中频电对大鼠脑缺血再灌注损伤保护作用的研究

目的研究中频电对大鼠脑缺血再灌注损伤的保护作用。方法50只动物被随机分成3组,假手术组、模型组及中频疗组,其中后2组参考Longa法制成大鼠脑缺血再灌注模型,中频疗组在缺血再灌注后立即将电极安置于耳后两侧乳突处,每次通电30min,每天1次,7d后眼球取血、断头取脑,测量血液流变学、红细胞膜流动性、抗氧化酶活性以及一氧化氮(NO)、一氧化氮合成酶(NOS)等各项指标的变化。结果模型组大鼠血液流变学、红细胞膜流动性、NO、NOS等含量显著高于假手术组,抗氧化酶活性显著低于假手术组;经过中频电治疗后,大鼠血液流变学、红细胞膜流动性、NO、NOS等含量有所下降,抗氧化酶活性有所升高,差异均有显著性。结论中频电能显著改善大鼠的脑部微循环,提高机体的抗氧化防御能力,有效地抑制了自由基、一氧化氮等对神经组织的损伤,通过作用于脑缺血病理生理过程中的多个靶点,发挥其对脑缺血再灌注损伤的保护作用。     

金黄色葡萄球菌锰超氧化物歧化酶的表达纯化及活性分析

目的克隆表达、纯化金黄色葡萄球菌(Staphylococcus aureus)锰超氧化物歧化酶(Mn-SOD)并测定其活性。方法使用Clustal Omega比对不同来源Mn-SOD的序列,使用Swiss model网站预测金黄色葡萄球菌Mn-SOD的三级结构。提取细菌DNA,以此为模板PCR扩增获得Mn-SOD基因并将其与pET28a连接,构建pET28a-Mn-SOD重组质粒。将重组质粒转化大肠埃希菌BL21(DE3)获得重组菌BL/pET28a-Mn-SOD,使用IPTG诱导表达重组Mn-SOD,通过镍柱亲和层析纯化Mn-SOD蛋白并测定不同pH条件下的酶活性。结果金黄色葡萄球菌Mn-SOD具有Mn-SOD的特征序列和锰离子结合位点。成功得到重组质粒pET28a-Mn-SOD,转化大肠埃希菌BL21后表达相对分子质量为24.8×10^3的Mn-SOD,使用Ni^2+柱纯化后得到高纯度的Mn-SOD,且在pH值为7.5时活性较高,约为3 200 U/mL。结论成功构建了pET28a-Mn-SOD重组质粒能,表达的Mn-SOD重组蛋白纯化后仍具有SOD活性。     

湿热环境暴露对氰化钠毒性和组织氧化应激反应的影响

目的探讨湿热环境下氰化物毒性作用变化规律及其对组织氧化应激反应的影响。方法以小动物湿热环境试验箱模拟高温高湿环境,测定不同温、湿度[温度（Ta）（20±0.5）℃、相对湿度（50±5）%,温度36℃及38℃、相对湿度（RH）（60±3）%]条件下氰化钠经腹腔注射KM小鼠的LD50。另将30只SD大鼠随机分为常温对照、常温中毒、湿热对照、湿热中毒及药物预防组,各组受试动物分别按以下因素单一或联合处理：（1）湿热应激：模拟箱内[温度（38±0.5）℃,相对湿度（60±3）%]60 min;（2）氰中毒：动物腹腔注射氰化钠3.6 mg/kg;（3）药物预防：给予谷胱甘肽、维生素C灌胃5 d。各组受试动物于热应激后60 min和（或）中毒30 min后测定脑、肝组织匀浆超氧化物歧化酶（superoxide dismutase,SOD）活性和丙二醛（malondialdehyde,MDA）含量。结果与20℃,RH50%时KM小鼠氰化钠中毒LD50（4.77 mg/kg）相比,（36±0.5）℃或（38±0.5）℃,RH 60%湿热环境中毒动物的LD50分别下降至4.66 mg/kg（P〉0.05）及4.17 mg/kg（P〈0.05）。20℃RH 50%条件下NaCN中毒后肝、脑组织SOD活力下降（P〈0.01）,MDA含量增加（P〈0.01）,而38℃RH 60%环境下NaCN中毒所致氧化应激改变更明显（P〈0.01）。药物预防可缓解相同条件下上述指标的改变（P〈0.01）。结论暴露于湿热环境下,小鼠氰化纳中毒的LD50可随环境温度的升高而降低。湿热环境和（或）氰化钠中毒两因素均可导致氧化应激指标的明显改变,二者同时作用可能具有联合效应。服用抗氧化药物可提高组织抗氧化应激能力。     

急诊多发伤患者血液SOD、LPO的测定及临床意义

目的：研究多发伤对血液SOD活性及LPO含量的影响以及与创伤严重度评分的关系。方法：采用邻苯三酚自氧化抑制法和硫代巴比妥酸反应产物比色分析法检测多发伤患者与正常健康成人的血液SOD活性及LPO含量，并对多发伤患者行创伤严重度评分。结果：多发伤组血液SOD平均活性显著降低（P＜0．001），LPO平均含量显著升高（P＜0．001），ISS值愈高，伤死率愈高。结论：多发伤患者创伤后体内氧自由基的产生与清除平衡失调，造成机体的自由基损伤及脂质过氧化损伤，而创伤严重度与患者的伤愈、死亡存在一定的关系。     

中西医结合治疗急性脑梗塞的疗效和其对促肾上腺激素及超氧化物歧化酶的影响

目的：探讨中西医结合治疗急性脑梗塞的疗效和其对促肾上腺激素（ＡＣＴＨ）和超氧化物歧化酶（ＳＯＤ）的影响。方法：对４５例急性脑梗塞患者行中西医结合〔紫外线照射充氧自血回输（ＵＢＩＯ）＋高压氧（ＨＢＯ）＋活血化瘀补肾中药〕治疗；３０例用ＵＢＩＯ＋ＨＢＯ治疗；３５例患者用复方丹参治疗作对照组。结果：中西医结合治疗急性脑梗塞治愈率及总有效率分别为４０．０％及９５．６％，复方丹参对照组分别为１４．３％及７１．４％，ＵＢＩＯ＋ＨＢＯ组分别为３３．３％和９０．０％。中西医结合治疗后ＡＣＴＨ及ＳＯＤ水平明显增高，与对照组比较差异有显著性，ＡＣＴＨ及ＳＯＤ变化趋势呈一致性。结论：中西医结合治疗使内分泌系统的垂体下丘脑肾上腺轴激素分泌作用增强，内环境ＳＯＤ对自由基清除力增高，疗效高。     

阿司匹林联合奥扎格雷钠对急性脑梗死患者血清hs-CRP、FIB、MDA、SOD及CAT表达水平的影响

目的观察阿司匹林联合奥扎格雷钠对急性脑梗死患者血清超敏C反应蛋白(hs-CRP)、纤维蛋白原(FIB)、丙二醛(MDA)、超氧化物歧化酶(SOD)及过氧化氢酶(CAT)表达水平的影响。方法将脑梗死急性发作患者107例随机分为对照组54例和观察组53例,对照组给予阿司匹林,观察组给予阿司匹林联合奥扎格雷钠。对比2组治疗前后血清hs-CRP、FIB、MDA、SOD和CAT表达水平,运用美国国立卫生研究院卒中量表(NIHSS)评分和日常生活能力表Barthel指数(BI)评估2组神经功能缺损程度改善情况。结果治疗后14 d,2组hs-CRP、FIB和MDA水平下降,SOD和CAT水平较治疗前上升(P0.05或P0.01),且观察组hs-CRP、FIB和MDA水平显著低于对照组(P0.01),SOD、CAT水平显著高于对照组(P0.05)。治疗后1个月,2组NHISS评分较治疗前下降(P0.05),BI指数较治疗前上升(P0.05),且观察组改善显著优于对照组(P0.05)。结论阿司匹林联合奥扎格雷钠能有效改善急性脑梗死患者氧自由基和抗氧化系统间平衡,减轻脑细胞损伤,恢复受损的神经功能。     

高原地区部队官兵腰椎间盘突出症患者血清SOD、MDA表达及临床意义

目的:通过检测高原地区部队官兵腰椎间盘突出症(lumbar disc herniation,LDH)患者血清中超氧化物歧化酶(SOD)的活力值及丙二醛(MDA)含量,探讨低氧环境下氧自由基对腰椎间盘突出症发病的影响。方法:采集腰椎间盘突出症患者血清标本作为患病组,共27例,随机抽取高原驻军健康机体血清标本27例为对照组,服役年限均为2～5年。取入伍1周的新兵血清标本27例为标准组进行比较。结果:27例腰椎间盘突出症患者血清中SOD活力值低于对照组高于标准组(P<0.05)。患病组血清中MDA高于对照组及标准组(P<0.05)。结论:高原地区部队官兵腰椎间盘突出症患者存在着不同程度的氧自由基代谢失衡,主要表现为清除超氧阴离子自由基的SOD活性下降,氧自由基含量的升高。氧自由基是加速椎间盘退变和致痛的重要因素。     

老年人胰岛素样生长因子-1、超氧化物歧化酶与骨质疏松的关系探讨

目的探讨老年人胰岛素样生长因子-1(IGF-1)、超氧化物歧化酶(SOD)与骨质疏松症(OP)之间的关系。方法测定150例老年OP患者(A组)和124例健康老年无OP者(B组)的IGF-1、SOD及骨密度(BMD)。结果A组患者和B组的IGF-1分别是(110.30±41.79)μg/L vs(186.13±68.13)μg/L;血清超氧化物歧化酶(T-SOD)分别是(89.57±18.67)kU/L vs(109.86±17.97)kU/L,差异有统计学意义(均P<0.01);各部位的BMD数值A组均小于B组(均P<0.01)。结论老年OP患者IGF-1、SOD明显低于无OP者,IGF-1、SOD与老年OP的发生、发展密切相关。     

Effects of vitamin C and melatonin on cysteamine-induced duodenal ulcer in a cholestatic rat model: A controlled experimental study

Background: Superoxide dismutase (SOD) is one of the defense mechanisms against free radicals. Cysteamine is a cytotoxic agent, acting through generation of reactive oxygen species (ROS) such as hydrogen peroxide, hydroxyl radical, and superoxide, and may decrease defense activity of SOD against ROS and induce duodenal ulcer. Melatonin is a suicidal antioxidant that has a protective effect against ROS and cytoprotective effect through inhibition of the decrease in SOD activity.Objectives: The primary aim of this study was to assess the effects of pretreatment with vitamin C and melatonin on cysteamine-induced duodenal ulcer. Secondary aims were to compare the ulcerogenic effect of cysteamine and the antiulcer effects of vitamin C and melatonin.Methods: This study was performed in male Wistar rats (200-250 g) in 3 groups of equal size (n = 24): bile duct ligation-induced cholestasis (test), sham, and control groups. In the test and sham groups, laparotomy was performed under general anesthesia and the common bile duct was identified; in sham rats, the common bile duct was left in situ, but in test rats, the common bile duct was isolated and doubly ligated to induce cholestasis. Animals in each group were also divided into 4 equal subgroups (n = 6). These subgroups were treated with vitamin C plus cysteamine, melatonin plus cysteamine, cysteamine alone, and saline, respectively. All animals were euthanized via overdose of ether anesthesia 24 hours after the last injection of cysteamine or saline, and 0.5 mL of blood was collected from the heart ventricle. The duodenum was cut open, washed with saline, fixed, and prepared for calculation of ulcer index (Szabo method) and histopathologic assessment. SOD activity was measured using a branded enzyme kit.Results: In all 3 groups, animals treated with cysteamine had significantly increased mean (SE) ulcer index (test, 4.00 [0.10] vs 1.17 [0.30]; sham, 3.83 [0.16] vs 0.50 [0.22]; control, 3.67 [0.21] vs 0 [0]) and decreased SOD activity (test, 146.41 [2.16] vs 299.83 [1.94] U/mL; sham, 154.75 [2.02] vs 303.08 [0.35] U/mL; control, 157.08 [1.67] vs 314.50 [1.14] U/mL) compared with saline-treated rats (all, P < 0.001). In the test rats, ulcer index was significantly increased and SOD activity was significantly decreased compared with the sham and control groups (both, P < 0.001). Pretreatment with vitamin C and melatonin was associated with attenuation of ulcer index and increased SOD activity compared with rats treated with cysteamine alone (P < 0.001). There were no significant differences in ulcer index or SOD activity between groups administered vitamin C or melatonin.Conclusions: In this experimental study, pretreatment with melatonin or vitamin C in all rats produced significant attenuation of the ulcer index and enhanced SOD activity. Cysteamine-induced duodenal mucosal damage was greater in cholestatic rats compared with sham and control rats.     

碱性成纤维细胞生长因子对慢性酒精中毒大鼠自由基与脂质过氧化作用的影响

目的观察碱性成纤维细胞生长因子(bFGF)对慢性酒精中毒大鼠脑和肝组织超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量和羟自由基含量的影响,探讨bFGF对慢性酒精中毒所致的脑损伤、肝损伤的保护作用。方法选择成年Wistar雄性大鼠,采用白酒灌胃建立慢性酒精中毒模型,慢性酒精中毒模型建立成功的大鼠随机抽签法分为酒精中毒组、生理盐水(NS)对照组和bFGF治疗组,每组10只。另10只不灌白酒作为正常对照组。bFGF治疗组大鼠按12μg/kg剂量肌肉注射bFGF,共14d。各组大鼠到d14后取出各组大鼠脑、肝组织制成匀浆,测定脑、肝组织SOD活力、MDA含量和抑制羟自由基能力。结果与正常对照组相比,慢性酒精中毒后大鼠脑和肝组织SOD活力显著降低,MDA含量和羟自由基含量均明显升高(P﹤0.05);经bFGF治疗后脑和肝组织中SOD活力显著升高,MDA含量和羟自由基含量均显著降低。结论 bFGF起到降低自由基,提高机体的抗氧化能力,提示bFGF对慢性酒精中毒所致的脑损伤和和肝损伤具有保护作用。