自发性高血压大鼠缺血再灌注后视网膜毛细血管细胞凋亡及p53基因表达

Objective To investigate the effect of apoptosis-related gene p53 on the apoptosis of retinal capillary cells in rats with spontaneously hypertensive (SHR) after ischemic reperfusion injury. Methods A total of 60 SHR rats were randomly divided into sham group (SHR-SH) and retinal ischemie reperfusion group (SHR-RIR), which were subdivided into 5 subgroups according to the time after RIR: 2, 6, 24, and 72 hours and 7 days, with 6 rats in each subgroup. Another 60 Wistar-Kyoto (WKY) rats were divided into the same groups as the SHR rats as the control. The RIR model was set up. The apoptosis of retinal capillary cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods and the expression of p53 was determined by streptavidin-perosidase (SP) immunohistochemistry. Results The apoptosis rate of retinal capillary cells in the 5 SHR-RIR groups was (8.64±0.56)%, (14.92±0.99)%, (24.72±2.98)%, (16.53±1.80)%, and (7.12±1.10)%,respectively. The expression of p53 in SHR-RIR groups increased at the 2nd hour after RIR, reached the peak at the 24th hour, kept the high level at the 72nd hour, and remained a little at the 7th day, which was significantly different from which in the SHR-SH groups (P<0. 01). The expression of p53 were higher in SHR-IR groups than that in the WKY-RIR groups (P<0. 01). Conclusions p53 may play a part in RIR injury by inducing or promoting apoptosis. The apoptosis of retinal capillary cells after RIR is more severe under the hypertension, and reaches the peak at the 24 hour after RIR.     

自发性高血压大鼠缺血再灌注后视网膜毛细血管细胞凋亡及p53基因表达

Objective To investigate the effect of apoptosis-related gene p53 on the apoptosis of retinal capillary cells in rats with spontaneously hypertensive (SHR) after ischemic reperfusion injury. Methods A total of 60 SHR rats were randomly divided into sham group (SHR-SH) and retinal ischemie reperfusion group (SHR-RIR), which were subdivided into 5 subgroups according to the time after RIR: 2, 6, 24, and 72 hours and 7 days, with 6 rats in each subgroup. Another 60 Wistar-Kyoto (WKY) rats were divided into the same groups as the SHR rats as the control. The RIR model was set up. The apoptosis of retinal capillary cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods and the expression of p53 was determined by streptavidin-perosidase (SP) immunohistochemistry. Results The apoptosis rate of retinal capillary cells in the 5 SHR-RIR groups was (8.64±0.56)%, (14.92±0.99)%, (24.72±2.98)%, (16.53±1.80)%, and (7.12±1.10)%,respectively. The expression of p53 in SHR-RIR groups increased at the 2nd hour after RIR, reached the peak at the 24th hour, kept the high level at the 72nd hour, and remained a little at the 7th day, which was significantly different from which in the SHR-SH groups (P<0. 01). The expression of p53 were higher in SHR-IR groups than that in the WKY-RIR groups (P<0. 01). Conclusions p53 may play a part in RIR injury by inducing or promoting apoptosis. The apoptosis of retinal capillary cells after RIR is more severe under the hypertension, and reaches the peak at the 24 hour after RIR.     

血压调控联合完全机械通气对重症颅脑损伤开颅术患者预后的影响

目的 采用血压调控联合完全机械通气治疗重症颅脑损伤开颅术后患者,观察术后脑氧摄取率(CERO₂),随访3个月内好转率与病死率。 方法 选择神经外科2013年7月-2015年6月重症颅脑损伤开颅术后患者54例,采用随机数字表法分为观察组28例和对照组26例。对照组采用ICU常规治疗;观察组采用ICU常规治疗合并血压调控及完全机械通气。比较2组患者一般情况,术前、术毕即刻、24、48、72小时CERO₂变化情况,随访3个月或终点事件(死亡)情况,比较2组预后。 结果 2组患者一般情况中,观察组呼吸机使用时间长于对照组,差异有统计学意义(P<0.05)。观察组术后24、48、72小时CERO₂较对照组降低,差异有统计学意义(P<0.05),提示该治疗方法对术后降低CERO₂有一定效果。观察组好转率53.57%,病死率3.57%;对照组好转率15.38%,病死率30.77%,观察组好转率高于对照组,病死率低于对照组,差异有统计学意义(P<0.05)。 结论 重症颅脑损伤患者开颅术后血压调控联合完全机械通气可降低CERO₂,改善患者预后。治疗过程中需要注意呼吸机相关医院感染的防治,确保治疗效果。      

自发性高血压大鼠缺血再灌注后视网膜毛细血管细胞凋亡及p53基因表达

Objective To investigate the effect of apoptosis-related gene p53 on the apoptosis of retinal capillary cells in rats with spontaneously hypertensive (SHR) after ischemic reperfusion injury. Methods A total of 60 SHR rats were randomly divided into sham group (SHR-SH) and retinal ischemie reperfusion group (SHR-RIR), which were subdivided into 5 subgroups according to the time after RIR: 2, 6, 24, and 72 hours and 7 days, with 6 rats in each subgroup. Another 60 Wistar-Kyoto (WKY) rats were divided into the same groups as the SHR rats as the control. The RIR model was set up. The apoptosis of retinal capillary cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods and the expression of p53 was determined by streptavidin-perosidase (SP) immunohistochemistry. Results The apoptosis rate of retinal capillary cells in the 5 SHR-RIR groups was (8.64±0.56)%, (14.92±0.99)%, (24.72±2.98)%, (16.53±1.80)%, and (7.12±1.10)%,respectively. The expression of p53 in SHR-RIR groups increased at the 2nd hour after RIR, reached the peak at the 24th hour, kept the high level at the 72nd hour, and remained a little at the 7th day, which was significantly different from which in the SHR-SH groups (P<0. 01). The expression of p53 were higher in SHR-IR groups than that in the WKY-RIR groups (P<0. 01). Conclusions p53 may play a part in RIR injury by inducing or promoting apoptosis. The apoptosis of retinal capillary cells after RIR is more severe under the hypertension, and reaches the peak at the 24 hour after RIR.     

自发性高血压大鼠缺血再灌注后视网膜毛细血管细胞凋亡及p53基因表达

Objective To investigate the effect of apoptosis-related gene p53 on the apoptosis of retinal capillary cells in rats with spontaneously hypertensive (SHR) after ischemic reperfusion injury. Methods A total of 60 SHR rats were randomly divided into sham group (SHR-SH) and retinal ischemie reperfusion group (SHR-RIR), which were subdivided into 5 subgroups according to the time after RIR: 2, 6, 24, and 72 hours and 7 days, with 6 rats in each subgroup. Another 60 Wistar-Kyoto (WKY) rats were divided into the same groups as the SHR rats as the control. The RIR model was set up. The apoptosis of retinal capillary cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods and the expression of p53 was determined by streptavidin-perosidase (SP) immunohistochemistry. Results The apoptosis rate of retinal capillary cells in the 5 SHR-RIR groups was (8.64±0.56)%, (14.92±0.99)%, (24.72±2.98)%, (16.53±1.80)%, and (7.12±1.10)%,respectively. The expression of p53 in SHR-RIR groups increased at the 2nd hour after RIR, reached the peak at the 24th hour, kept the high level at the 72nd hour, and remained a little at the 7th day, which was significantly different from which in the SHR-SH groups (P<0. 01). The expression of p53 were higher in SHR-IR groups than that in the WKY-RIR groups (P<0. 01). Conclusions p53 may play a part in RIR injury by inducing or promoting apoptosis. The apoptosis of retinal capillary cells after RIR is more severe under the hypertension, and reaches the peak at the 24 hour after RIR.     

自发性高血压大鼠缺血再灌注后视网膜毛细血管细胞凋亡及p53基因表达

Objective To investigate the effect of apoptosis-related gene p53 on the apoptosis of retinal capillary cells in rats with spontaneously hypertensive (SHR) after ischemic reperfusion injury. Methods A total of 60 SHR rats were randomly divided into sham group (SHR-SH) and retinal ischemie reperfusion group (SHR-RIR), which were subdivided into 5 subgroups according to the time after RIR: 2, 6, 24, and 72 hours and 7 days, with 6 rats in each subgroup. Another 60 Wistar-Kyoto (WKY) rats were divided into the same groups as the SHR rats as the control. The RIR model was set up. The apoptosis of retinal capillary cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods and the expression of p53 was determined by streptavidin-perosidase (SP) immunohistochemistry. Results The apoptosis rate of retinal capillary cells in the 5 SHR-RIR groups was (8.64±0.56)%, (14.92±0.99)%, (24.72±2.98)%, (16.53±1.80)%, and (7.12±1.10)%,respectively. The expression of p53 in SHR-RIR groups increased at the 2nd hour after RIR, reached the peak at the 24th hour, kept the high level at the 72nd hour, and remained a little at the 7th day, which was significantly different from which in the SHR-SH groups (P<0. 01). The expression of p53 were higher in SHR-IR groups than that in the WKY-RIR groups (P<0. 01). Conclusions p53 may play a part in RIR injury by inducing or promoting apoptosis. The apoptosis of retinal capillary cells after RIR is more severe under the hypertension, and reaches the peak at the 24 hour after RIR.     

自发性高血压大鼠缺血再灌注后视网膜毛细血管细胞凋亡及p53基因表达

Objective To investigate the effect of apoptosis-related gene p53 on the apoptosis of retinal capillary cells in rats with spontaneously hypertensive (SHR) after ischemic reperfusion injury. Methods A total of 60 SHR rats were randomly divided into sham group (SHR-SH) and retinal ischemie reperfusion group (SHR-RIR), which were subdivided into 5 subgroups according to the time after RIR: 2, 6, 24, and 72 hours and 7 days, with 6 rats in each subgroup. Another 60 Wistar-Kyoto (WKY) rats were divided into the same groups as the SHR rats as the control. The RIR model was set up. The apoptosis of retinal capillary cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) methods and the expression of p53 was determined by streptavidin-perosidase (SP) immunohistochemistry. Results The apoptosis rate of retinal capillary cells in the 5 SHR-RIR groups was (8.64±0.56)%, (14.92±0.99)%, (24.72±2.98)%, (16.53±1.80)%, and (7.12±1.10)%,respectively. The expression of p53 in SHR-RIR groups increased at the 2nd hour after RIR, reached the peak at the 24th hour, kept the high level at the 72nd hour, and remained a little at the 7th day, which was significantly different from which in the SHR-SH groups (P<0. 01). The expression of p53 were higher in SHR-IR groups than that in the WKY-RIR groups (P<0. 01). Conclusions p53 may play a part in RIR injury by inducing or promoting apoptosis. The apoptosis of retinal capillary cells after RIR is more severe under the hypertension, and reaches the peak at the 24 hour after RIR.     

姜黄素对动脉粥样硬化兔基质金属蛋白酶9的影响

目的研究姜黄素对动脉粥样硬化兔主动脉基质金属蛋白酶9表达的影响。方法将30只雄性日本大耳白兔给予高脂饲料喂养2个月。成功复制动脉粥样硬化模型兔20只,随机分成两组,治疗组给予姜黄素200mg/(kg·d)灌胃,对照组每日给予生理盐水灌胃,均以基础饲料喂养,共治疗1月。采血检测血浆总胆固醇、甘油三酯、低密度脂蛋白胆固醇和高密度脂蛋白胆固醇水平变化;兔处死后取主动脉观察粥样斑块面积比;取主动脉弓做病理切片,进行光镜检查,用免疫组织化学检测主动脉壁基质金属蛋白酶9的表达。结果姜黄素治疗组血浆甘油三酯、总胆固醇、低密度脂蛋白胆固醇水平与对照组相比显著降低,高密度脂蛋白胆固醇水平显著升高(P<0.05)。姜黄素治疗组斑块面积/主动脉面积比显著低于对照组(P<0.05),基质金属蛋白酶9免疫组织化学染色强度、阳性细胞率、总积分均低于对照组。结论姜黄素可以显著降低动脉粥样硬化兔主动脉壁基质金属蛋白酶9的表达,抑制动脉粥样硬化的形成。     

自发性高血压大鼠缺血再灌注后视网膜毛细血管细胞凋亡及p53基因表达

目的 探讨凋亡相关基因p53在自发性高血压大鼠(SHR)视网膜缺血再灌注损伤（RIR）后视网膜毛细血管细胞凋亡中的作用。方法 将60只SHR随机分为假手术组(SHR-SH)和缺血组(SHR-RIR),每组各30只大鼠;每组又按照不同再灌注时间分别再分为再灌注后2、6、24、72 h和7 d共5个小组,每小组各6只大鼠。选取60只Wistar-Kyoto大鼠（WKY）同样分为假手术组(WKY-SH)和缺血组(WKY-IIR)作为对照。建立大鼠RIR损伤动物模型,采用末端脱氧核苷酸转移酶介导的dUTP 缺口翻译法（TUNEL）法观察大鼠视网膜毛细血管细胞凋亡,通过免疫组织化学链酶卵白素-生物素复合体法(SP)检测RIR后不同时段视网膜组织中p53基因的表达变化。结果 SHR视网膜毛细血管细胞凋亡率在RIR后2、6、24、72 h和7 d时分别为（8.64±0.56）%、（14.92±0.99）%、（24.72±2.98）%、（16.53±1.80）%和（7.12±1.10）%。SHR视网膜毛细血管在RIR后2 h p53表达即开始增加,6 h继续增多,24 h达到高峰,72 h仍维持在较高水平,7 d时仍有少量表达,与SHR SH比较,差异有统计学意义（P＜0.01）。WKY-SH和SHR-SH组各时间点细胞凋亡和p53表达无明显差异。WKY RIR与SHR RIR相应时间点比较,差异有统计学意义（P＜0.01）。结论 p53可能通过诱导或促进细胞凋亡参与大鼠RIR;高血压状态下发生RIR视网膜毛细血管细胞凋亡更为严重,且尤以缺血再灌注后24 h为著。     

姜黄素对动脉粥样硬化兔血脂和血管内皮功能的影响

目的观察姜黄素对动脉粥样硬化(AS)家兔血脂和血管内皮功能的影响。方法复制AS模型家兔20只随机分两组,治疗组(10只)和对照组(10只),均予基础饲料喂养,治疗组每日加予姜黄素200mg灌胃一次,对照组每日给予生理盐水灌胃一次,治程1个月。治疗前后观察血浆甘油三脂(TG)、总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、血管性血友病因子(vWF)、组织型纤溶酶原激活物(t-PA)和纤溶酶原激活抑制物-1(PAI-1)的变化。结果治程结束时治疗组、对照组各8只家兔进入统计学分析。治疗组较对照组显著降低血浆TG、TC、LDL-C及升高HDL-C水平(P<0.05),PAI-1水平和PAI-1/t-PA比值下降(P<0.01)。结论姜黄素有显著的降低TC、LDL-C、TG和升高HDL-C的作用,一定程度上改善血管内皮功能作用。