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目的:研究放射复合伤口愈合中外周血淋巴细胞凋亡规律并探讨其与愈合延迟的关系。方法:用原位末端标记(TUNEL)方法检测细胞凋亡,碱磷酶免疫组织化学方法检测 Bax、Bcl-2蛋白表达。结果:创伤复合照射组动物白细胞数出现下降,伤后3d 降至最低,伤后5d 仍显著低于单伤组;伤后两组动物外周血淋巴细胞凋亡率均出现升高,然而在整个伤口愈合过程中,伤照组凋亡率始终高于单伤组;伤后不同时间淋巴细胞 Bax 蛋白出现升高,伤照组明显高于单伤组,而 Bcl-2呈现相反的变化趋势。结论:照射后外周血白细胞数的降低和淋巴细胞凋亡的增加是辐射延迟伤口愈合的重要原因;Bax 和 Bel-2蛋白参与了淋巴细胞凋亡的调控。
Objective: To study the rule of apoptosis of peripheral blood lymphocytes during radiation combined wound healing and to explore its relationship with the delay of healing. Methods: Apoptosis was detected by TUNEL method. The expressions of Bax and Bcl-2 protein were detected by alkaline phosphatase immunohistochemical method. Results: The number of white blood cells of trauma combined irradiation group decreased, the level of white blood cells decreased to the lowest level on the 3rd day after injury, and was significantly lower than that of the single injury group on the 5th day after injury. The apoptotic rates of peripheral blood lymphocytes in both groups increased after injury, During wound healing, the apoptotic rate of the injured group was always higher than that of the single injured group. The expression of Bax protein in the lymphocytes increased at different time points after injury. The injury group was significantly higher than the single injury group, while Bcl-2 showed the opposite trend. CONCLUSION: The decrease of peripheral leukocyte count and the increase of lymphocyte apoptosis after radiation are the important reasons of radiation delayed wound healing. Bax and Bel-2 are involved in the regulation of lymphocyte apoptosis.