姜黄素对大鼠肝缺血再灌注早期肝组织一氧化氮和内皮素-1水平的影响

目的探讨姜黄素对大鼠肝脏缺血再灌注早期损伤(再灌注1 h)的微循环影响。方法将大鼠随机分为假手术组(A组)、对照组(B组)和实验组(C组)。通过检测再灌注早期1 h血清转氨酶的水平、肝组织中NO和ET-1水平来评价姜黄素对大鼠肝脏缺血再灌注早期损伤(再灌注1h)的微循环影响。结果姜黄素可降低大鼠肝脏缺血再灌注早期损伤血清转氨酶的水平,减少肝组织中NO水平和抑制肝组织中ET-1生成。且肝组织中NO生成与血清ALT存在正相关,肝组织ET-1水平与血清ALT存在正相关。结论姜黄素可通过减少肝组织中NO生成、降低肝组织中ET-1表达来改善肝缺血再灌注早期损伤中微循环的紊乱,从而减少对肝缺血再灌注肝实质细胞的损伤。     

葛根素对肝硬化大鼠肝脏缺血再灌注损伤保护作用及其保护机制的研究

目的观察葛根素（Pue）对肝硬化大鼠肝脏缺血再灌注损伤是否具有保护作用，及其保护机制。方法首先建立大鼠肝硬化动物模型，在此模型基础上建立大鼠全肝缺血再灌注模型，比较用Pue预处理对缺血再灌注后，肝组织光镜下的形态学改变；血清中丙氨酸氨基转移酶（ALT）、天冬氮酸氨基转移酶（AST）和氧化亚氮（NO）、丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性，及肝组织中NO、肿瘤坏死因子α（TNF-α）、MDA含量、SOD活性变化。结果Pue预处理可使大鼠血清NO含量、肝组织NO含量及SOD活性明显增高；而血清ALT、AST、MDA含量及肝组织TNF—α、MDA含量明显降低；肝组织形态损伤也有所减轻。结论葛根素对肝硬化大鼠肝缺血再灌注损伤有显著的保护作用，其主要机制是减少NO的降低、扩张血管、改善微循环；清除氧自由基、减轻脂质过氧化。     

缺血后处理对肝脏缺血再灌注中肝窦内皮细胞损伤的保护作用

目的探讨缺血后处理对肝脏缺血再灌注中肝窦内皮细胞损伤的保护作用.方法建立大鼠局部肝脏缺血再灌注模型,将24只健康雄性Wistar大鼠随机分为假手术、缺血再灌注、缺血后处理3组,以缺血再灌前、反复多次的短暂预再灌、停灌作后处理,观察各组血浆肝酶及透明质酸(HA)水平变化和肝组织中丙二醛(MDA)、超氧化物歧化酶(SOD)、内皮素-1(ET-1)含量,并行肝组织病理形态学检查.结果与缺血再灌注组相比,缺血后处理组肝酶的漏出、血浆HA水平及肝组织中MDA、ET-1的含量明显降低(P＜0.01),而SOD活性则显著升高(P＜0.01),肝组织病理学损伤亦明显减轻.结论缺血后处理可通过抑制再灌注后氧自由基的过量生成而保护肝窦内皮细胞,减轻肝脏缺血再灌注损伤.     

白藜芦醇对肝脏缺血再灌注损伤的保护作用

摘要：探讨白藜芦醇对肝脏缺血再灌注损伤的防护作用。将雄性SD大鼠随机分为空白对照组、缺血再灌注组（I/R组）、I/R加生理盐水处理组和I/R加白藜芦醇处理组。观察肝脏缺血40 min再灌注1，3，6，12h后血清谷丙转氨酶（ALT）、谷草转氨酶（AST）及肝组织丙二醛（MDA）含量的变化以及肝组织病理学改变。结果示肝脏I/R后血清ALT，AST及肝组织MDA含量均显著升高，肝脏缺血再灌注前用白藜芦醇15 mg/kg者，血清ALT，AST及肝组织MDA含量均明显降低，且肝组织病理学损害明显减轻。结果表明白藜芦醇对肝脏I/R损伤具有保护作用     

高渗氯化钠羟乙基淀粉40注射液高容量血液稀释对大鼠肝脏缺血再灌注损伤的影响

目的 探讨高渗氯化钠羟乙基淀粉40注射液高容量血液稀释对大鼠肝脏缺血再灌注损伤的影响.方法 雄性Wistar大鼠30只,体重300～350 g,随机分为3组(n=10):假手术组(S组)、缺血再灌注组(IR组)和高容量血液稀释组(HH组).S组仅开腹,不阻断血管;IR组阻断肝门静脉和左肝动脉30 min,再灌注2 h;HH组30 min内经尾静脉输注高渗氯化钠羟乙基淀粉40注射液10 ml/kg进行高容量血液稀释,输注完毕后15 min,行肝脏缺血再灌注.再灌注2 h时,下腔静脉取血样,测定血清谷丙转氨酶(ALT)和谷草转氨酶(AST)的活性;取左肝叶组织,光镜下观察病理学结果,采用比色法测定丙二醛(MDA)含量,采用黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)活性.结果 与S组比较,IR组和HH组血清ALT和AST的活性、肝组织MDA含量升高,肝组织SOD活性降低(P<0.01),肝组织病理学损伤明显;与IR组比较,HH组血清ALT和AST的活性、肝组织MDA含量降低,肝组织SOD活性升高(P<0.01),肝组织病理学损伤减轻.结论 高渗氯化钠羟乙基淀粉40注射液高容量血液稀释可减轻大鼠肝脏缺血再灌注损伤,可能与氧自由基生成减少有关.     

缺血预处理对肝缺血再灌注后氧自由基损伤的保护作用

目的 探讨缺血预处理(PC)对肝缺血再灌注损伤的保护作用机制。方法 将18只犬随机分为三组:非缺血对照组、缺血再灌注组和缺血预处理组。对各组肝上下腔静脉血进行谷丙转氨酶(ALT)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)以及丙二醛(MDA)和超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化酶(GSH-PX)活性及总抗氧化(TAX)能力测定。结果 全肝缺血再灌注后ALT、AST、LDH和MDA含量明显上升(P<0.01),SOD、CAT、GSH-PX活性及TAX能力明显下降(P<0.01,P<0.05);而缺血预处理组与缺血再灌注组比较,ALT、AST、LDH和MDA含量明显下降(P<0.01,P<0.05),SOD、CAT、GSH-PX活性及TAX能力明显上升(P<0.01,P<0.05)。结论 缺血预处理能增强肝组织自身抗氧化能力,减轻肝缺血灌注后氧自由基对肝脏的损伤。     

雌激素对大鼠肝缺血再灌注损伤中SOD和MDA及细胞凋亡的影响

目的：探讨雌激素对大鼠切除肝缺血再灌注损伤的肝脏超氧化物歧化酶（SOD）、丙二醛（MDA）及细胞凋亡的影响。方法：制作肝切除缺血再灌注损伤动物模型,雄性SD大鼠随机分为3组,即假手术组（Sham组）,肝切除缺血再灌注组（I/R组）和肝切除缺血再灌注＋雌激素组（I/R＋E2组）。分别在缺血再灌注后1、3、6 h于光学显微镜下观察肝组织病理学改变,检测血清ALT的水平、肝组织MDA的含量及SOD的活性,并应用流式细胞仪检测细胞凋亡率。结果：I/R＋E2组在各时相点血清ALT、肝组织MDA和SOD及肝细胞凋亡率的变化幅度明显低于I/R组。在光学显微镜下观察I,/R组肝小叶结构紊乱,肝窦淤血,肝细胞水肿变性,肝细胞片状坏死。Sham组和I/R＋E2组上述改变明显减轻。结论：雌激素对肝切除缺血再灌注损伤有显著保护作用,其作用机制可能与雌激素减少氧自由基产生、减轻脂质过氧化反应及抑制细胞凋亡有关。     

亚低温对肝缺血再灌注损伤的保护作用

目的　探讨亚低温对肝缺血再灌注损伤的保护作用机制。方法　将 18只犬随机分为 3组 :非缺血对照组 (n =6 )、缺血再灌注组 (n =6 )和亚低温处理组 (肝周充填碎冰块造成肝脏亚低温 ,n =6 )。对各组肝上下腔静脉血进行谷丙转氨酶 (ALT)、谷草转氨酶(AST)、乳酸脱氢酶 (LHD )以及丙二醛 (MDA)和超氧化物歧化酶 (SOD)、过氧化氢酶 (CAT)、谷胱甘肽过氧化酶 (GSH PX)活性及总抗氧化 (TAX )能力测定。结果　全肝缺血再灌注后ALT ,AST ,LDH和MDA含量明显上升 (P <0 .0 1) ,SOD ,CAT ,GSH PX活性及TAX能力明显下降 (P <0 .0 1) ;而亚低温处理组与缺血再灌注组比较 ,ALT ,AST ,LDH和MDA含量明显下降 (P <0 .0 1) ,SOD ,CAT ,GSH PX活性及TAX能力明显上升 (P <0 .0 1,P <0 .0 5 )。结论　亚低温能增强肝组织自身抗氧化能力 ,减轻肝缺血再灌注后氧自由基对肝脏的损伤。     

七氟醚预处理对右肝癌切除患者肝脏缺血再灌注损伤的保护作用

目的：探讨七氟醚预处理对右肝癌切除患者肝脏缺血再灌注损伤的保护作用及其机制。方法：择期全麻下行右肝癌手术切除患者40例．ASAI或II级,术中经第一肝门阻断．血流阻断时间10～30min．随机分为2组（n=20）：缺血再灌注组（IR组）和七氟醚预处理组（S组）。两组麻醉维持期间均保持脑电双频谱指数40-50。s组麻醉诱导后吸入1MAC七氟醚（呼气末浓度）．30min后洗脱15min。于麻醉诱导前（T0）、缺血再灌注即刻（T1）、1h（T2）、6h（T3）抽血测血清中谷丙转氨酶（ALT）．谷草转氨酶（AST）,乳酸脱氢酶（LDH）的含量以及肝脏组织匀浆中丙二醛（MDA）含量和超氧化物岐化酶（SOD）活性,并行肝组织病理学观察。结果：与麻醉诱导前比较．两组缺血再灌注即刻．1h、6h血清ALT．AST,LDH含量均显著增加（P〈0．05）;与IR组比较,s组肝脏缺血再灌注后相应各时点血清ALT．AST、LDH含量均降低．肝组织匀浆MDA含量减少,SOD活性增加（P〈0．05）;肝组织病理学损伤减轻。结论：七氟醚预处理对右肝癌切除患者肝脏缺血再灌注损伤有保护作用．可能与其抑制氧自由基生成．减少脂质过氧化有关。     

参附注射液对大鼠肢体缺血再灌注后肝脏损伤的保护作用

目的观察参附注射液对大鼠肢体缺血再灌注损伤后肝功能、血红素加氧酶-1（HO-1）表达的影响,并对其保护机制做一初步探讨。方法 64只清洁级SD雄性大鼠,用随机数字表法随机分为4组,每组16只,分别为假手术组、缺血再灌注组、参附干预组、参附＋锌原卟啉Ⅸ（Znpp）干预组。假手术组：大鼠麻醉后仅分离不夹闭股动脉,分离血管前10 min以7.5 mL/kg腹腔注射生理盐水;缺血再灌注组：夹闭股动脉前10 min以7.5 mL/kg腹腔注射生理盐水,夹闭股动脉缺血3 h,再灌注4 h;参附干预组：夹闭股动脉前10 min以7.5 mL/kg腹腔注射参附注射液,夹闭股动脉缺血3 h,再灌注4 h;参附＋Znpp干预组：术前30 min腹腔注射Znpp 5 mg/kg,余同参附干预组。再灌注完毕后取材,取外周静脉血测血清谷丙转氨酶（GPT）、谷草转氨酶（GOT）含量;取肝组织测定肝组织中丙二醛（MDA）含量、超氧化物歧化酶（SOD）活性;采用免疫组织化学法测定肝脏组织中HO-1蛋白表达;光镜下观察肝脏病理学改变。结果 1与假手术组比较,各肢体缺血再灌注造模组MDA含量均明显升高（P〈0.05）,SOD活性明显降低（除参附干预组外,P〈0.05）,GPT、GOT含量均明显升高（P〈0.05）,HO-1蛋白表达明显升高（P〈0.05）。2与缺血再灌注组比较,参附干预组MDA含量明显降低（P〈0.05）,SOD活性明显升高（P〈0.05）,血清GPT、GOT含量明显降低（P〈0.05）,肝组织中HO-1蛋白表达升高（P〈0.05）。3与参附干预组比较,参附＋Znpp干预组MDA含量明显升高（P〈0.05）,SOD活性明显降低（P〈0.05）,血清GPT、GOT含量明显升高（P〈0.05）,而肝组织HO-1蛋白表达差异无统计学意义（P〉0.05）。结论肢体缺血再灌注可造成肝脏功能损伤,给予参附注射液预处理可以减轻肝脏损害程度,这种保护作用可能与参附注射液预处理上调HO-1蛋白在肝组织中的表达、抑制氧自由基生成?     

Curcumin protects against ischemia/reperfusion injury in rat kidneys

OBJECTIVES: Renal ischemia followed by reperfusion leads to acute renal failure in both native kidneys and renal allograft. We investigated the effect of curcumin on ischemia-reperfusion (I/R) injury and the antioxidant effects of curcumin in rats. METHODS: Thirty rats were randomly divided into five experimental groups (control, sham, curcumin, I/R and I/R+curcumin, n=6 each). Curcumin was administered (200 mg kg(-1)) orally to curcumin and I/R+curcumin groups for 7 days. Then, the rats were subjected to bilateral renal ischemia for 45 min and followed by reperfusion for 24 h. All rats were killed and kidney function tests, serum and tissue nitric oxide (NO), protein carbonyl (PC), malondialdehyde (MDA), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) levels were determined. Histopathological examinations were also performed. RESULTS: Curcumin significantly improved the urea and cystatin C levels in I/R+curcumin group compared to I/R group (p<0.05). Reduction of serum GSH-Px was significantly improved by curcumin (p<0.001), but SOD enzyme activity did not alter (p>0.05). Treatment with curcumin also resulted in significant reduction in serum and tissue MDA, NO and PC and for tissue that were increased by renal I/R injury (p<0.001 for serum and p<0.05 for tissue, respectively). In histological examination, the rats treated with curcumin had nearly normal morphology of the kidney. CONCLUSIONS: Based on our results, it can be concluded that curcumin protects the kidneys against I/R injury via its antioxidant effects.     

Inhibition of NFkappaB activation with curcumin attenuates plasma inflammatory cytokines surge and cardiomyocytic apoptosis following cardiac ischemia/reperfusion

BACKGROUND: Following cardiopulmonary bypass (CPB) and cardiac global ischemia and reperfusion, pro-inflammatory cytokines are activated and cause cardiomyocytic injury. Nuclear factor (NF)-kappaB is involved in regulating inflammatory signal transduction. Curcumin inhibits NF-kappaB activation and blocks the inflammatory responses. We studied whether curcumin could decrease myocardial ischemia/reperfusion injury with cardioplegia during CPB and attenuate the appearance of apoptosis of cardiomyocytes. MATERIALS AND METHODS: Rabbits received normal saline (group 1) or curcumin (70 mum/kg, group 2; 100 mum/kg, group 3) injection 2 h before CPB. Total CPB was initiated and cold (4 degrees C) antegrade intermittent crystalloid cardioplegia was delivered every 20 min for 60 min of cardiac arrest. Rabbits were weaned from CPB and reperfused for 4 h. Blood was sampled at various time points and then the reperfused hearts were harvested. RESULTS: Postoperative elevation of plasma levels of interleukin (IL)-8 (14.5, 0.9, 2.9 times over baseline in groups 1-3, respectively, P < 0.05), IL-10 (201.1, 6.0, 14.9 times over baseline in groups 1-3, respectively, P < 0.05), TNF-alpha (9.4, 3.1, 3.9 times over baseline in groups 1-3, respectively, P < 0.05), and cardiac troponin I (141.2, 14.9, 15.0 times over baseline) significantly decreased in the curcumin groups. Appearance of apoptotic cardiomyocytes significantly decreased in the curcumin groups (5.69 +/- 1.64, 1.51 +/- 0.41, 2.43 +/- 0.49 per 1000 nuclei in groups 1-3, respectively, P < 0.01). The activation of neutrophil in the myocardium, which was measured using myocardial myloperoxidase activity assay, was significantly attenuated in the curcumin group. There was a significant increase in apoptosis-related cleavage fragments of caspase-3 and poly-ADP-ribose polymerase in group 1 compared to the other groups. CONCLUSIONS: Curcumin, an inhibitor of NF-kappaB, ameliorated the surge of pro-inflammatory cytokines during CPB and decreased the occurrence of cardiomyocytic apoptosis after global cardiac ischemia/reperfusion injury.     

姜黄素预处理对大鼠缺血再灌注肾小管上皮细胞凋亡的影响

目的：建立大鼠。肾脏缺血再灌注损伤（IRI）模型,观察姜黄素预处理对大鼠肾脏缺血再灌注肾小管上皮细胞凋亡的影响。方法：36只SD雄性大鼠随机分为3组,分别为假手术（Sham）组、肾脏缺血再灌注模型（IR）组、姜黄素预处理（CUR）组,每组12只。CUR组在缺血前2h给予姜黄素100mg／kg剂量溶于0．1％二甲基亚砜1ml中,注入腹腔。24小时后沿原切口进入,切除左。肾。肾组织用4％多聚甲醛固定24h,常规石蜡包埋切片。采用TUNEL法检测各组缺血肾小管上皮细胞凋亡。结果：与Sham组相比,IR组肾小管上皮细胞凋亡明显增加。与IR组比较,CUR组肾小管上皮细胞凋亡减少（P＜0．05）。结论：姜黄素预处理可减轻肾脏IRI的肾小管上皮细胞凋亡。     

Curcumin and dexmedetomidine prevents oxidative stress and renal injury in hind limb ischemia/reperfusion injury in a rat model

Curcumin and dexmedetomidine have been shown to have protective effects in ischemia–reperfusion injury on various organs. However, their protective effects on kidney tissue against ischemia–reperfusion injury remain unclear. We aimed to determine whether curcumin or dexmedetomidine prevents renal tissue from injury that was induced by hind limb ischemia–reperfusion in rats. Fifty rats were divided into five groups: sham, control, curcumin (CUR) group (200?mg/kg curcumin, n?=?10), dexmedetomidine (DEX) group (25?μg/kg dexmedetomidine, n?=?10), and curcumin–dexmedetomidine (CUR–DEX) group (200?mg/kg curcumin and 25?μg/kg dexmedetomidine). Curcumin and dexmedetomidine were administered intraperitoneally immediately after the end of 4?h ischemia, just 5?min before reperfusion. The extremity re-perfused for 2?h and then blood samples were taken and total antioxidant capacity (TAC), total oxidative status (TOS) levels, and oxidative stress index (OSI) were measured, and renal tissue samples were histopathologically examined. The TAC activity levels in blood samples were significantly lower in the control than the other groups (p?0.01 for all comparisons). The TOS activity levels in blood samples were significantly higher in Control group and than the other groups (p??0.01 for all comparison). The OSI were found to be significantly increased in the control group compared to others groups (p?0.001 for all comparisons). Histopathological examination revealed less severe lesions in the sham, CUR, DEX, and CUR–DEX groups, compared with the control group (p?< 0.01). Rat hind limb ischemia–reperfusion causes histopathological changes in the kidneys. Curcumin and dexmedetomidine administered intraperitoneally was effective in reducing oxidative stress and renal histopathologic injury in an acute hind limb I/R rat model.     

姜黄素对自发性高血压大鼠脑缺血再灌注时海马神经元凋亡及c-Jun氨基末端激酶3和突触后密度蛋白95表达的影响

目的 探讨姜黄素对自发性高血压(SH)大鼠脑缺血再灌注时海马神经元凋亡及c-Jun 氨基末端激酶3(JNK3)和突触后密度蛋白95(PSD95)表达的影响.方法 与雄性WKY同源的SH大鼠135只和雄性WKY大鼠90只,清洁级,体重275～325 g,采用随机数字表法,将WKY大鼠随机分为2组(n=45):假手术组(W-S组)及脑缺血再灌注组(W-I/R组),将SH大鼠随机分为3组(n=45):假手术组(S-S组)和脑缺血再灌注组(S-I/R组)及姜黄素组(S-C组).采用四血管阻断法制备全脑缺血再灌注模型.W-S组和S-S组仅分离双侧颈总动脉,W-I/R组和S-I/R组于再灌注30 min时腹腔注射玉米油10 ml/kg,S-C组于再灌注30 min时腹腔注射姜黄素100 mg/kg.于再灌注2 h,6 h、1 d、3 d和7d时进行海马凋亡神经元计数,并测定海马JNK3和PSD95蛋白的表达水平.结果 与W-S组比较,S-S组海马凋亡神经元计数增加(P<0.05),JNK3蛋白表达差异无统计学意义(P>0.05);与S-S组比较,S-I/R组海马凋亡神经元计数增加,JNK3蛋白表达上调(P<0.05);与S-I/R组比较,S-C组海马凋亡神经元计数减少,JNK3蛋白表达下调(P<0.05).各组海马PSD95蛋白表达比较差异无统计学意义(P>0.05).结论 姜黄素可抑制SH大鼠脑缺血再灌注时神经元凋亡,其机制与下调海马JNK3蛋白表达有关,姜黄素下调海马JNK3蛋白表达可能与PSD95途径无关.

Abstract：

Objective To investigate the effect of curcumin on apoptosis in hippocampal neurons and the expression of c-Jun N-terminal kinase 3 (JNK3) and postsynaptic density protein 95 (PSD95) in hippocampus during cerebral ischemia-reperfusion (I/R) in rats with spontaneous hypertension (SH) .Methods One hundred and thirty-five male rats (homologous with WKY) with SH and 90 male normotensive WKY rats, weighing 275-325 g,were used in this study. The WKY rats were randomized into 2 groups ( n = 45 each) : sham operation group (WS group) and cerebral I/R group (W-I/R group) . The rats with SH were randomly divided into 3 groups ( n = 45each) : sham operation group (S-S group), cerebral I/R group (S-I/R group) and curcumin group (S-C group) .Global cerebral ischemia was produced by 4 vessel-occlusion method. The bilateral common carotid arteries were only exposed but not ligated in W-S and S-S groups. Intraperitoneal corn oil 10 ml/kg was injected at 30 min of reperfusion in W-I/R and S-I/R groups. Intraperitoneal curcumin 100 mg/kg was injected at 30 min of reperfusion in S-C group. Three animals in each group were sacrificed at 2 h, 6 h, 1 d, 3 d and 7 d of reperfusion and their brains were harvested for determination of apoptosis in hippocampal neurons and the expression of JNK3 and PSD95in hippocampus. Results The number of apoptotic neurons was significantly increased in S-S group compared with W-S group ( P < 0.05) . The number of apoptotic neurons was significantly increased and the expression of JNK3was up-regulated in S-I/R group compared with S-S group ( P < 0.05) . The number of apoptotic neurons was significantly decreased and the expression of JNK3 was down-regulated in S-C group compared with S-I/R group (P <0.05) . There was no significant difference in the expression of PSD95 among all the groups ( P > 0.05) . Conclusion Curcumin can inhibit apoptosis in hippocampal neurons and the mechanism is related to down-regulation of the expression of JNK3 in hippocampus. The mechanism by which curcumin down-regulates the expression of JNK3in hippocampus may not be related to PSD95 pathway.     

姜黄素对自发性高血压大鼠脑缺血再灌注时海马神经元凋亡及c-Jun氨基末端激酶3和突触后密度蛋白95表达的影响

目的 探讨姜黄素对自发性高血压(SH)大鼠脑缺血再灌注时海马神经元凋亡及c-Jun 氨基末端激酶3(JNK3)和突触后密度蛋白95(PSD95)表达的影响.方法 与雄性WKY同源的SH大鼠135只和雄性WKY大鼠90只,清洁级,体重275～325 g,采用随机数字表法,将WKY大鼠随机分为2组(n=45):假手术组(W-S组)及脑缺血再灌注组(W-I/R组),将SH大鼠随机分为3组(n=45):假手术组(S-S组)和脑缺血再灌注组(S-I/R组)及姜黄素组(S-C组).采用四血管阻断法制备全脑缺血再灌注模型.W-S组和S-S组仅分离双侧颈总动脉,W-I/R组和S-I/R组于再灌注30 min时腹腔注射玉米油10 ml/kg,S-C组于再灌注30 min时腹腔注射姜黄素100 mg/kg.于再灌注2 h,6 h、1 d、3 d和7d时进行海马凋亡神经元计数,并测定海马JNK3和PSD95蛋白的表达水平.结果 与W-S组比较,S-S组海马凋亡神经元计数增加(P<0.05),JNK3蛋白表达差异无统计学意义(P>0.05);与S-S组比较,S-I/R组海马凋亡神经元计数增加,JNK3蛋白表达上调(P<0.05);与S-I/R组比较,S-C组海马凋亡神经元计数减少,JNK3蛋白表达下调(P<0.05).各组海马PSD95蛋白表达比较差异无统计学意义(P>0.05).结论 姜黄素可抑制SH大鼠脑缺血再灌注时神经元凋亡,其机制与下调海马JNK3蛋白表达有关,姜黄素下调海马JNK3蛋白表达可能与PSD95途径无关.     

姜黄素对自发性高血压大鼠脑缺血再灌注时海马神经元凋亡及c-Jun氨基末端激酶3和突触后密度蛋白95表达的影响

目的 探讨姜黄素对自发性高血压(SH)大鼠脑缺血再灌注时海马神经元凋亡及c-Jun 氨基末端激酶3(JNK3)和突触后密度蛋白95(PSD95)表达的影响.方法 与雄性WKY同源的SH大鼠135只和雄性WKY大鼠90只,清洁级,体重275～325 g,采用随机数字表法,将WKY大鼠随机分为2组(n=45):假手术组(W-S组)及脑缺血再灌注组(W-I/R组),将SH大鼠随机分为3组(n=45):假手术组(S-S组)和脑缺血再灌注组(S-I/R组)及姜黄素组(S-C组).采用四血管阻断法制备全脑缺血再灌注模型.W-S组和S-S组仅分离双侧颈总动脉,W-I/R组和S-I/R组于再灌注30 min时腹腔注射玉米油10 ml/kg,S-C组于再灌注30 min时腹腔注射姜黄素100 mg/kg.于再灌注2 h,6 h、1 d、3 d和7d时进行海马凋亡神经元计数,并测定海马JNK3和PSD95蛋白的表达水平.结果 与W-S组比较,S-S组海马凋亡神经元计数增加(P<0.05),JNK3蛋白表达差异无统计学意义(P>0.05);与S-S组比较,S-I/R组海马凋亡神经元计数增加,JNK3蛋白表达上调(P<0.05);与S-I/R组比较,S-C组海马凋亡神经元计数减少,JNK3蛋白表达下调(P<0.05).各组海马PSD95蛋白表达比较差异无统计学意义(P>0.05).结论 姜黄素可抑制SH大鼠脑缺血再灌注时神经元凋亡,其机制与下调海马JNK3蛋白表达有关,姜黄素下调海马JNK3蛋白表达可能与PSD95途径无关.     

姜黄素对肝缺血再灌注损伤保护作用的研究

目的探讨姜黄素对自体肝移植大鼠肝脏缺血再灌注损伤(IRI)的保护作用及其可能机制。方法54只SD雄性大鼠随机分为假手术(SO)组、自体肝移植模型姜黄素预处理(CU)组以及自体肝移植模型溶剂对照(CM)组,术后或再灌注2,6,24 h每组分别处死6只大鼠进行谷丙转氨酶(ALT)、谷草转氨酶(AST)、髓过氧化物酶(Myeloperoxidase MPO)的含量检测。结果血清ALT及AST水平,CM组及CU组均较SO组明显升高,但CM组又明显高于CU组;MPO在SO组含量明显低于CM组和CU组,而CU组又显著低于CM组。结论姜黄素对自体肝移植大鼠肝缺血再灌注损伤有保护作用,其机制可能与减轻中性粒细胞浸润有关。     

Curcumin Nutrition for the Prevention of Mesenteric Ischemia-Reperfusion Injury: An Experimental Rodent Model

Background

Curcumin is an anti-oxidant molecule known to be a potent inhibitor of nuclear factor-κB (NF-κB). It has been shown to attenuate ischemia/reperfusion (I/R) injury in several organ systems. In this study, we sought to investigate the effects of curcumin on the prevention of superior mesenteric artery I/R injury in rats.

Methods

Wistar albino rats were randomly allocated to 3 groups: group I, sham operated (n = 10); group II, I/R injury only (n = 10); group III, curcumin-treated I/R cohort (n = 10). Group I animals underwent laparotomy without I/R injury. After group II animals underwent laparotomy, 60 minutes of superior mesenteric artery ligation were followed by 3 hours of reperfusion. In the curcumin group, 15 days before I/R, curcumin (40 mg/kg) was administered by gastric gavage. All animals were sacrificed at the end of reperfusion. Intestinal tissue samples were obtained to investigate intestinal mucosal injury; in addition we estimated levels of myeloperoxidase (MPO) activity, malondialdehyde (MDA), nitric oxide (NO), glutathione (GSH), interleukin (IL)-6, and tumor necrosis factor (TNF)-α.

Results

There were statistically significant decreases in GSH levels, along with an increase in intestinal mucosal injury scores, MPO activity, MDA levels, NO, IL-6, and TNF-α in group I when compared with groups II and III (P = .01). Curcumin treatment in group III produced a significant increase in GSH levels, as well as a decrease in intestinal mucosal injury scores, MPO activity, MDA, and NO levels when compared with group II (P < .05).

Conclusion

This study showed that curcumin treatment significantly attenuated reperfusion injury in a superior mesenteric artery I/R model in rats.