血红素氧化酶(脱环)

摘要： Objective To observe the effect oftert-Butylhydroquinone (tBHQ) on the expression of nuclear factor erythroid 2-related factor 2 (Nrf2),heme oxygenase (HO)-1 and phosphatidylinositol 3-kinase (PI3K) in high glucose cultured retinal Müller cells;and to investigate the anti-oxidative stress and anti-apoptotic effects oftBHQ.Methods Retinal Müller cells were divided into normal glucose group (5.5 mmol/L,N group),high glucose group (45 mmol/L,HG group) and tBHQ intervention group (HG+tBHQ group).After retinal Müller cells were cultured with high glucose for 48 hours,the pretreatment with tBHQ (20 μmol/L) induced the expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and HO-1.The Müller cells were identified by immunofluorescence staining.The expressions of Nrf2,HO-1,PI3K,B-cell lymphoma-2 (Bcl-2) and Bax were detected by Western blot and real-time fluorescence quantitative PCR.Flow cytometry was used to detect the apoptosis of retinal Müller cells in rats.Results Müller cytoplasm and nucleus GS showed strong positive,large cell body,abundant cytoplasm,uniform green fluorescence;nuclear DAPI staining round or oval,clear boundary.The expression of Nrf2 protein (t=4.114,P=0.006),HO-1 protein (t=9.275,P=0.000),Nrf2 mRNA (t=7.292,P=0.000) and HO-1 mRNA (t=15.014,P=0.000) in the HG group were higher than those in the N group.The expressions of Nrf2 protein (t=7.847,P=0.000),HO-1 protein (t=7.947,P=0.000),PI3K protein (t=5.397,P=0.002),Bcl-2 protein (t=6.825,P=0.000),Nrf2 mRNA (t=18.046,P=0.000),HO-1 mRNA (t=39.458,P=0.000),PI3K mRNA (t=4.979,P=0.003) and Bcl-2 mRNA (t=9.535,P=0.000) in the HG+tBHQ group were significantly higher than those in the HG group.The protein and mRNA expressions of Bax protein in the HG+tBHQ group were significantly lower than those in the HG group (t=14.998,16.520;P=0.000,0.000).Flow cytometry showed that the apoptosis rate of Müiller cells in the HG group was significantly higher than that in the N group (t=39.905,P=0.000).The apoptosis rate of Müller cells in the HG+tBHQ group was significantly lower than that in the HG group (t=21.083,P=0.000).Conclusion tBHQ can inhibit the apoptosis of retinal Müller cells by up-regulating the expression ofNrf2,HO-1 and PI3K.%目的 观察叔丁基对苯二酚(tBHQ)对高糖环境下视网膜Müller细胞中核因子E2相关因子2(Nrf2)、血红素氧合酶1(HO-1)、磷脂酰肌醇-3激酶(PI3K)的表达影响;初步探讨tBHQ的抗氧化及抗凋亡作用.方法 大鼠视网膜Müller细胞分为正常糖组(5.5 mmol/L)(N组)、高糖组(45.0 mmol/L)(HG组)、tBHQ干预组(HG+tBHQ组).HG+tBHQ组Müller细胞培养48h后,加入tBHQ 20 μmol/L预处理剂诱导Nrf2和HO-1的表达.免疫荧光染色法鉴定Müller细胞;蛋白免疫印迹法和实时荧光定量聚合酶链反应检测各组Müller细胞中Nrf2、HO-1、PI3K、B淋巴细胞瘤-2(Bcl-2)、Bax蛋白和基因的表达;流式细胞仪检测各组Müller细胞的凋亡.结果 培养的Müller细胞细胞体大,细胞浆丰富;细胞核呈圆形或卵圆形,边界清晰.HG组Müller细胞中Nrf2 (t=4.114)、HO-1(t=9.275)蛋白表达较N组升高,差异有统计学意义(P=0.006、0.000).HG+tBHQ组Müller细胞中Nrf2(t=7.847)、HO-1(t=7.947)、PI3K(t=5.397)、Bcl-2(t=6.825)蛋白表达较HG组升高,差异有统计学意义(P=0.000、0.000、0.002、0.000);Bax蛋白表达较HG组降低,差异有统计学意义(t=14.998、P=0.000).HG组Müller细胞中Nrf2(t=7.292)、HO-1(t=15.014) mRNA较N组升高,差异有统计学意义(P=0.000、o.ooo).HG+tBHQ组Müller细胞中Nrf2(t=18.046)、HO-1(t=39.458)、PI3K(t=4.979)、Bcl-2(t=9.535) mRNA较HG组升高,差异有统计学意义(P=0.000、0.000、0.003、0.000);Bax mRNA较HG组降低,差异有统计学意义(t=16.520、P=0.000).HG组Müller细胞凋亡率较N组增高,差异有统计学意义(t=39.905、P=0.000);HG+tBHQ组Müller细胞凋亡率较HG组降低,差异有统计学意义(t=21.083、P=0.000).结论 tBHQ通过上调视网膜Müller细胞中Nrf2、HO-1、PI3K的表达,抑制Müller细胞的凋亡.

摘要： 目的 观察莲房原花青素(LSPC)对老年脑老化大鼠学习记忆能力的影响,并探讨血红素氧合酶(HO)系统在其中的可能作用机制.方法 以40只4月龄年轻雌性SD大鼠Morris水迷宫实验第3～5天的平均潜伏期为基础,从100只18月龄雌性SD大鼠中筛选出老年认知功能正常(aged unimpaired,AU)大鼠(其平均潜伏期小于年轻大鼠平均潜伏期3个标准差)和老年认知障碍(aged impaired,AI)大鼠(其平均潜伏期大于年轻大鼠0.5个标准差).随机选取12只4月龄大鼠为年轻对照组,随机选取12只AU大鼠为AU组,随机选取36只AI大鼠并随机分为AI组、低剂量LSPC(L-LSPC,50 mg/kg)干预组、高剂量LSPC(H-LSPC,100 mg/kg)干预组.采用Morris水迷宫试验评估各组大鼠的学习记忆能力,采用ELISA法检测各组大鼠皮质、海马中HO-1及HO-2表达水平.结果 AI组大鼠Morris水迷宫实验平均潜伏期较年轻对照组大鼠明显延长(P＜0.05),L-LSPC和H-LSPC干预组大鼠第3～5天平均潜伏期和游泳距离均明显短于AI组(P＜0.05或P＜0.01).各组大鼠皮质HO-1和HO-2表达水平组间比较差异无统计学意义(均P＞0.05).各组大鼠海马组织HO-1和HO-2表达存在统计学差异(均P＜0.01),与年轻对照组和AU组比较,AI组大鼠海马HO-1水平明显升高(均P＜0.01),而海马HO-2水平降低(均P＜0.05);与AI组比较,L-HSPC和H-LSPC组海马HO-1水平降低(均P＜0.01),而海马HO-2表达水平升高(P＜0.01),且H-LSPC组升高海马HO-2水平较L-LSPC组更明显(P＜0.01).结论 LSPC可明显改善老年脑老化大鼠的记忆功能,其机制可能通过降低大脑海马组织HO-1水平、上调HO-2表达水平来发挥神经保护作用.

摘要： Objective To compare the difference of serum heme oxygenase-1 (HO-1) and carbon monoxide(CO) levels between the patients with coronary heart disease(CHD) caused chronic heart failure(CHF) and CHD patients with normal cardiac function,and further to explore the protective mechanism of HO-1/CO system during the pathogenesis process of CHF.Methods Ninety-one patients with CHF were selected as the observation group and 72 CHD cases with normal cardiac function were taken as the control group.The concentration of HO-1 was determined by ELISA arid the Chalmer S method was used to detect serum CO concentration.The general clinical data of the two groups were recorded by the using the heart failure questionnaire.And the liver and kidney functions,blood lipids,NT-proBNP,BNP and cardiac echocardiography examination were performed.Results The serum HO-1 level in the observation group was (8.13±0.27)ng/mL,which was higher than (2.80±0.52)ng/mL in the control group;the CO level in the observation group was (0.35±0.06)mg/L,which was lower than(0.59±0.07)mg/L in the control group,the difference was statistically significant(P＜0.01);the HO-1 level in the observation group was gradually increased with the increase of cardiac function grade (P＜0.01);while the CO level was decreased with the increase of cardiac function grade (P＜0.01).Conclusion The serum HO-11evel in the patients with CHF is highly expressed with the heart failure aggravation;endogenous CO is gradually decreased due to consumption after cardiac failure aggravation.%目的 通过比较冠心痛所致慢性心力衰竭患者及冠心痛心功能正常患者血清血红素加氧酶-1(HO-1)及一氧化碳(CO)水平差异,进一步探讨HO-1/CO系统在慢性心力衰竭发病中的保护机制.方法 选择慢性心力衰竭患者91例作为观察组,以72例冠心病心功能正常患者作为对照组,采用双抗体酶联免疫吸附(ELISA)测定HO-1浓度,Chalmer S法检测血清CO浓度;通过心力衰竭调查表记录入两组病例一般临床资料,并进行肝肾功能、血脂、NT-proBNP、BNP及心脏超声心动图等检查.结果 观察组血清HO-1水平(8.13±0.27) ng/mL高于对照组(2.80±0.52)ng/mL;观察组CO水平(0.35±0.06)mg/L低于对照组(0.59±0.07) mg/L,差异均有统计学意义(P＜0.01);观察组HO-1水平随心功能分级增高而逐渐增高(P＜0.01),而CO水平随心功能分级增高而逐渐降低(P＜0.01).结论 慢性心力衰竭患者随着心力衰竭加重血清HO-1水平高表达,内源性CO因心力衰竭加重后消耗而逐渐降低.

摘要： Objective To investigate the cellular viability and mitochondrial reactive oxygen species (ROS) production of the Müller cells under high glucose condition,and explore the protection role of the 5,6-dihydrocyclopenta-1,2-dithiole-3-thione (CPDT) on Müller cells.Methods Müller cells from Sprague Dawley rats were divided into 5 groups randomly,including 25 mmol/L normal glucose group (group A) and 65 mmol/L high glucose group (group B).High glucose group with 45,60,70 μmol/L CPDT and cultured them 72 hour was set as group C,D and E.Water soluble tetrazolium salt (WST)-8 was used to measure the cellular viability.Flow cytometry was used to measure the active oxygen and apoptosis index.The expression of nuclear factor erythroid 2-related factor 2 (Nrf2),hemeoxygenase-1 (HO-1),Bcl-2 and Bax protein were measured by Western blot.Results Compared with group A,the WST-8 showed that the viability of Müller cells apparently decreased in group B (t=39.59,P＜0.05).Compared with the group B,the viability of Müller cells had changes in group C (t=0.97,P＞0.05),but recovered in group D and E (t=-4.17,-7.52;P＜0.05).Compared with group A,the FCM showed that the mitochondrial ROS levels was higher in group B (t=-30.99,P＜0.05).Compared with group B,the mitochondrial ROS levels were decreased in group D (t=27.68,P＜0.05).Compared with group A,Bax,Nrf2 and HO-1 increased (t=-11.03,-63.17,-11.44;P＜0.05),while the bcl-2 decreased in group B (t=7.861,P＜0.05).Compared with the group B,Nrf2,HO-1 and Bax decreased (t=15.11,26.59,6.27;P＜0.05),while the bcl-2 increased in group D (t=-6.53,P＜0.05).Conclusions Under the high glucose,CPDT may reduce the mitochondrial ROS levels and the expression of Nrf2,HO-1 and Bax protein of Müller cells.It may inhibit apoptosis through activating the Nrf2/HO-1 pathway and balancing of level of Bcl-2 protein and mitochondrial ROS.%目的 观察5,6-二氢环戊烯1,2-二硫杂环戊烯-3-硫酮(CPDT)对高糖环境下大鼠视网膜Müller细胞活性及其线粒体活性氧(ROS)生成量的影响,初步探讨CPDT对高糖环境下Müller细胞的保护作用及其机制.方法 Sprague Dawley大鼠Müller细胞分为25 mmol/L对照组(A组)、65 mmol/L高糖(B糖)组、高糖+45 μmol/L CPDT组(C组)、高糖+60 μmol/L CPDT组(D组)、高糖+70 μmol/L CPDT组(E组).培养72 h后,水溶性四唑盐(WST)-8法检测各组Müller细胞的细胞相对增生率;流式细胞仪测定各组Müller细胞ROS生成量及细胞凋亡率;蛋白免疫印迹法(Western blot)测定Müller细胞中核因子-E2相关因子2(Nrf2)、血红素合晦-1 (HO-1)、B细胞淋巴瘤/白血病-2(Bcl-2)和Bcl相关X蛋白(Bax蛋白)表达的变化.结果 WST-8法检测结果显示,与A组比较,B组Müller细胞活性明显下降,差异有统计学意义(t=39.59,P＜0.05).与B组比较,C组Müller细胞活性无明显提高,差异无统计学意义(t=0.97,P＞0.05);D、E组Müller细胞活性恢复,差异有统计学意义(t=-4.67、-7.52,P＜0.05).流式细胞仪检测结果显示,与A组比较,B组Müller细胞中ROS生成量增加,差异有统计学意义(t=-30.99,P＜0.05);与B组比较,D组Müller细胞中ROS含量明显下降,差异有统计学意义(t=27.68,P＜0.05).Western blot检测结果显示,与A组比较,B组Müller细胞Bax、Nrf2、HO-1蛋白表达显著上调,差异有统计学意义(t=-1 1.03、-63.17、-11.44,P＜0.05);Bcl-2蛋白表达明显下调,差异有统计学意义(t=7.861,P＜0.05).与B组比较,D组Müller细胞Nrf2、HO-1、Bax蛋白表达均下调,差异有统计学意义(t=15.11、26.59、6.27,均P＜0.05);Bcl-2蛋白表达上调,差异有统计学意义(t=-6.53,P＜0.05). 结论 CPDT降低高糖环境下Müller细胞中ROS含量,下调Nrf2、HO-1、Bax蛋白表达;其机制与激活Nrf2/HO-1氧化应激通路,改变Bcl-2蛋白之间的平衡性,影响线粒体氧自由基量生成,从而抑制细胞凋亡有关.

摘要： 目的:研究补充外源性雌激素对去势大鼠海马和皮质组织中核转录因子2/血红素加氧酶1(Nrf2/HO-1)、沉默信息调节因子相关酶1(SIRT1)表达含量及大鼠海马和皮质区域神经元排列形态和数量的影响,探讨雌激素对神经系统的作用.方法:选取清洁级3个月龄Sprague-Dawley(SD)雌性大鼠40只,随机分为4组.空白组(CON组)、假手术组(SHAM组)、去势对照组(OVX组)、去势实验组(OVX+E2组),每组10只.OVX+E2组给予17β-雌二醇(E2)灌胃,其余3组予生理盐水灌胃.16周后测定各组大鼠海马和皮质组织中的Nrf2、HO-1、SIRT1表达量,同时对大脑皮质及海马CA1区域神经元行形态学检查.结果:①OVX组大鼠海马及皮质中Nrf2、HO-1水平高于SHAM组,SIRT1水平低于SHAM组;OVX+E2组大鼠海马及皮质中Nrf2、SIRT1水平高于OVX组,HO-1水平则低于OVX组;②OVX+E2组海马及皮质组织中神经元数量及排列情况与SHAM组无明显差异,而OVX组海马及皮质尼氏体数量减少,神经元排列紊乱.结论:补充外源性雌激素可下调去势大鼠海马及皮质中HO-1表达,上调Nrf2、SIRT1表达,维持神经元数量及排列结构,从而保护神经系统.%Objective:Investigate the effects of exogenous estrogen on the expression of nuclear transcription factor (Nrf2),heme oxygenase-1 (HO-1),silent information regulator 1 (SIRT1),and the changes of the neuronal morphology and volume in the hippocampus and cortex of those ovariectomized rats,so as to explore the beneficial effects of estrogen on the nervous system. Methods:Forty female Sprague-Dawley (SD) rats aged three months were randomly divided as follows:①control group(CON),②sham operation group(SHAM),③ovariectomized group(OVX),④treated group(OVX+E2). There were 10 rats in each group. The OVX+E2 group were treated with 17β-oestradiol intragastric administration,the other groups were given saline daily. After 16 weeks,Nrf2/HO -1 and SIRT1 levels in the hippocampus and cortex were detected by immunohistochemistry. Then observe the morphology of neurons from cerebral cortex and hippocampus CA1 region. Results:①Compared with the SHAM group,the Nrf2/HO-1 level in hippocampus and cortex of the OVX group was significantly increased , while SIRT1 level was significantly decreased;Compared with the OVX group,Nrf2 and SIRT1 level of the OVX+E2 group was significantly increased,while HO-1 level was significantly decreased. ②There were not significant differences in the number and arrangement of neurons between OVX+E2 group and SHAM group,and the number of tigroid body in hippocampus and cortex of the OVX group was reduced,the morphological alteration of the neuron were disordered. Conclusions:Exogenous oestradiol increased the Nrf2/SIRT1 level but reduced HO-1 level in the hippocampus and cortex of the ovariectomized rats , maintaining neuronal number and structure,thereby protecting the nervous system.

摘要： [Objective] To explore whether heme oxygenase‐1 (HO‐1) and mitochondrial ATP sensitive potas‐sium (mitoKATP ) channel are involved in morphine‐induced delayed cardioprotection .[Methods] Wistar rats were randomly divided into 5 groups .And 25 min regional ischemia plus 2 h reperfusion (IR) at 24 h post‐treatment of 0 .9% sodium chloride 5 mL in group IR;morphine 3mg/kg in group Mor ;HO‐1inhibitor ZnPP‐IX 20μg/kg plus morphine 3 mg/kg in group ZnPP+ Mor;mitoKATP channel antagonist 5‐hydroxydecanoic acid (5‐HD) 5 mg/kg plus morphine 3 mg/kg in group 5‐HD+Mor .In group Mor+5‐HD ,IR 24 h after morphine 3mg/kg and 10 min after 5‐HD 5 mg/kg .Heart rate (HR) and mean arterial blood pressure (MAP) were recorded at pre‐ischemia , 30 ,60 ,120 min post‐reperfusion .Infarct size (percentage area at risk) was assessed at the end of reperfusion .[Results] No statistical differences in HR or MAP existed among five groups .Infarct size was 60 .0% ± 10 .5% in group IR .Pretreatment with morphine reduced infarct size to 27 .4% ± 8 .2% after 24 h in group Mor .The reduc‐tion of infarct size by morphine was abolished by 5‐HD given either before morphine application or before ischemia . And cardioprotection was abolished by ZnPP‐IX given before morphine in group ZnPP+Mor .[Conclusion]Both HO‐1 and mitoKATP are probably involved in delayed cardioprotection evoked by morphine .And mitoKATP channel may serve as both a trigger and a effector in cardioprotection .%【目的】研究血红素氧合酶‐1（HO‐1）和线粒体ATP敏感性钾（Mitochondrial KATP ，mitoKATP ）通道与吗啡预处理的延迟性心肌保护作用的关系。【方法】雄性Wistar大鼠随机分为5组。IR组（A组），腹腔注射生理盐水5 mL ，24 h后行心肌缺血再灌注（IR）；Mor组（B组），腹腔注射吗啡3 mg／kg（用生理盐水稀释至5 mL），24 h后行心肌IR；HO‐1阻滞剂（ZnPP‐IX）＋ Mor组（C组），腹腔注射ZnPP‐IX 20μg／kg ，30 min后腹腔注射吗啡3 mg／kg ，24 h后行心肌IR；mitoKATP通道阻滞剂（5‐HD）＋Mor组（D组），腹腔注射5‐HD 5 mg／kg ，20 min后腹腔注射吗啡3 mg／kg ，24 h后行心肌IR；Mor＋5‐HD组（E组），腹腔注射吗啡3 mg／kg ，24 h后行IR ，但在缺血前10 min腹腔注射5‐HD 5 mg／kg。各组于缺血前、缺血25 min、再灌注30、60、120 min记录大鼠心率（HR ）、平均动脉压（MAP）。心肌缺血再灌注结束即刻采用 EB ／TTC双重染色，称重法测定心肌梗死面积，比较各组心肌梗死面积发生情况。【结果】和A组相比，B组心肌梗死面积明显减小，且差异有显著性（ P＜0．05）；C组、D组和E组心肌梗死面积无明显差异（ P ＞0．05）。【结论】HO‐1和mitoKATP通道参与了吗啡预处理的延迟性心肌保护作用；mitoKATP通道既是启动因子又是效应器。

摘要： 子痫前期是妊娠期最常见的疾病之一,其不仅能导致胎盘早剥、妊娠妇女肝肾功能受损、早产、胎儿生长受限等,也是孕产妇及围生儿死亡的常见原因,由于其严重危害母儿健康,其发病机制一直是产科领域的研究热点.子宫螺旋动脉重塑障碍、血管内皮受损、遗传、免疫失衡及炎症反应等与子痫前期关系密切,其中广泛的血管内皮受损是该病发生的关键环节.近年研究发现,氧化应激及可溶性血管内皮因子(sEng)、可溶性血管内皮生长因子受体1(sFlt-1)升高是导致血管内皮受损的主要原因,而血红素加氧酶1(HO-1)是一种可诱导的抗氧化酶,HO-1及其催化代谢产物一氧化碳(CO)、胆红素不仅对正常妊娠的胎盘形成、胎盘功能的维持及胎儿的生长发育具有重要保护作用,还能通过激活胎盘保护型信号通路、合成还原型烟酰胺腺嘌呤二核苷酸磷酸(NADPH)还原酶来抑制子痫前期妇女体内的氧化应激以及通过降低血管内皮损伤因子如sEng、sFlt-1对血管内皮的损害、促进血管内皮保护因子如血管内皮生长因子(VEGF)对血管的保护作用来抑制子痫前期的发生,推测HO-1及其催化代谢产物能够为子痫前期预防及治疗带来新的突破.

摘要： 本发明公开了一种脱血红素猪血血红蛋白酶解物和血红素肽的制备方法。该方法以猪血红细胞为原料，通过溶血、复合蛋白酶酶解、等电离心分离制备脱血红素猪血血红蛋白酶解物及血红素肽。本发明反应条件温和，脱血红素酶解物的蛋白质回收率达80～85%，血红素肽中血红素回收率达到90～93%以上，血红素含量达到25～30%。两种产物均无不良风味，可直接添加于食品。

摘要： 本申请提供了一种基于滚环扩增的串联G‑四链体‑血红素DNA酶免标记信号放大方法，包括以下步骤：1)采用亲和洗脱液和生物素化捕获探针对链霉亲和素功能化微球进行处理，得到预处理微球；2)将样品基因组DNA进行循环扩增和纯化，得到环化DNA；3)将所述步骤1)得到的预处理微球和所述步骤2)得到的环化DNA混合后进行滚环扩增，得到滚环扩增产物；4)将所述步骤3)得到的滚环扩增产物与血红素结合，得到信号放大的滚环扩增产物，所述信号放大的滚环扩增产物形成放大的检测信号；所述步骤1)和步骤2)之间没有时间顺序限定。本发明的方法对沙门氏菌的检测限为0.03pmol/L，检测成本低、操作简单、灵敏度极高、检测快速且可通过肉眼判断样品中是否含有沙门氏菌。

摘要： 本发明公开了一种脱血红素猪血血红蛋白酶解物和血红素肽的制备方法。该方法以猪血红细胞为原料，通过溶血、复合蛋白酶酶解、等电离心分离制备脱血红素猪血血红蛋白酶解物及血红素肽。本发明反应条件温和，脱血红素酶解物的蛋白质回收率达80～85％，血红素肽中血红素回收率达到90～93％以上，血红素含量达到25～30％。两种产物均无不良风味，可直接添加于食品。

摘要： 本发明涉及血红素氧化酶-2在制备抑制器官移植免疫排斥制剂中的应用。本发明公开了血红素氧化酶-2及其基因在制备抑制器官移植免疫排斥反应制剂中的应用。本发明的制剂可用于抑制器官移植免疫排斥反应，提高器官移植的存活率，为治疗肝脏、肾脏和心脏等慢性终末期疾病提供了有效方法。

摘要： 本发明涉及一种扩增血红素氧化酶基因的方法，属于分子生物学和临床医学领域。本发明选择在GenBank上发表的HOX－1的编码基因，利用DNAman生物学软件进行同源性分析，根据保守序列设计了一对简并引物。以COPD吸烟患者和健康吸烟者的HOX－1基因组DNA作为模板，利用简并引物扩增得到蛋白酶编码基因的保守序列。本发明扩增得到的HOX－1蛋白酶基因多态性在中国西南地区汉族人与COPD的易感性有关，且携带HOX－1I类基因型(包含有L等位基因)的个体更易感COPD。本发明的方法具有快捷、简便、经济、结果更准确等优点。本发明得到的基因可指导易感COPD人群避免从事一些接触煤灰、粉尘等的工作，从而减少COPD的发病率，提高COPD的防治水平。

摘要： 在本发明及其研究中，我们通过重组腺相关病毒向器官移植物内导入抗氧化基因——血红素氧化酶－1(HO－1)，通过重组腺相关病毒载体的作用使血红素氧化酶－1在器官移植物内长期表达。通过本实验研究，我们希望知道长期表达HO－1基因对慢性移植排斥会有什么影响。在本研究中，我们应用重组腺相关病毒介导HO－1基因在移植物中长期表达，观察其对慢性排斥反应的影响。结果发现rAAV/HO－1可以预防移植物的动脉粥样硬化和间质纤维化。HO－1基因的长期稳定表达不但是延长移植物存活期的先决条件，而且可以防止移植物的动脉粥样硬化和间质纤维化。rAAV/HO－1对移植物的长期保护作用与显著下调移植物内的前炎症因子、生长因子和组织蛋白酶抑制剂的表达有关。我们的研究结果预示了rAAV/HO－1将成为临床器官移植中抑制慢性移植排斥的一种新的治疗方法。

摘要： 本发明公开了一种多肽--人亚铁血红素铜离子呼吸氧化酶亚基1－17.27,编码此多肽的多核苷酸和经DNA重组技术产生这种多肽的方法。本发明还公开了此多肽用于治疗多种疾病的方法,如疖,痈,皮肤鳞状细胞癌,骨(肉)瘤,神经系统功能紊乱等。本发明还公开了抗此多肽的拮抗剂及其治疗作用。本发明还公开了编码这种新的人亚铁血红素铜离子呼吸氧化酶亚基1－17.27的多核苷酸的用途。

摘要： 本发明涉及使用氧化氮(NO)、血红素加氧酶－1(HO－1)和血红素降解产物如一氧化碳(CO)、胆绿素、胆红素和铁治疗疾病。

摘要： 本申请提供了一种基于滚环扩增的串联G‑四链体‑血红素DNA酶免标记信号放大方法，包括以下步骤：1)采用亲和洗脱液和生物素化捕获探针对链霉亲和素功能化微球进行处理，得到预处理微球；2)将样品基因组DNA进行循环扩增和纯化，得到环化DNA；3)将所述步骤1)得到的预处理微球和所述步骤2)得到的环化DNA混合后进行滚环扩增，得到滚环扩增产物；4)将所述步骤3)得到的滚环扩增产物与血红素结合，得到信号放大的滚环扩增产物，所述信号放大的滚环扩增产物形成放大的检测信号；所述步骤1)和步骤2)之间没有时间顺序限定。本发明的方法对沙门氏菌的检测限为0.03pmol/L，检测成本低、操作简单、灵敏度极高、检测快速且可通过肉眼判断样品中是否含有沙门氏菌。

摘要： 一种采用次血红素六肽模拟酶的过氧化氢光度测定法，属于医学、食品、环境技术领域，方法是：1、检测原理，H2O2在DhHP‑6的催化下产生氧自由基，氧化的氯代苯酚体系显色。在分析仪测定反应前后吸光度值变化，计算出H2O2的量。2、试剂组成，①磷酸盐缓冲液，离子强度300mmol/L,pH7.7、②DhHP‑6、③4‑氨基安替比林、④氯代苯酚、⑤过氧化物酶。3、操作过程，①在37°C水浴中将试剂加入到3个试管中，1分钟后再将液体样品、标准液和水分别加入到各试管中，反应10分钟；②测定F、B、C吸光度值。通过比对，计算过氧化氢的量。有益效果是：具有灵敏度高、稳定性好及经济实用等特点，可对医药及食品、质监、环监等部门对过氧化氢量监测。