富氢生理盐水对缺血再灌注皮瓣核因子-κB、α肿瘤坏死因子及细胞凋亡的影响  

Effect of hydrogen-rich saline on TNF-α, NF-κB and apoptosis in skin flap after ischemia/reperfusion injury

作　　者：赵岭[1] 王友彬[2] 覃仕瑞[1] 马雪梅[1] 

机构地区：[1]北京工业大学生命学院,100022 [2]北京协和医院

出　　处：《中华医学美学美容杂志》2013年第2期130-133,共4页Chinese Journal of Medical Aesthetics and Cosmetology

基　　金：基金项目：北京市自然科学基金资助项目（编号：7132169）

摘　　要：目的探讨富氢生理盐水（hydrogen-rich saline，HRS）腹腔注射对缺血再灌注皮瓣细胞凋亡的影响及其机制。方法18只雄性SD大鼠随机分为3组，分别为实验组、对照组1和对照组2。每只大鼠进行麻醉后，以右侧腹壁下浅动脉为蒂，形成约宽6cm、长9cm的腹部皮瓣。显做血管夹阻断皮瓣供血3h，恢复供血前10min实验组大鼠腹腔注射HRS，对照组1和对照组2注射普通生理盐水；对照组2进行手术，但不夹闭血管。术后5d处死大鼠，取皮瓣组织用末端脱氧核苷酸转移酶介导的d-UTP缺口末端标记技术（TUNEL）染色观察皮瓣中细胞凋亡状况，酶联免疫法（ELISA）测定组织α肿瘤坏死因子（TNF-α）表达水平、Western印迹法测定核因子-κB（nuclear factor -κB，NF-κB）水平。结果实验组中凋亡阳性指数为（39．72±8．09）％，与对照组1凋亡指数（69．43±13．27）％相比明显降低；TNF-α表达水平分别为实验组（269．136±24．530）pg／ml、对照组1（516．408±38．674）pg／ml，表达水平明显降低；实验组NF-κB表达低于对照组1。对照组2由于没有夹闭血管，末见明显细胞凋亡情况，TNF-α及NF-κB表达无明显升高。结论HRS可有效抑制皮瓣缺血再灌注损伤引起的细胞凋亡，其作用机制可能与分子氢对NF-κB和TNF—α的抑制有关。Objective To study the protemive effect of hydrogen rich saline （HRS） on apoptosis in skin flap after ischemia/reperfusion injury. Methods Total 18 Sprague-Dawley rats were randomly divided into three groups： a HRS treated group and two physiological saline treated groups （controls 1, 2）. The rats were anesthetized and an extended abdominal skin flap （6 cm × 9 cm） was elevated in each animal, lschemia was induced by clamping the left right pedicle for 3 h, then HRS was administered intraperitoneally 10 min before reperfusion, and physiological saline was injected in control groups 1 and 2. In the control group 2, the flaps were elevated without occluding the artery and vein. Five days postoperation, apoptosis, TNF -α level in flap were measured with EI.ISA, NF -κB in nucleus was determined by Western blot. Results Apoptotic rate represented （39. 72±8. 09） in HRS group and （69,43±13.27） % in control group 1, respectively. Treatment with HRSresuited in a marked reduction in apoptotic rate. TNF-α level was （516.408±38. 674） pg/ml in the control group 1, a significant reduced TNF-α was measured in HRS group, accounting for （269. 136 ± 24. 530） pg/ml. Moreover, NF-κB activation was significantly down regulated by HRS. In control group 2, no significant apoptosis was observed because of non-blood occlusion, and there was no marked elevation of TNF-α and NF-κB. Conclusions HRS can protect skin from ischemia/reperfusion injury, attenuate apoptosis in flaps, which may be associated with the inhibition of TNF -α and NF kb elevation.

关 键 词：富氢生理盐水 皮瓣 凋亡 核因子 Α肿瘤坏死因子 

分 类 号：R285.5[医药卫生—中药学]