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北京市自然科学基金(7132169)

作品数:3 被引量:18H指数:2
相关作者:马雪梅王友彬刘艺芳张明子赵岭更多>>
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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被引量:2
2013年
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。
赵岭王友彬覃仕瑞马雪梅
关键词:皮瓣核因子Α肿瘤坏死因子
JNK激酶抑制剂SP600125对大鼠皮瓣缺血再灌注损伤的保护作用被引量:4
2016年
目的探讨SP600125对SD大鼠腹部皮瓣缺血再灌注损伤的保护作用及其机制。方法雄性SD大鼠36只随机分为3组,假手术组(SH组),缺血再灌注/注射SP600125组(I/R-SP组)和缺血再灌注/注射DMSO溶液组(I/R-D组),每组12只,后两组大鼠通过夹闭左腹腹壁下浅动脉3 h后恢复血流供给制备腹部皮瓣缺血再灌注模型。血流恢复24 h,每组随机挑选6只大鼠进行免疫组化检测,比较p JNK、Bcl-2和Bax蛋白的表达水平;血流恢复72 h,采用激光多普勒血流灌注成像仪检测各组剩余(6只)大鼠皮瓣的血流灌注情况,并通过HE染色和TUNEL染色观察组织学变化和细胞的早期凋亡。结果免疫组化结果显示,与I/R-D组相比,I/R-SP组p JNK,Bax蛋白表达水平显著降低,Bcl-2表达水平显著增高;皮瓣血流灌注情况显示,I/R-SP组成活率及血流灌注量均显著高于I/R-D组,差异有统计学意义(P<0.01);皮瓣组织细胞凋亡率,I/R-SP组显著低于I/R-D组(P<0.01)。结论 SP600125可能通过抑制JNK通路,减少细胞凋亡,从而缓解皮瓣缺血再灌注损伤。
刘艺芳张明子王友彬马雪梅
关键词:皮瓣缺血再灌注损伤SP600125
Protective effect of hydrogen-rich saline on ischemia/reperfusion injury in rat skin flap被引量:13
2013年
Objective: Skin damage induced by ischemia/reperfusion (I/R) is a multifactorial process that often occurs in plastic surgery. The mechanisms of I/R injury include hypoxia, inflammation, and oxidative damage. Hydrogen gas has been reported to alleviate cerebral I/R injury by acting as a free radical scavenger. Here, we assessed the protective effect of hydrogen-rich saline (HRS) on skin flap I/R injury. Methods: Abdominal skin flaps of rats were elevated and ischemia was induced for 3 h; subsequently, HRS or physiological saline was administered intraperitoneally 10 min before reperfusion. On postoperative Day 5, flap survival, blood perfusion, the accumulation of reactive oxygen species (ROS), and levels of cytokines were evaluated. Histological examinations were performed to assess inflammatory cell infiltration. Results: Skin flap survival and blood flow perfusion were improved by HRS relative to the controls. The production of malondialdehyde (MDA), an indicator of lipid peroxidation, was markedly reduced. A multiplex cytokine assay revealed that HRS reduced the elevation in the levels of inflammatory cytokines, chemokines and growth factors, with the exception of RANTES (regulated on activation, normal T-cell expressed and secreted) growth factor. HRS treatment also reduced inflammatory cell infiltration induced by I/R injury. Conclusions: Our findings suggest that HRS mitigates I/R injury by decreasing inflammation and, therefore, has the potential for application as a therapy for improving skin flap survival.
Ling ZHAOYou-bin WANGShi-rui QINXue-mei MAXue-jun SUNMing-lian WANGRu-gang ZHONG
关键词:ISCHEMIA/REPERFUSION
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