大鼠肝缺血/再灌注损伤时c-fos、Bcl-2在肝组织的表达及与肝细胞凋亡的关系

目的:观察大鼠肝缺血/再灌注损伤时c-fos、Bcl-2在肝组织中的表达及与肝细胞凋亡的关系,并探讨可能的机制。方法:选健康雄性Wistar大鼠48只,随机分为对照组、缺血30min组(I组)、缺血30min即刻再灌注组(I/R组)、缺血30min再灌注1h组(I/R1h组)、缺血30min再灌注2h组(I/R2h组)、缺血30min再灌注后4h组(I/R4h组),每组8只。应用免疫组化法分别测定各组大鼠肝组织c-fos、Bcl-2的表达,应用原位细胞凋亡法测定肝细胞凋亡的情况,同时观察肝脏组织病理变化。结果:肝脏I/R可出现肝细胞明显损伤、肝细胞水肿、炎性细胞浸润,甚至有细胞坏死。与对照组比较,cfos在I组表达就有增高(P<0.01),I/R4h组达到高峰。I/R组与I组、I/R4h组与I/R2h组相比差异有统计学意义(P<0.01)。肝组织Bcl2在I组表达增高(P<0.01),I/R2～4h达到高峰。I/R4h组与I/R2h组相比差异无统计学意义(P>0.01)。细胞凋亡指数:I组、I/R组与对照组比较明显增加(P<0.01),随着时间的延长细胞凋亡指数逐渐增加。c-fos与细胞凋亡指数呈正相关(r=0.889,P<0.01),Bcl-2与细胞凋亡指数呈正相关(r=0.901,P<0.01)。结论:肝缺血/再灌注损伤可引起肝组织的损伤及肝细胞凋亡。肝细胞凋亡与cfos的表达有关。Bcl2在缺血期发挥了其抑凋亡作用,随着再灌注时间的延长,其抑凋亡作     

大鼠局灶性脑缺血再灌注损伤中各脑区NO含量的变化

目的探讨局灶性脑缺血再灌注损伤中各脑区NO含量的变化。方法用改良的血管内栓线法复制大鼠局灶性脑缺血再灌注模型，应用亚硝酸盐还原法反映脑组织中NO的含量。结果①脑缺血再灌注损伤后．左右皮层、海马的NO含量明显升高，与正常对照组相比有显著性差异（P〈0．05）；②缺血侧与其自身对照侧相比，升高不明显。结论大鼠一侧脑缺血再灌注后，两侧同时受到损伤。     

下丘脑室旁核对大鼠胃缺血/再灌注损伤保护作用的细胞机制

目的 研究电刺激下丘脑室旁核（PVN）对胃缺血/再灌注损伤（GI/RI）大鼠胃黏膜细胞凋亡和增殖的影响,探讨电刺激PVN对GI/RI保护作用的细胞机制.方法 采用电刺激、电解损毁PVN的手段,以夹闭大鼠腹腔动脉30 min、松开 动脉夹恢复血流灌注1 h制备GI/RI模型,计算胃黏膜损伤指数,检测胃黏膜细胞的凋亡和增殖情况.结果 夹闭大鼠腹腔动脉30 min,再灌注1 h后可造成胃黏膜的明显损伤,电刺激PVN后GI/RI明显减轻,而且胃黏膜细胞的增殖增加,凋亡减少.结论 电刺激PVN对GI/RI具有明显的保护作用.这种保护作用是通过促进胃黏膜细胞增殖、抑制胃黏膜细胞凋亡而实现的.     

二氮嗪对缺血再灌注致大鼠心肌细胞坏死和凋亡的影响

目的研究二氮嗪对大鼠心肌缺血再灌注损伤的保护效果。方法健康SD大鼠随机分为两组，实验组静脉注射二氮嗪12.5mg／kg进行预处理，对照组静脉注射相应量溶媒，10min后每组大鼠均行左侧开胸，结扎左前降支，造成局部心肌缺血2h，恢复再灌注2h后取心脏，测量心肌梗死面积大小及采用TUNEL法原位标记缺血区凋亡心肌细胞。结果与对照组相比，二氮嗪预处理组心肌梗死面积显著减小（P〈0．05），心肌细胞凋亡发生率明显降低（P〈0．05）。结论二氮嗪对大鼠心肌缺血再灌注损伤具有较好的保护作用，能减少心肌细胞坏死和凋亡。     

氟烷和安氟醚对大鼠心肌缺血再灌注损伤的保护作用

目的研究氟烷和安氟醚对缺血再灌注心肌功能和代谢、氧自由基的影响。方法SD大鼠80只,随机分为10小组,每组8只。采用Langendorff离体大鼠心脏模型。按给药方式又分为3大组,对照组(含4小组):平衡15min为1小组,平衡后续灌15min为1小组,平衡续灌后缺血10min为1小组,平衡续灌缺血25min后复灌30min为1小组。氟烷组(含3小组):平衡15min后,灌注含1.5MAC氟烷灌注液15min为1小组,平衡续灌后缺血10min为1小组,平衡续灌缺血25min复灌含1.5MAC氟烷的灌注液30min为1小组。安氟醚组:包括3小组,情况同氟烷组。各组记录平衡后,给药后(或续灌15min)复灌30min左室收缩压(LVSP)、左室舒张末期压(LVEDP)、左室发展压(LVDP)、左室压力升高或降低最大速率(±dp/dtmax)、心率(HR)、冠脉流量(CF)。实验结束后测定心肌超氧化物歧化酶(SOD)活性、心肌丙二醛(MDA)含量、高能磷酸盐(ATP)含量。结果安氟醚具有明显扩张冠状动脉的作用。安氟醚能促进缺血再灌注心肌冠脉流量的恢复。两用药组明显降低LVDP、+dp/dt,升高LVEDP(P<0.05);缺血再灌注后,氟烷、安氟醚的LVDP分别恢复到基础值的57%、62%,+dp/dt分别恢复到基础值的56%、67%;与对照组相比差异具有显著性。两用药组均能提高心肌ATP含量,缺血后心肌ATP下降较慢,复灌后恢复较快。复灌     

Effects of 2-APB on Store-operated Ca~(2+) Channel Currents of Hepatocytes after Hepatic Ischemia/Reperfusion Injury in Rats

In clinical practice of hepatobiliary surgery,various factors, such as shock, inflammation, he patic trauma, the operations of liver and biliarytract (in case of necessities of interrupting hepaticportal), liver transplantation, are mutually relatedto commonly pathophysiological procedures,named hepatic ischemia/reperfusion injury, whichcauses Ca2+ overload of hepatocytes and hepatocel lular apoptosis and necrosis and eventually leads toliver dysfunction ( and even …     

Effect of Electroacupuncture on TRPM7 mRNA Expression after Cerebral Ischemia／reperfusion in Rats via TrkA Pathway

TRPM7 ion channel protein is a member ofthe transient receptor potential (TRP) cation chan-nel superfamily .It is an unusual bifunctional pro-tein that contains anα-kinase domain fused to aCa2 +-permeable cation channel . Aarts and col-leagues provide evidence that TRPM7 initiatesCa2 +overload. TRPM7 may play a key role in an-oxic neuronal death[1]. Electroacupuncture (EA)has been shown to be an effective treat ment onstroke . The detailed mechanisms mediating thebeneficial effects of…     

当归对大鼠缺血再灌注心肌HSP70和NF-κB的影响

目的 :观察当归注射液对缺血再灌注 (I/R)过程心肌热休克蛋白 70 (HSP70 )和核转录因子κB(NF κB)表达的影响 ,探讨当归抗心肌缺血再灌注损伤的可能作用机理。方法 :4 5只SD大鼠随机分成 3组 (每组n =15 ) :假手术组 (Ⅰ组 ) ,缺血再灌注组 (Ⅱ组 ) ,当归治疗组 (Ⅲ组 ) ,建立在体心肌缺血再灌注动物模型。每组 5只动物再灌注 4 0min用化学扩增法测定SOD活性 ,TBA法测定MDA含量 ;10只动物再灌注 12 0min测定HSP70免疫组化SP法观察心肌细胞HSP70蛋白表达 ,用ESMA法观察NF κB的变化 ,在电镜下观察心肌细胞的超微结构。结果 :再灌注前注射当归注射液显著降低了再灌注心肌MDA水平 (P <0 .0 1) ,增强了SOD活性 (P <0 .0 1)和HSP70的表达 (P <0 .0 1) ,减低NF κB的活性 ,同时减轻了心肌的超微结构损伤。结论 :当归注射液可通过抗氧化作用、增加HSP70的表达和减低NF κB的活性发挥抗心肌缺血再灌注损伤 ,对心肌有明显的保护作用。     

GM-1对大鼠局灶性脑缺血再灌注后Fas蛋白的表达与细胞凋亡的影响

目的研究大鼠脑缺血再灌注后凋亡相关基因Fas在海马区表达的变化，进一步探讨脑缺血再灌注后细胞凋亡的机制和GM-1的脑保护作用。方法线栓法制作大鼠局灶性脑缺血再灌注模型，同时给予GM-1治疗，采用TUNEL和免疫组化方法观察细胞凋亡及Fas蛋白在脑缺血再灌注后的变化规律。结果脑缺血再灌注后海马区神经细胞过度地表达Fas蛋白，并且该区出现明显的神经细胞凋亡；GM-1能够使Fas蛋白的表达高峰及神经细胞凋亡高峰下调。结论Fas的过度表达可能是脑缺血再灌注后神经细胞凋亡的重要原因。GM-1可能通过抑制Fas的表达，减少神经细胞凋亡发挥脑保护作用。     

Local hypothermia and optimal temperature for stroke therapy in rats

Background Local hypothermia induced by intravascular infusion of cold saline solution effectively reduces brain damage in stroke. We further determined the optimal temperature of local hypothermia in our study. Methods Seventy-eight adult male Sprague Dawley rats (260-300 g) were randomly divided into 3 groups: group A, ischemia/reperfusion without cold saline infusion (n=-26) (control group); group B, infusion with 20℃ saline before reperfusion (n=26); group C: infusion with 10~C saline before reperfusion (n=26). In each group, we chose 15 rats for monitoring physical indexes and the temperature of the brain (cortex and striatum) and body (anus), measurement of brain infarction volume, assessment of neurological deficits and the survival rate of reperfusion at 48 hours. Another 8 rats from each group was chosen for examining brain edema, another 3 from each group for histological observation by electron microscopy (EM) and light microscopy (LM) at 48 hours after reperfusion. Results There was no significant difference among the 3 groups for physical indexes during the examination (F(2,45)=0.577, P=0.568; F(2, 45)= 0.42, P=0.78 for blood pressure and blood gas analysis, respectively). The brain temperature was significantly reduced in the group C compared to the other groups (F(2, 45)=37.074, P=0.000; F(2, 45)=32.983, P=0.000, for cortex and striatum temperature respectively), while the difference in rectal temperature between group A and B or C after reperfusion was not significant (F(2, 45)= 0.17115, P=0.637). And the brain infarct volume was significantly reduced in group C (from 40%±10% in group A, 26%±8% in group B, to 12%±6% in group C, F<(2,45)=43.465, P=0.000) with the neurological deficits improving in group C (X2=27.626, P=0.000). The survival rate at 48 hours after 10℃ and 20℃ saline reperfusion was increased by 132.5% and 150%, respectively, as compared to the control group (X2=10.489, P=0.005). The extent of the brain edema showed no significant difference (F(2, 21)=0.547, P=0.587) after cold saline infusion compared to the control group. No obvious vascular injury was found by electron or light microscopy in either infusion group.Conclusions Regional hypothermia with 10~C cold saline infusion can significantly decrease the infarction volume, improve the neurological deficits, and 10~C seems to be the optimal temperature in inducing a cerebral protection effect during stroke. This procedure could be adopted as a further treatment for acute stroke patients.