弱阳性表达;③免疫组织化结果表明,低浓度CO组bcl-2、bax蛋白均有升高,以bax为著。低氧肺动脉高压组虽然也有表达,但程度较弱,且bcl-2表达处于优势。结论低浓度CO可以调节bcl-2、bax凋亡基因的表达,从而促进肺动脉组织的凋亡。
Objective To investigate the expressions of bcl-2,bax apoptosis relative genes in the pulmonary artery of hypoxic pulmonary hypertension rats,and explore its mechanism and prevention measure.Methods 36 rats were randomly divided into normal,hypoxic pulmonary hypertension and low concentration CO groups （n=12）.In situ TUNEL method,in situ hybridization and immunohistochemistry were used to detect the apoptosis of the pulmonary artery.Results The apoptosis rates of the pulmonary artery in normal,hypoxic pulmonary hypertension and low concentration CO groups were 8.1%,37.6% and 76.5% respectively.The expressions of bax protein and mRNA in low concentration CO group were significantly higher than those of normal and hypoxic pulmonary hypertension group （P0.01）.The expressions of bcl-2 protein and mRNA were not obvious in the low concentration CO group.Conclusions Low concentration of CO can regulate the expressions of bcl-2 and bax mRNA and promote the apoptosis of pulmonary artery.
出处
《中国老年学杂志》
CAS
CSCD
北大核心
2010年第6期800-802,共3页
Chinese Journal of Gerontology
基金
全军攻关课题(06G083
08G093)
国家自然科学基金(30770928)
第三军医大学校科研创新基金(2006HG04)
重庆市自然科学基金(2007BB5072)
关键词
低氧
肺动脉高压
凋亡
Hypoxia
Pulmonary hypertension
Apoptosis
