胰高血糖素样肽-2对小鼠小肠缺血/再灌注损伤的保护作用

目的:观察胰高血糖素样肽-2(GLP-2)对缺血/再灌注损伤小鼠小肠的保护效应.方法:采用肠缺血/再灌注(I/R)模型,将32只小鼠随机分为4组(n=8)假手术(Sham)组、I/R组、I/R GLP-2保护组和I/R 谷氨酰胺(GLN)阳性对照组.光镜观察小肠黏膜形态学改变.检测小肠绒毛高度和隐窝深度;小肠组织二胺氧化酶(DAO)活性;肠系膜淋巴结(MLN)细菌易位率.结果:与假手术组相比,I/R组部分小肠绒毛坏死脱落,绒毛高度下降,隐窝变浅(P＜0 01);小肠组织DAO活性降低(P＜0.01);MLN细菌易位率增加(P＜0.05).与I/R组比,GLP-2组肠绒毛损害明显减轻,DAO活性回升(P＜0.01),细菌易位率回降(P＜0.05).结论:GLP-2对缺血/再灌注损伤小鼠小肠的形态结构及肠屏障功能具有保护作用.     

缺血预适应对肢体缺血/再灌注骨骼肌、小肠和肺损伤的影响

目的:观察肢体缺血/再灌注(LI/R)后骨骼肌、小肠、肺功能损伤变化,并探讨缺血预适应(IPC)的保护效应及机制。方法:实验用雄性Wistar大鼠24只,随机分为3组(n=8):对照(Control)组,缺血/再灌注(I/R)组和缺血预适应(IPC+I/R)组。分别测定血浆乳酸脱氢酶(LDH)、肌酸激酶(CK)、活性氧(ROS)、丙二醛(MDA)、动脉血氧分压(PaO2)和二氧化碳分压(PaCO2),测定血浆血栓素B2(TXB2),6-酮-前列腺素F1α(6-keto-PGF1α)的含量以及TXB2/6-keto-PGF1α比值的变化;测定骨骼肌、小肠、肺组织髓过氧化物酶(MPO)含量,肺湿干比(W/D)及小肠组织DAO含量。观察骨骼肌组织的形态学变化。结果:IPC+I/R组血浆LDH、CK、ROS、MDA、TXB2/6-keto-PGF1α比值明显低于I/R组,PaO2较I/R组明显升高。IPC+I/R组肺湿干比(W/D),骨骼肌、肺、小肠组织MPO含量明显低于I/R组,而小肠DAO活性升高。骨骼肌组织病理学改变减轻。结论:缺血预适应减轻了缺血/再灌注后骨骼肌、小肠、肺功能的损伤,其机制可能与降低氧化损伤、改善TXB2/6-keto-PGF1α的平衡关系有关。     

缺血预适应对大鼠肢体缺血/再灌注后肺损伤的影响

目的:观察肢体缺血预适应对大鼠肢体缺血/再灌注(I/R)后肺损伤的影响并探讨其机制。方法:将雄性Wistar大鼠随机分为4组(n=8):对照组(C),肢体缺血/再灌注组(LI/R),缺血预适应组(IPC)和L-NAME组。各组大鼠均于肢体缺血4h再灌注4h处死,分别测定其动脉血氧分压(PaO2)和二氧化碳分压(PaCO2),血浆及肺组织丙二醛(MDA)、一氧化氮(NO)、内皮素(ET)含量,计算血浆NO/ET比值;以及肺湿干比(W/D)、肺系数(LI),肺组织髓过氧化物酶(MPO)含量。结果:大鼠LI/R后4h,PaO2明显降低;W/D、LI、血浆及肺组织的MDA、NO、ET和肺组织MPO活性均明显增加,而血浆NO/ET比值明显减小。与LI/R组比较,IPC组各项损伤指标明显减轻,NO水平升高,血浆NO/ET比值明显增大。与对照组和IPC组比较,L-NAME处理组,各项损伤指标数值明显增加,NO水平降低;血浆NO/ET比值明显减小,差异均具有显著性。各组大鼠PaCO2的变化无显著性。结论:缺血预适应对肢体缺血/再灌注后肺损伤具有保护作用,其机制可能与内源性NO合成增加有关。     

银杏提取物对大鼠肺缺血/再灌注损伤的保护作用

目的：观察银杏提取物（EGB）对大鼠体外循环肺缺血／再灌注损伤（I／R）的保护作用。方法：建立离体大鼠肺灌流模型．SD大鼠随机分成假手术组（Sham）、I／R组和EGB组,观察大鼠肺组织形态学改变、分别测定肺组织匀浆及灌流液中超氧化物歧化醇（SOD）、丙二醛（MDA）的含量、肺湿干重比（W／D）和平均肺动脉压（MPAP）。结果：HE染色显示EGB组肺损伤明显减轻、肺组织湿／干重比和MPAP显著低于I／R组：EGB组肺脏灌流液和组织匀浆中SOD的活性显著高于I／R组,MDA含量则显著低于I／R组。结论：EGB对大鼠肺I／R损伤具有保护作用。     

七叶皂苷钠对肠缺血/再灌注肠过氧化损伤的影响

目的：探讨七叶皂苷钠对肠缺血/再灌注肠过氧化损伤的影响及其机制。方法：复制大鼠肠缺血/再灌注（I/R）损伤模型,观察七叶皂苷钠对血浆和肠组织超氧化物歧化酶（SOD）、丙二醛（MDA）、二胺氧化酶（DAO）、髓过氧化物酶（MPO）的影响,同时观察肠组织水肿和病理损害。结果：七叶皂苷钠可显著改善肠损伤,降低肠组织湿/干比值及含水率,同时升高血浆和肠组织SOD活性,降低血浆和肠组织MPO活性及MDA含量（P〈0.01）。结论：七叶皂苷钠对肠I/R后肠黏膜具有保护作用,其机制可能与抑制中性粒细胞的聚集与活化,对抗脂质过氧化损伤有关。     

TLR2促进大鼠肾缺血再灌注损伤中的炎症反应和氧化应激

目的:探究肾缺血再灌注损伤对Toll样受体2(Toll-like receptors 2, TLR2)信号路径的影响,以及TLR2在肾缺血灌注中的作用。方法:将21只Wistar大鼠随机分为假手术组(Sham)、肾缺血再灌注模型组(I/R)和T2.5处理组(T2.5)。缺血再灌注24小时后,采集心脏血和左肾组织。对肾组织进行病理学分析,采用试剂盒检测血清肌酐(Cr)和血尿素氮(BUN)水平,采用酶联免疫吸附试验(ELISA)和免疫印迹分析(Western blot)检测肾组织炎症和氧化应激变化。结果:与假手术组相比,模型组大鼠肾组织出现明显损伤,T2.5处理能有效改善肾组织损伤,差异具有统计学意义(P0.05)。与假手术组相比,模型组大鼠血清Cr、BUN水平显著上升,而T2.5能显著抑制血清Cr、BUN升高、减轻肾损伤(P0.05)。与假手术组相比,模型组大鼠肾组织TLR2、TLR4相对表达量显著上升,T2.5能显著抑制肾组织TLR2、TLR4的升高,调节TLR信号通路(P0.05)。与假手术组相比,模型组大鼠的NF-k B表达及磷酸化水平显著上升(P0.05),T2.5能够显著下调I/R大鼠的NF-kB磷酸化水平(P0.05),对NF-kB的表达则无明显影响(P0.05)。与假手术组相比,模型组大鼠肾组织中促炎因子IL-6、IL-1β和TNF-α的浓度均显著上升(P0.05),T2.5能通过显著下调IL-6和IL-1β水平来改善I/R大鼠的炎症水平(P0.05),但对TNF-α的水平无明显影响(P0.05)。与假手术组相比,模型组大鼠的SOD活力显著下降,T2.5能显著逆转该下降趋势(P0.05);而模型组大鼠的MDA活力显著上升(P0.05),T2.5处理对I/R大鼠的MDA活力无明显影响(P0.05)。结论:TLR2在缺血再灌注损伤中促进了炎症反应和氧化应激,其机制与激活TLR信号路径,促进NF-kB磷酸化,进一步调节促炎因子的释放和抗氧化酶的活性有关。     

缺血预适应对大鼠肢体缺血/再灌注后小肠细胞凋亡的影响

目的：观察大鼠肢体缺血再灌注后小肠粘膜自由基及钙含量改变与细胞凋亡情况．以及缺血预适应对其变化的影响。方法：将雄性Wistar大鼠18只,随机分为对照（Control）组,缺血／再灌注（I／R）组和缺血预适应（IPC＋I／R）组,分别测定血浆和小肠组织超氧化物歧化酶（SOD）、黄嘌呤氧化酶（XOD）、丙二醛（MDA）的含量,小肠组织钙及线粒体钙含量;小肠组织的Bel-2和Bax蛋白的表达水平;检测小肠细胞凋亡情况。结果：肢体I／R后血浆和小肠粘膜SOD减少而XOD和MDA增加;小肠组织钙及线粒体钙含量增多;Bel-2蛋白表迭和Bax表达增多,但Bel-2／Bax比值降低;凋亡细胞增多。IPC减轻了I／R后引起的XOD、MDA含量的升高,并且增加了SOD的含量;减轻了组织和线粒体钙超载;Bel-2的表达则明显升高而Bax表达较I／R组明显减少,Bel-2／Bax比值升高;凋亡细胞减少。结论：肢体IR引起小肠粘膜自由基的增多,钙超栽,凋亡细胞增多;IPC可能通过减少自由基的产生及钙超载,抑制细胞凋亡而对肢体I／R继发的小肠功能损伤起保护作用。     

红花对兔肺缺血/再灌注损伤及环氧酶表达的影响

目的：探讨红花（safflor injection,SI）抗肺缺血/再灌注损伤作用及其机制。方法：复制在体兔肺缺血/再灌注损伤模型。30只日本大耳兔,随机均分为三组：假手术组（S组）,缺血/再灌注组（I/R组）和缺血/再灌注＋红花注射液组（SI组）。实验结束时,自颈动脉抽血检测丙二醛（MDA）含量、超氧化物歧化酶（SOD）和黄嘌呤氧化酶（XO）活力。取肺组织测湿干重比（W/D）,计算肺泡损伤率（IAR）,电镜观察细胞超微结构改变。免疫组化法检测肺组织COX-1、COX-2蛋白表达的变化 组织原位杂交法检测肺组织COX-1mRNA、COX-2mRNA表达的变化。结果：I/R组血清MDA、XO均显著高于S组,SOD明显低于S组（P〈0.01） I/R组和SI组的W/D与IAR均高于S组（均P〈0.05和P〈0.01）,SI组显著低于I/R组（P〈0.01） I/R组肺组织的超微结构损伤严重,SI组损伤程度明显较轻 免疫组化和原位杂交发现I/R组肺组织COX-2蛋白和COX-2mRNA表达皆显著高于SI组（均P〈0.01）,肺组织COX-1蛋白和COX-1mRNA表达三组间无明显变化。结论：肺缺血/再灌注损伤可诱导肺组织COX-2的表达,SI可能通过抗氧化应激和下调肺组织COX-2蛋白及其基因的表达而减轻肺缺血/再灌注损伤。     

维甲酸X受体介导的氧化应激通路在大鼠肺缺血/再灌注损伤中的调控作用

本研究旨在探讨维甲酸X受体(retinoid X receptor, RXR)介导的氧化应激通路对大鼠肺缺血/再灌注损伤(pulmonary ischemia/reperfusion injury, PIRI)的干预作用及机制。选取雄性Sprague Dawley (SD)大鼠77只,随机分为7组(n=11):正常对照组(Control组)、假手术组(Sham组)、假手术+9-顺式维甲酸(9-cis retinoid acid,9-cRA,RXR激动剂)组(Sham+9-cRA组)、假手术+HX531 (RXR抑制剂)组(Sham+HX531组)、缺血/再灌注(ischemia/reperfusion, I/R)组、I/R+9-cRA组、I/R+HX531组。采用大鼠在体左侧肺门夹闭30 min再灌注180 min方法制备肺缺血/再灌注(I/R)模型。I/R+9-cRA组和I/R+HX531组大鼠于开胸前腹腔注射9-cRA和HX531。再灌注结束后取左肺组织,评估肺组织损伤,用试剂盒检测肺组织氧化应激等相关指标,用HE染色法和透射电镜分别观察肺组织形态和肺泡上皮细胞超微结构,用免疫荧光标记法观察肺组织RXRα的表达情况,用Western blot检测核因子E2相关因子(nuclear factor E2-related factor 2, Nrf2)蛋白表达情况。结果显示,与Sham组相比,I/R组肺组织出现明显损伤,SOD活性下降,MDA含量和MPO活性升高,Nrf2蛋白表达水平显著降低;与I/R组相比,I/R+9-cRA组肺组织损伤减轻,SOD活性升高,MDA含量和MPO活性下降,RXR和Nrf2蛋白表达水平明显上调。9-cRA的上述改善作用可被HX531逆转。上述结果提示,激动RXR可有效减轻大鼠肺I/R损伤,对肺组织有一定的保护作用,具体机制可能与其激活Nrf2信号途径,增强抗氧化水平,减轻氧化应激反应有关。     

EPO对缺血/再灌注损伤大鼠心肌细胞Mfn2蛋白表达及心肌细胞凋亡的影响

目的观察重组人促红细胞生成素（recombinant human erythropoietin,rhEPO）对缺血/再灌注损伤大鼠心肌细胞Mitofusin2（Mfn2）蛋白表达的影响及其抗心肌细胞凋亡的作用。方法选取成年SD大鼠35只,随机分为正常组（Normal）,假手术组（Sham）,缺血再灌注组（I/R）,缺血再灌注EPO治疗组（I/R＋EPO）。各组分别于再灌注3h和24h后,剪取心脏缺血/再灌注损伤区域,用脱氧核苷酸末端转移酶介导的缺口末端标记法（TUNEL）检测心肌细胞凋亡,免疫组化法检测Mfn2蛋白的表达。结果再灌注3h和24h后,与正常组和假手术组相比,I/R组Mfn2蛋白的表达和心肌细胞凋亡均显著增加;与I/R组相比,I/R＋EPO组Mfn2蛋白的表达和心肌细胞凋亡均显著降低。结论EPO可以下调缺血再灌注损伤后心肌细胞Mfn2蛋白的表达,抑制心肌细胞的凋亡。     

硫酸镁对脑源性肺损伤综合征的影响

目的探讨不同剂量的硫酸镁(MgSO4)对大鼠脑源性肺损伤后神经源性肺水肿、血浆炎性因子TNF-α及肺组织病理形态学变化的影响。方法将30只SD雄性大鼠按随机数字法分为假手术组(A组)、模型组(B组)及硫酸镁50mg/kg干预组(C组)、硫酸镁100mg/kg干预组(D组)、硫酸镁200mg/kg干预组(E组),每组6只。建立大鼠颅脑损伤模型后,硫酸镁干预组即刻按50mg/kg 25%MgSO4腹腔注射,C组注射1次、D组注射2次、E组注射4次,每8h注射1次。A组及B组的大鼠注射相同剂量生理盐水作对照,C组大鼠注射1次及D组大鼠注射2次MgSO4后给予注射相同剂量的生理盐水作对照,注射方法及间隔时间同E组。伤后48h测定大鼠肺组织含水量、血浆TNF-α浓度,肺组织常规HE染色,光镜观察肺组织病理形态学变化。结果大鼠颅脑创伤后肺组织含水量均高于假手术组,以C组最明显(P0.05),差异有统计学意义。B、C、D、E组大鼠之间肺组织含水量比较差异无统计学意义。B、C、D、E组大鼠TNF-α浓度均明显高于假手术组(P0.05),D组血浆TNF-α浓度明显低于B组(P0.05),E组血浆TNF-α浓度明显低于B组(P0.01),其他各组间差异无统计学意义。假手术组肺组织形态正常,肺血管无扩张,无炎症细胞浸润;B、C、D、E组与假手术组比较均可见终末支气管腔内充满炎症细胞,周围肺组织的肺泡腔内可见炎细胞浸润,肺血管扩张、充血。B、C、D、E组在炎症细胞浸润及肺毛细血管扩张方面无明显差异。结论脑外伤可导致脑源性肺损伤综合征,可导致神经源性肺水肿;硫酸镁可降低大鼠脑损伤后血浆TNF-α浓度,对肺水肿无明显影响。     

脑缺血再灌注损伤大鼠血浆蛋白C活性变化的研究

目的探讨脑缺血再灌注损伤大鼠血浆蛋白C活性的变化及其检测意义。方法取SD大鼠30只,随机分为正常对照组(NC组)、假手术组(SH组)及脑缺血再灌注模型组(IR组),每组10只。线栓法制备左侧局灶性脑缺血再灌注模型,缺血2 h,再灌注24 h,神经功能缺损评分后,右侧颈总动脉取血,离心后取血浆50μl,于-20℃冰冻保存,发色底物法检测蛋白C活性;余血浆2 h内检测凝血功能各指标。结果 IR组大鼠蛋白C活性较NC组及SH组明显降低(P0.01),SH组PC活性较NC组也降低(P0.05);IR组较NC组及SH组PT、APTT明显降低(P0.01),FIB显著增高(P0.01)。结论脑缺血再灌注损伤后PC活性明显改变,检测血浆PC活性的变化对缺血再灌注脑损伤的早期诊断与治疗监测具有重要意义。     

Intestinal inflammation caused by magnesium deficiency alters basal and oxidative stress-induced intestinal function

The aim of this study was to determine the effect of magnesium deficiency on small intestinal morphology and function. Rats were assigned to 4 groups and placed on magnesium sufficient or deficient diet for 1 or 3 weeks. Infiltration of neutrophils and mucosal injury were assessed in stained sections of small intestine. Magnesium deficiency alone induced a significant increase in neutrophil infiltration and increased vascular ICAM-1 expression, in the absence of changes in mucosal injury or expression of proinflammatory mediators. Magnesium deficiency was associated with hyposecretory epithelial cell responses and vascular macromolecular leak in the small intestine and lung, which was attributed partly to reduced expression of NOS-3. To determine the effect of hypomagnesmia on the intestinal responses to a known oxidative stress, groups of rats were randomized to either sham operation or superior mesenteric artery occlusion for 10 (non-injurious) or 30 (injurious) minutes followed by a 1- or 4-hour reperfusion period. In response to mesenteric ischemia/reperfusion, deficient rats showed exaggerated PMN influx, but similar mucosal injury. Intestinal ischemia in sufficient animals induced vascular macromolecular leak in the small intestine and lung at 4 hours of reperfusion, with levels similar to those observed in untreated deficient rats. Acute magnesium repletion of deficient rats 24 h before surgery attenuated the exaggerated inflammation in deficient rats. These data show that magnesium deficiency induced a subclinical inflammation in the small intestine in the absence of mucosal injury, but with significant functional changes in local and remote organs and increased sensitivity to oxidative stress. The opinions contained herein are those of the authors and are not to be construed as official policy or reflecting the views of the Department of Defense     

阿托伐他汀预处理对心肌缺血再灌注损伤大鼠心室重构、炎症反应和氧化应激的影响

目的:研究阿托伐他汀预处理对心肌缺血再灌注损伤大鼠心室重构、炎症反应和氧化应激的影响。方法:选取90只SD级大鼠进行研究,将其随机分成假手术组、缺血再灌注组、阿托伐他汀组,每组30只。假手术组与缺血再灌注组大鼠予以生理盐水(5 m L/d)连续灌胃7d处理,阿托伐他汀组予以阿托伐他汀20 mg/(kg·d)连续灌胃7 d,上述干预结束后,缺血再灌注组与阿托伐他汀组大鼠通过阻断大鼠冠状动脉左前降支的方式建立心肌缺血再灌注损伤模型。比较三组大鼠心室重构指标水平、炎症反应以及氧化应激相关指标水平。结果:缺血再灌注组、阿托伐他汀组大鼠的左室相对重量、右室相对重量、室间隔厚度、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、丙二醛(MDA)、乳酸脱氧酶(LDH)水平均高于假手术组,且阿托伐他汀组大鼠上述指标均低于缺血再灌注组(均P<0.05);缺血再灌注组、阿托伐他汀组大鼠白介素-10(IL-10)、超氧化物气化酶(SOD)水平低于假手术组,且阿托伐他汀组大鼠IL-10、SOD水平高于缺血再灌注组(均P<0.05)。结论:阿托伐他汀预处理可有效预防心肌缺血再灌注损伤大鼠心室重构,同时可在一定程度上改善大鼠的炎症反应和氧化应激反应。     

Dexamethasone blocks sepsis-induced protection of the heart from ischemia reperfusion injury

Previous investigations have shown that sepsis, while causing cardiac dysfunction, can protect the heart from ischemia-reperfusion injury. Sepsis-induced protection may be due to nitric oxide produced by an inducible form of nitric oxide synthase generated in response to cytokines released during sepsis. The glucocorticoid dexamethasone has been shown to inhibit the synthesis of the inducible form of nitric oxide synthase (iNOS). The goals of this study were to determine if dexamethasone would prevent sepsis-induced cardiac dysfunction and sepsis-induced protection of the heart from ischemia-reperfusion injury. In this experiment, rats were made septic by injecting Escherichia coli into the dorsal subcutaneous space. Control rats were injected with sterile saline. At the time of surgery, some of the control and septic animals were injected intraperitoneally with dexamethasone (3 mg/kg). The next day, 24-26 hr after injection of the first dose of E. coli, animals were anesthetized, and hearts were removed and studied in the isovolumic beating-heart preparation. Left ventricular end diastolic pressure was set to 5 mmHg, and left ventricular pressure was measured continuously throughout the protocol. Left ventricular developed pressure (LVDP) was used as an index of LV function. After stabilization, hearts were made globally ischemic for 35 min and then reperfused for 25 min. As has been shown previously, sepsis depressed LVDP but also protected the heart from further depression of LVDP by ischemia and reperfusion. Dexamethasone prevented both sepsis-induced cardiac dysfunction and sepsis-induced protection of the heart from ischemia-reperfusion injury. In addition plasma nitrite/nitrate levels were not different from control levels in the dexamethasone-treated septic rats whereas levels were elevated in the septic animals. The dexamethasone mediated abrogation of sepsis-induced cardiac dysfunction and protection during ischemia-reperfusion injury may be due to suppression of nitric oxide production.     

Effects of dexamethasone on late radiation injury following partial-body and local organ exposures.

Dexamethasone was evaluated as a treatment for radiation-induced lung, kidney, liver, and spinal cord injuries in rats. One experimental group was partial-body-irradiated (22.5 Gy) with the head, femur, and exteriorized intestine shielded to prevent acute mortality. Other animals received local irradiation to the kidney (20 Gy), liver (25 Gy), or a 1-cm segment of cervical spinal cord (18 to 40 Gy). Following irradiation half of the animals in each radiation group were given drinking water containing 188 micrograms/liter of dexamethasone. Tests were done to assess kidney function (hematocrit, plasma urea nitrogen, ethylenediaminetetraacetic acid clearance), liver function (rose bengal clearance, plasma glutamic oxaloacetic acid transaminase), or spinal cord injury (paralysis). The effectiveness of dexamethasone in preventing radiation injury was tissue specific. Dexamethasone eliminated lethal pleural fluid accumulation after partial-body irradiation and delayed development of kidney dysfunction after local kidney irradiation. As a result, dexamethasone increased the median survival time from 63 to 150 days after partial-body irradiation and from 126 to 175 days after local kidney irradiation. After whole-liver irradiation, development of hepatic functional injury was retarded by dexamethasone treatment but without significantly changing survival time. Dexamethasone had no effect on spinal cord tolerance but significantly shortened the latent period between radiation and paralysis.     

Brief small intestinal ischemia lessens renal ischemia-reperfusion injury in rats

Ischemic preconditioning (IPC) not only reduces local tissue injury caused by subsequent ischemia-reperfusion (IR) but may also have a beneficial effect on IR injury of tissues remote from those undergoing preconditioning. In this study, we investigated the effect of small intestinal IPC on renal IR injury in rats. Renal IR injury was induced by a 45-min renal artery occlusion and reperfusion for 2 or 24 h in rats with a previous contralateral nephrectomy, and ischemic preconditioning was induced by 3 cycles of 8-min ischemia and 5-min reperfusion of the small intestine. We then measured the concentrations of plasma creatinine (Cr) and blood urine nitrogen (BUN) and the level of malondialdehyde (MDA) and activities of superoxide dismutase (SOD) and catalase (CAT) in the renal cortex. Renal histopathology also was evaluated. Pretreatment with intestinal ischemic preconditioning significantly alleviated renal IR injury, as shown by decreases in the levels of Cr, BUN, and MDA, decreased renal morphologic change, and improved preservation of SOD and CAT activities. These results suggest that remote ischemic preconditioning of the small intestine protects against renal IR injury by inhibition of lipid peroxidation and preservation of antioxidant enzyme activities.     

Exogenous hydrogen sulfide attenuates gastric ischemia-reperfusion injury via activation of K(ATP) channel

The present study aimed to investigate the protective effect and mechanism of hydrogen sulfide donor NaHS administration against gastric mucosal injury induced by gastric ischemia-reperfusion (GI-R) in rats. GI-R injury was induced by clamping the celiac artery of adult male SD rats for 30 min and followed by reperfusion for 1 h. The rats were randomly divided into sham group, GI-R group, NaHS group, glibenclamide group and pinacidil group. Gastric mucosal damage was analyzed with macroscopic injured area, deep damage was assessed with histopathology scores, and the hydrogen sulfide concentration in plasma was determined by colorimetric method. The results showed that pretreatment of NaHS significantly reduced the injured area and deep damage of the gastric mucosa induced by GI-R. However, NaHS did not significantly alter the levels of hydrogen sulfide in plasma 14 d after NaHS administration. The gastric protective effect of NaHS during reperfusion could be attenuated by glibenclamide, an ATP-sensitive potassium channel (K(ATP)) blocker. However, K(ATP) opener pinacidil inhibited the GI-R-induced injury. These results suggest that exogenous hydrogen sulfide plays a protective role against GI-R injury in rats possibly through modulation of K(ATP) channel opening.     

梓醇对大鼠脑缺血再灌注损伤的保护作用研究

目的:探讨梓醇对缺血再灌注大鼠脑损伤后的保护作用.方法:采用传统大脑中动脉阻塞(MCAO)方法制备大鼠局灶性缺血模型,根据随机数字表法将SD大鼠分为MCAO组、对照组(vehicle组)及梓醇处理组(catalpol组),缺血再灌注48 h后观察各组大鼠神经功能学评分和脑梗死容积.分别于术前、术后6h、24 h、48 h取大鼠脑组织样本,检测匀浆中谷胱甘肽过氧化物酶(GSH-PX)和丙二醛(MDA)的变化情况.结果:与vehicle组和MCAO组相比,catalpol处理组神经功能学评分降低(P＜0.05);其梗死容积较小(P＜0.05).组织匀浆结果显示catalpol处理组脑匀浆中GSH-PX活力升高,MDA含量下降(P＜0.05).结论:梓醇可能通过降低脑内自由基水平、控制脂质过氧化程度,对缺血再灌注引起的大鼠脑损伤产生神经保护作用.