脓毒症大鼠急性肺损伤机制研究

目的探讨脓毒症大鼠急性肺损伤的机制。方法采用盲肠结扎穿孔术(CLP)建立大鼠脓毒症模型。健康成年雄性SD大鼠48只,随机分为假手术组、脓毒症组,每组24只。动物模型制备成功后,于术后3、12、24h检测肺组织匀浆标本黄嘌呤氧化酶(XO)、丙二醛(MDA)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)含量。光学显微镜下观察肺组织病理改变。结果术后3、12、24h假手术组XO分别为(2.4±0.3)U/g、(2.3±0.5)U/g、(2.4±0.4)U/g,MDA为(15.7±2.7)nmol/mg、(15.2±2.9)nmol/mg、(15.6±2.6)nmol/mg,SOD为(58.8±8.0)U/mg、(58.1±10.1)U/mg、(58.7±9.5)U/mg,GSH-Px为(33.2±5.4)U/mg、(32.5±7.0)U/mg、(33.1±6.3)U/mg;脓毒症组XO分别为(4.2±0.6)U/g、(5.5±0.7)U/g、(5.7±0.5)U/g,MDA为(29.3±5.7)nmol/mg、(36.3±6.6)nmol/mg、(41.4±7.3)nmol/mg,SOD为(43.3±7.0)U/mg、(41.8±6.9)U/mg、(38.2±7.4)U/mg,GSH-Px为(27.9±4.0)U/mg、(26.4±3.9)U/mg、(24.3±3.3)U/mg。与假手术组比较,脓毒症大鼠肺组织XO、MDA含量显著升高,SOD、GSH-Px含量显著降低,差异有统计学意义(P0.01)。结论脓毒症大鼠存在急性肺损伤,其机制可能与氧化应激相关。     

牛奶和辅酶Q10对丙烯腈致血管内皮功能紊乱的影响

目的 探讨牛奶或辅酶Q10预处理对丙烯腈致大鼠血管内皮功能紊乱的影响.方法 将80只大鼠分为4组:对照组、单纯丙烯腈组、牛奶组、辅酶Q10组.采用灌胃染毒法,对照组仅予玉米油(丙烯腈的溶剂,1 ml/100 g),其他3组予丙烯腈25 mg/kg染毒.牛奶组和辅酶Q10组在染毒前30 min分别给予牛奶、辅酶Q10预处理.染毒12周后检测血清及主动脉组织中诱导型一氧化氮合酶(iNOS)和内皮型一氧化氮合酶(eNOS)的活力.结果 单纯丙烯腈组、牛奶组、辅酶Q10组血清iNOS水平[(42.9±2.5)U/ml、(26.5±4.4)U/ml、(26.7±3.3)U/ml]比对照组[(21.9±1.6)U/ml,P＜0.05]升高.主动脉组织中iNOS在单纯丙烯腈组、牛奶组、辅酶Q10组[(0.812±0.008)、(0.773±0.019)、(0.622±0.013)U/mg蛋白]比对照组[(0.540±0.028)U/mg蛋白,P＜0.05]高;而辅酶Q10组的主动脉eNOS活力[(0.471±0.011)U/mg蛋白]高于对照组、单纯丙烯腈组和牛奶组[(0.371±0.029)、(0.380±0.016)、(0.425±0.020)U/mg蛋白,P＜0.05].结论 牛奶和辅酶Ql0可以缓解丙烯腈致血管内皮功能紊乱作用.

Abstract：

Objective To explore the influences of milk or coenzyme Q10 pretreatment to acrylonitrile on vascular endothelial functions in rats.Methods A total of 80 rats were randomly divided into 4 groups:control group(Con),acrylonitrile exposure group(ACN),milk pretreatment group (M + ACN)and coenzyme Q10 pretreatment group(Q10 + ACN).The experiment was conducted by the method of gavage exposure in rats.Control group was exposed to corn oil;acrylonitrile was administered to other three groups at the doses of 25 mg/kg.The M + ACN and Q10 + ACN groups were pretreated by milk or coenzyme Q10 at 30 minutes before acrylonitrile exposureAfter a 12-week exposure,the activities of inducible nitric oxide synthase(iNOS)and endothelial nitric oxide synthase(eNOS)were measured in serum and aortal tissues.Results As compared with Con group[(21.9 ± 1.6)U/ml],the activity of blood serum iNOS was higher in ACN,M + ACN and Q10 + ACN groups[(42.9 ± 2.5)U/ml,(26.5 ± 4.4)U/ml,(26.7 ±3.3)U/ml,P＜0.05].As compared with Con group[(0.540 ± 0.028)U/mgprot],the activity of aortal iNOS was higher in ACN,M + ACN and Q10 + ACN groups[(0.812 ± 0.008),(0.773 ± 0.019),(0.622 ±0.013)U/mgprot,(P ＜0.05)].Furthermore the activity of aortal eNOS in Q10 + ACN group[(0.471 ±0.011)U/mgprot]was higher than Con,ACN or M +ACN group[(0.371 ±0.029),(0.380 ±0.016),(0.425 ±0.020)U/mgprot,P ＜0.05].Conclusion Chronic administration of ACN by gavages results in vascular endothelial dysfunctions.Milk and coenzyme Q1o pretreatment reduce this effect in rats.     

解偶联蛋白2在PM2.5所致的氧化应激损伤心肌细胞中的作用机制探讨

目的:初步探讨解偶联蛋白2(UCP2)在PM2.5致心肌细胞氧化应激损伤中的作用。方法:培养大鼠心肌细胞株H9C2细胞,分为NC组、PM2.5组、PM2.5+si RNA组三组,分别给予常规的培养基、PM2.5培养基、si RNA+PM2.5培养基刺激,48 h后比色法检测线粒体的活性氧(ROS)、丙二醛(MDA)含量、谷胱甘肽(GSH)含量以及超氧化物歧化酶(SOD)活性。结果:PM2.5组心肌细胞内ROS、MDA含量、GSH含量、SOD活性分别为(69.2±6.3)U/Well、(68.33±1.96)nmol/mgprot、(533.05±10.83)mg/gprot、(50.37±1.98)U/mgprot,PM2.5+si RNA组心肌细胞内ROS(90.2±6.2)U/Well明显增多、MDA含量(88.44±1.27)nmol/mgprot明显升高,GSH含量(421.17±16.90mg/gprot)明显减少,SOD活性(30.09±2.02)U/mgprot明显降低。三组两两比较差异均有统计学意义(P<0.05)。结论:PM2.5可以通过氧化应激途径损伤心肌细胞,RNA干扰UCP2基因表达后,PM2.5致氧化应激增强所介导的心肌细胞损伤加剧,这提示UCP2在PM2.5致氧化应激心肌损伤过程中可能起着保护性作用。     

参附注射液对糖尿病大鼠缺血再灌注损伤心肌DJ-1表达的影响

目的：观察参附注射液(SFI)对糖尿病大鼠缺血再灌注损伤(IR)心肌DJ-1表达的影响,并探究其对糖尿病IR心肌保护作用的分子机制。方法健康雄性SD大鼠腹腔注射60 mg/kg链尿佐菌素制备糖尿病模型。取糖尿病造模成功大鼠30只,随机数字表法分为三组(n=10)：假手术组(S组)、IR组、IR+SIF组。心肌IR模型采用结扎冠脉左前降支(LAD)30 min后松开120 min制备,S组只穿线包绕LDA而不结扎。IR+SFI组开胸前SFI以10 mL·kg-1·h-1持续泵注,开胸后以3 mL·kg-1·h-1持续输注至手术结束,其余两组泵注等量晶体液。检测SD大鼠心梗面积、血清肌酸激酶-MB(CK-MB)含量、心肌DJ-1表达,超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量。结果与S组比较,IR组大鼠的心梗面积[(49.0±5.3)%vs (0.0±0.0)%],CK-MB [(1982±275) U/L vs (1076±262) U/L]、MDA [(13.1±1.9) nmol/mg vs (7.6±1.1) nmol/mg]含量显著增加,差异均有统计学意义(P<0.05),而DJ-1表达[(0.65±0.14) vs (1.0±0.0)]和SOD活性[(79.0±19.3) U/mg vs (143±15.4) U/mg]显著降低,差异均具有统计学意义(P<0.05);与IR组相比,IR+SFI组大鼠的心梗面积[(35.7±5.3)%vs (49.0±5.3)%],CK-MB [(1364±228) U/L vs (1982±275) U/L]和MDA [(7.3±1.25) nmol/mg vs (13.1±1.9) nmol/mg]含量显著降低,差异均有统计学意义(P<0.05),而DJ-1表达[(0.9±0.14) vs (0.65±0.14)]和SOD活性[(119.4±14.6) U/mg vs (79.0±19.3) U/mg]显著降低,差异均有统计学意义(P<0.05)。结论 SFI能显著降低糖尿病心肌IR损伤的易损性,其机制可能与其上调心肌DJ-1表达、增强内源性抗氧化应激有关。     

醛酮类物质染毒对小鼠肺脏抗氧化能力的影响

目的:通过模拟生物燃料烟气中主要醛酮类物质染毒小鼠观察其对小鼠肺脏抗氧化能力的影响.方法:选用小鼠40只,随机分为2组:实验组和对照组,每组20只,雌雄各半.取甲醛(0.0663 mg)、乙醛(0.1181 mg)、苯甲醛(0. 147 mg)、丙酮(0. 609 mg)加水至1 000 ml,置于超声波雾化器中向已放入20只小鼠的染毒柜喷雾,每天喷雾1次,每次5 h,连续13 d.对照组放于另一柜中,除喷雾蒸馏水外,其它同实验组.以化学分析方法检测小鼠外周血和肺组织中丙二醛(MDA)含量、超氧歧化酶(SOD)与谷胱甘肽过氧化物酶(GSH-Px)活力.结果:染毒小鼠肺脏MDA含量明显高于对照组[(17.88±2.08)nmol/mgprot vs (8.00±2.89) nmol/mgprot,P《0.001)]; SOD与GSH-Px活力明显降低[(24.08±2.04)NU/mgprot vs (38.77±8.95) NU/mgprot;(28.75±4.82) U/mgprot vs (34.76±1.43) U/mgprot],P《0.001),染毒小鼠外周血中MDA含量变化不明显[(6.06±1.91) nmol/mgprot vs (5.62±2.54) nmol/mgprot,P》0.05],但SOD与GSH-Px活力明显低于对照组[(81.78±8.83) NU/mgprot vs(108.63±14.13) NU/mgprot;(50.94±3.20) U/mgprot vs(60.46±4.14) U/mgprot,P《0.001].结论:模拟生物燃料烟气中主要醛酮类物质染毒小鼠可影响肺脏的抗氧化能力.     

吡格列酮对2型糖尿病患者氧化应激的影响

目的 探讨吡格列酮对2型糖尿病患者氧化应激的影响.方法 收集于本院就诊的2型糖尿病患者130例,随机分成对照组和吡格列酮组,每组65例.对照组给予门冬胰岛素30和二甲双胍控制血糖;吡格列酮组使用门冬胰岛素30、二甲双胍和吡格列酮(15 mg/d)降糖治疗,均治疗3个月.治疗前后检测并比较两组患者血清氧化应激指标:超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA).结果 治疗后吡格列酮组患者血清SOD、GSH-Px活性[(54±18)U/ml和(82±18)U/ml]较治疗前[(39±16)U/ml和(71±22)U/ml]显著升高,MDA水平[(2.6±1.7)nmol/ml]较治疗前[(3.8±2.3)nmol/ml]显著降低,差异有统计学意义(P＜0.05),且治疗后吡格列酮组上述3种指标与对照组[(42±18)U/ml、(73±19)U/ml和(3.5±1.8)nmol/ml]比较,差异有统计学意义(P＜0.01).结论 吡格列酮能提高2型糖尿病患者血清SOD和GSH-Px活性,降低MDA水平,而且吡格列酮的这种作用不依赖于降糖作用.     

Caveolin-1 is involved in radiation-induced ERBB2 nuclear transport in breast cancer cells

This study examined the radiation-induced ERBB2 nuclear transport in the BT474 breast cancer cell line and the relationship between caveolin-1 and radiation-induced ERBB2 nuclear transport. The BT474 cells were treated with herceptin (200 nmol/L), PP2 (a caveolin-1 inhibitor, 100 nmol/L) and irradiation combined or alone. Confocal microscopy was used to observe the nuclear import of ERBB2 and caveolin-1 after irradiation. Western blotting was employed to detect the expression of ERBB2, caveolin-1 and DNA-PKcs after irradiation, and immunoprecipitation to identify the ERBB2 and caveolin-1 complex before perinuclear ERBB2 localization. Confocal microscopy showed the transport of ERBB2 and caveolin-1 from the cell membrane to the nucleus 15 min after irradiation and the proteins accumulated at the perinuclear region within 45 min. Western blotting revealed that the expression levels of ERBB2, caveolin-1 and DNA-PKcs were increased after irradiation and reached a peak 45 min later. Both herceptin and PP2 treatments were found to decrease ERBB2 expression. An immune complex composed of ERBB2 and caveolin-1 was found in the herceptin group after irradiation. It was concluded that after irradiation, ERBB2 may be transported from the cell membrane to the nucleus and activate DNA-PKcs to trigger DNA double-strand break (DSB) repair; caveolin-1 may participate in this process. Treatments involving the downregulation of caveolin-1 may increase the radio-sensitization of breast cancer cells.     

丹红注射液对脓毒症大鼠心肌组织氧自由基及HMGB1表达的影响

目的观察丹红注射液对脓毒症大鼠心肌损伤的保护作用,探讨其可能作用机制。方法24只雄性Wistar大鼠随机分为正常组、假手术组、模型组、丹红组,每组6只。盲肠结扎并穿孔(CLP)法建立脓毒症大鼠动物模型,观察各组心肌组织超微结构改变,心肌组织丙二醛(MDA)、超氧化物岐化酶(SOD)和高迁移率族蛋白1(HMGB1)含量的变化。结果 CLP术后24h,与手术组比较,模型组、丹红组大鼠心肌组织MDA含量[(5.5706±1.3251)μ/mg prot、(3.9900±1.0559)μ/mg prot比(1.1506±0.1771)μ/mg prot]、HMGB1蛋白表达量(0.6074±0.0504、0.5010±0.1049比0.1427±0.0345)升高,差异有统计学意义(P0.05),而模型组、丹红组大鼠心肌组织SOD活力[(10.5276±3.0568)nmol/mg prot、(15.5129±3.4425)nmol/mg prot比(20.5604±3.1312)nmol/mg prot]降低,差异有统计学意义(P0.05);与模型组比较,丹红组大鼠心肌组织MDA含量表达降低[(3.9900±1.0559)μ/mg prot比(5.5706±1.3251)μ/mg prot,P0.05],SOD活力升高[(15.5129±3.4425)nmol/mg prot比(10.5276±3.0568)nmol/mg prot,P0.05],心肌组织HMGB1表达量降低(0.5010±0.1049比0.6074±0.0504,P0.05);相同时间点心肌超微结构提示模型组大鼠心肌细胞线粒体肿胀,部分空泡变性;丹红组心肌细胞损伤轻于模型组。结论丹红注射液对脓毒症大鼠心肌损伤有一定程度的保护作用,其作用机制可能与清除氧自由基,降低HMGB1含量有关。     

Effects of the Combined Use of Benazepril and Valsartan on Apoptosis in the Kidney of Rats with Adriamycin-induced Nephritic Gomerulosclerosis

The effects of the combined use of angiotensin converting enzyme inhibitor (ACEI) benazepril and angiotensin 11 type 1 receptor antagonist (AT1RA) valsartan on apoptosis and the expression of apoptosis-related proteins Fas and FasL in the kidney of rats with adriamycin-induced nephritic glomerulosclerosis was investigated. Uninephrectomy and the injection of adriamycin induced the rat model of glomerulosclerosis. Benazepril (6 mg/kg), valsantan (20 mg/kg), or benazepril (3 mg/kg) plus valsantan (20 mg/kg) was respectively delivered daily by gavage to the rats in three treatment groups for 12 weeks. Apoptosis was examined by means of terminal-deoxynucleotidyl transferase mediated d-UTP nick end labeling (TUNEL). Immunohistochemistry was adopted to detect the expression of Fas and FasL. Software of pathological analysis quantitated the levels of Fas and FasL. The results showed that as compared with those in the control group, the kidneys in the model group had more severe glomerulosclerosis, much more apoptotic cells and higher levels of expression of Fas and FasL. The degree of glomerulosclerosis, the number of apoptotic cells and the levels of expression of Fas and FasL were reduced by benazepril and valsartan. The combined use of benazepril and valsartan had the best therapeutic effect. It was concluded that benazepril and valsartan could suppress the excessive apoptosis of kidney cells by lowering the expression of the apoptosis-related proteins Fas and FasL, so as to postpone the process of glomerulosclerosis. The combined use of benazeoril and valsartan has better theraoeutic effect.     

酒精性心肌病大鼠中成腱蛋白表达与心肌纤维化的关系

目的 探讨酒精性心肌病心肌中成腱蛋白X(TN-X)表达以及与心肌重构和心肌纤维化的关系.方法 实验动物分为酒精喂养组(酒精组)和对照组,6个月后检测心脏结构、功能和心肌胶原含量,免疫组化法和Westem免疫印迹法测定心肌TIN-X、信号转导蛋白(smad)3和smad-7的蛋白表达.结果 6个月后,酒精组左室射血分数(LVEF)和左室短轴缩短率(FS)低于对照组、左室舒张末期内径(LVEDd)和胶原容积分数(CVF)高于对照组(均P＜0.05).酒精组TN-X和smad-3蛋白表达(88%±6%、82%±8%)明显高于对照组(33%±11%、29%±8%);smad-7蛋白表达(37%±9%)低于对照组(79%±10%)(均P＜0.01).TN-X表达与LVEF、FS和smad-7呈显著负相关,与LVEDd、CVF和smad-3呈显著正相关(均P＜0.01).结论 TN-X在酒精性心肌病中表达增加,可能促进酒精性心肌病心肌纤维化和心肌重构.     

Effects of chrysotile fibres lipid peroxides reaction in exposed female workers and in rat lung macrophages

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同型半胱氨酸在酒精性心肌病发病中的作用

目的 探讨同型半胱氨酸(Hcy)在酒精性心肌病(ACM)发病中的作用.方法 Wistar大鼠分为两组,酒精组(41只)和对照组(28只).酒精组通过随意饮用白酒及定量灌胃6个月建立ACM模型.对照组以水代酒.动态检测各组大鼠心脏功能、测定血浆Hcy水平、光镜观察心室肌组织病理改变、免疫组化法检测心肌组织基质金属蛋白酶9(MMP-9)表达以及Masson染色观察心肌纤维化程度.结果 大量饮酒4个月时,酒精组较对照组左室舒张末期内径增大(7.0 mm±0.6 mm比5.0 mm±0.4 mm,P＜0.05),左室射血分数(52%±8%比78%±4%,P＜0.05)和左室短轴缩短率降低(31%±3%比47%±2%,P＜0.05),6个月时上述指标改变更明显(P＜0.01);酒精组血浆Hcy水平自2个月起明显升高[(18.1±3.1)μmol/L比(9.8±2.1)μmol/L,P＜0.01],4个月[(26.3±4.0)μmol/L,P＜0.05]、6个月更高[(30.9±3.6)μmol/L,P＜0.05].4、6个月酒精组MMP-9表达高于实验前(0.161%±0.019%、0.263%±0.014%比0.050%±0.008%,P＜0.01),4、6个月酒精组Masson染色分析显示心肌胶原纤维高于实验前(10.23%±1.20%、22.41%±2.57%比0.50%±0.09%;P＜0.01).在ACM发病过程,酒精组血浆Hcy与心肌组织MMP-9显著正相关(r=0.848,P＜0.01).结论 长期大量饮白酒可导致血浆Hcy水平显著升高,并通过增加心肌组织MMP-9的表达参与心脏重构及酒精性心肌病的发病.

Abstract：

Objective To explore the role of homocysteine in the pathogenesis of alcoholic cardiomyopathy. Methods A total of 69 male Wistar rats were randomly assigned into two groups: alcoholfed group and the control. Cardiac function was assessed by pulse Doppler. Plasma Hcy levels were examined using automatic biochemical instrument (chemiluminescence). The protein expression of MMP-9 was evaluated using immunohistochemical method, and collagen fiber of myocardium was quantitative analyzed by Masson stain. Results After heavy drinking, the LVEDd of alcohol-fed group were larger than the control group [( 7. 0 ± 0. 6) mm vs ( 5.0 ± 0. 4 ) mm, P ＜ 0. 05], the LVEF and FS were lower in the 4thmonth(52%±8% vs 78%±4%,31%±3% vs 47%±2%,P ＜0.05), the data changed more significantly (P ＜0. 01 ) in the 6th month. The level of plasma Hcy from alcohol-fed group was significantly higher from the 2nd month than that before the experiment [( 18. 1 ± 3. 1 ) μ mol/L vs ( 9. 8 ± 2. 1 )μ mol/L,P ＜ 0. 01], and it was higher in 4th month than that in 2nd month [(26. 3 ± 4. 0) μmol/L vs (18. 1 ±3. 1) μ mol/L,P＜0.05], it was highest in 6 months. After 4-month and 6-month drinking, the expression of MMP-9 protein from alcohol group was higher than before the experiment (0. 161%±0. 019%,0. 263%±0. 014% vs 0. 050% ± 0. 008%, P ＜ 0. 0l ). Masson staining showed myocardial collagen of alcohol group was more after 4-month and 6-month drinking than those before the experiment ( 10. 23% ±1.20% vs 0. 50%±0. 09%; 22. 41% ± 2. 57% vs 0. 50% ± 0. 09%, P ＜ 0. 01 ). Plasma Hcy and cardiac tissue MMP-9 is a significant positive correlation ( r = 0. 848, P ＜ 0. 01 ). Conclusion Long-term and large drink liquor can lead to plasma Hcy levels significantly increased, and participate cardiac remodeling and the pathogenesis of ACM through increasing the expression of myocardial tissue MMP-9 protein.     

红景天总黄酮对大鼠心肌成纤维细胞增殖的抑制作用

目的:研究红景天总黄酮对转化生长因子β1(TGF-β1)诱导的新生大鼠心肌成纤维细胞(CFB)增殖的抑制作用,探讨红景天总黄酮改善心肌纤维化的作用机制。方法:采用TGF-β1(5 μg·L^-1)诱导大鼠CFB增殖,构建心肌纤维化细胞模型。将正常培养的大鼠CFB分为对照组、模型组和25、50及100 mg·L^-1红景天总黄酮组。给药48 h后,MTT法检测细胞活力,ELISA法检测细胞培养上清液中Ⅰ型胶原蛋白(ColⅠ)和Ⅲ型胶原蛋白(Col Ⅲ)的水平,检测上清液中总超氧化物歧化酶(T-SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性以及丙二醛(MDA)、谷胱甘肽(GSH)的水平。结果:MTT法检测,与对照组比较,模型组细胞活力明显升高(P<0.01);与模型组,红景天总黄酮各剂量组细胞活力均明显下降(P<0.05)。T-SOD和MDA检测,与对照组比较,模型组细胞T-SOD活性下降(P<0.05),MDA水平明显升高(P<0.05);与模型组比较,50和100 mg·L^-1组细胞T-SOD活性明显升高(P<0.01),25和50 mg·L^-1红景天总黄酮组MDA水平明显下降(P<0.05)。GSH-Px和GSH检测,与对照组比较,模型组细胞GSH-Px活性及GSH水平均明显降低(P<0.01);与模型组比较,红景天总黄酮各剂量组细胞GSH-Px活性和GSH水平均升高(P<0.05)。ColⅠ和Col Ⅲ水平测定,模型组ColⅠ和Col Ⅲ水平明显升高(P<0.01);与模型组比较,红景天总黄酮各剂量组细胞2种蛋白水平均明显下降(P<0.05)。结论:红景天总黄酮可以抑制大鼠CFB的增殖,并可能经抗氧化应激途径改善心肌纤维化。     

乙酰半胱氨酸对大鼠酒精性肝病的保护作用研究

目的:探讨乙酰半胱氨酸在改善大鼠酒精性肝损伤中的作用。方法:采用酒精灌胃法建立大鼠酒精性肝病模型,同时以乙酰半胱氨酸300mg/kg,进行干预,每日1次。第12周末处死大鼠,留取血、肝组织标本,检测大鼠血清丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)、丙二醛(MDA)和超氧化物歧化酶(SOD)含量,并观察光镜下肝组织病理学改变。结果:酒精模型组动物血清ALT、AST、MDA值分别为76.50±8.70U/L,188.10±24.2U/L和20.60±3.60nmol/ml,较正常对照组升高(P<0.05),SOD值为196.12±24.03U/L,较正常对照组明显降低(P<0.01);同时模型组大鼠肝组织可见大量脂滴浸润和炎症改变。而乙酰半胱氨酸组动物血清ALT、AST、MDA值分别为49.40±9.61U/L,150.60±26.90U/L和8.90±1.41nmol/ml,较酒精模型组明显降低(P<0.01),SOD值为279.9±7.9U/L,较酒精模型组明显升高(P<0.01),乙酰半胱氨酸组肝组织仅见少数肝细胞肿胀及少量脂滴浸润。结论:乙酰半胱氨酸可通过抗氧化作用减轻酒精性肝损伤。     

老年重症患者术中应用自由基清除剂依达拉奉的多中心疗效分析

目的 观察老年重症患者手术中应用依达拉奉对预后的影响.方法 2008年7月1日至9月30日在北京朝阳医院、北京同仁医院、北京安贞医院和卫生部北京医院4家医院的400例老年重症手术患者按随机数字表法分为试验组与对照组,各200例.麻醉开始前试验组患者静脉泵入依达拉奉(60mg/40 ml)直至手术结束,对照组以等量生理盐水代替.分别于桡动脉穿刺后、手术开始后1 h及缝皮前检测超氧化物歧化酶(SOD)与丙二醛水平,记录术中情况及术后病死率、总住院日、重症监护病房(ICU)停留时间、术后机械通气时间与术后并发症情况.其中行不停跳冠状动脉旁路移植术患者于术前和术后24 h检查肌钙蛋白Ⅰ(cTn Ⅰ)与左室射血分数(LVEF).结果 试验组手术开始后1 h与缝皮前SOD水平均高于对照组[(87±14)U/ml比(78±14)U/ml,(83±13)U/ml比(77±14)U/ml,P＜0.01、＜0.05];丙二醛则均低于对照组[(11±5)nmol/L比(14±7)nmol/L,(11±5)nmol/L比(14±6)nmol/L,P＜0.05、＜0.01].术中低血压需持续应用血管活性药物支持者对照组多于试验组(37例比19例,P＜0.01),试验组总住院日、ICU住院日都短于对照组[(21±9)d比(23±9)d,(10±7)d比(13±9)d,均P＜0.05],行不停跳冠状动脉旁路移植术患者试验组术后cTn Ⅰ和LVEF与术前和对照组相比差异均有统计学意义(均P＜0.05).结论 老年重症患者术中应用依达拉奉可防止丙二醛升高、SOD下降,降低术中低血压发生率,减少老年重症患者总住院日与ICU住院日.特别是行不停跳冠状动脉旁路移植术患者术中应用依达拉奉,术后cTn Ⅰ与LVEF测量值试验组与术前和对照组相比都有明显改善.

Abstract：

Objective To observe the effects of intraoperative application of radical scavenger edaravone in severe elderly cases. Methods A total of 400 severe elderly patients scheduled for surgery were randomly assigned to receive edaravone 60 mg/40 ml ( Group Y) or an equal volume of normal saline (Group C). The arterial blood samples were harvested at immediately after pricking, 1 hour after the beginning of surgery and before saturation to determine the levels of superoxide dismutase (SOD) and malondialdehyde (MDA). The operative duration, fluid volume, blood loss, blood transfusion volume,urine output, intraoperative adverse events, mortality rate, total hospital stay, intensive care unit (ICU)stay, postoperative mechanical ventilation time and complications were recorded. Patients undergoing offpump coronary artery bypass graft (OPCABG) were evaluated for troponin Ⅰ (cTn Ⅰ ) and left ventricular ejection fraction (LVEF) before and after 24 hours of surgery. Results SOD was higher and MDA lower in Group Y than those in Group C at 1 hour intraoperation and before saturation[SOD: (87 ± 14)U/ml vs(78 ±14)U/ml, (83±13)U/mlvs(77±14)U/ml, P＜0.01, ＜0.05; MDA : (11 ±5)nmol/Lvs(14±7)nmol/L,( 11 ± 5 ) nmol/L vs ( 14 ± 6) nmol/L, P ＜ 0. 05, ＜ 0. 01]. There were more intraoperative hypotension cases requiring a continuous application of vasoactive drugs in Group C(37 cases vs 19 cases),total hospital stay[(21 ±9 )d vs (23±g)d, P＜0.05] and ICU stay[(10±7)dvs (13±9)d, P＜0. 05] were also longer. Postoperative cTn Ⅰ and LVEF of Group Y significantly improved in OPCABG cases ( all P ＜ 0. 05 ). Conclusion The intraoperative application of edaravone in severe elderly patients may prevent MDA increase and SOD decrease and reduce free radical damage. Especially in OPCABG patients,cTn Ⅰ and LVEF improve significantly.     

丹参川芎嗪注射液治疗早期高血压肾病的疗效以及对氧化应激的影响

探讨丹参川芎嗪注射液治疗早期高血压肾病的疗效以及对氧化应激的影响。方法方便选取该院自2015年1月—2015年6月收治的78例早期高血压肾病患者按照随机数字表法分为对照组和研究组,每组39例。对照组患者给予黄葵胶囊治疗,研究组患者在对照组治疗基础上加用丹参川芎嗪注射液治疗,14天为一个疗程,共进行两个疗程的治疗。比较两组患者治疗前后血清β2-微球蛋白(β2-MG)、血清胱抑素C(Cys-C)、血清超氧化物歧化酶(SOD)及丙二醛(MDA)水平差异。结果治疗前对照组与研究组血β2-MG和Cys-C水平分别为(3.89±0.45)、(5.43±0.36)mg/L和(3.92±0.63)、(5.52±0.43)mg/L,治疗后对照组与研究组血β2-MG和Cys-C水平分别为(1.99±0.32)、(1.55±0.26)mg/L和(1.16±0.46)、(0.89±0.37)mg/L,治疗后两组血β2-MG和Cys-C水平均较前明显降低(与同组治疗前相比,均P﹤0.05),且研究组降低更为明显(与对照组治疗后相比,均P﹤0.05)。治疗前对照组与研究组血SOD和MDA水平分别为(29.34±4.58)U/mL、(8.06±1.25)nmol/mL和(29.64±5.04)U/mL、(8.14±1.34)nmol/mL,治疗后对照组与研究组血SOD和MDA水平分别为(42.85±6.67)U/mL、(4.58±0.97)nmol/mL和(62.57±9.04)U/mL、(2.84±0.64)nmol/mL,治疗后两组血SOD水平较前均明显升高而MDA水平均明显降低(与同组治疗前相比,均P﹤0.05),且研究组变化更为明显(与对照组治疗后相比,均P﹤0.05),差异均有统计学意义。结论丹参川芎嗪注射液能够明显减轻早期高血压肾病患者体内的氧化应激程度,保护肾功能,提高治疗效果,值得在临床中推广应用。     

L-精 氨酸对病理性心肌肥大抑制作用的研 究

目的观察L-精氨酸对心肌肥厚的保护作用及相关机制。方法雄性Wistar大鼠36只,随机分为3组,每组各12只：对照组、模型组（ISO组）、L-精氨酸治疗组。皮下注射异丙肾上腺素（ISO）复制大鼠心肌肥厚模型,检测心脏重量参数（心重／体重,左室重／体重）,心肌组织胶原含量,心房利钠肽（ANP）的转录水平,观察L-精氨酸对心肌肥大的影响;检测各组大鼠血清一氧化氮（NO）、一氧化氮合酶（NOS）、丙二醛（MDA）和乳酸脱氢酶（LDH）含量。结果L-精氨酸治疗组心重／体重[（3．52±0．21）mg/g]和左室重／体重[（2．39±0．23）mg／g]均低于ISO组[心重／体重（3．89±0．25）mg／g,左室重／体重（2．67±0．26）mg／g）],差异有统计学意义（P〈0．05）。同时,L-精氨酸治疗组ANPmRNA表达相对值（1．2）低于ISO组（1．5）,差异有统计学意义（P〈0．05）;心肌间质胶原含量,L-精氨酸治疗组[（14．52±3．09）％]低于ISO组[（35．24±4．78）％],差异有高度统计学意义（P〈0．01）;L-精氨酸治疗组NO含量[（34．15±6．12）μmol／L]和NOS活性[（23．9±3．12）U／mL]与ISO组NO含量[（20．96±5．06）μmol／L]和NOS活性[（16．58±3．12）U／mL]比较均增加．差异有高度统计学意义（P〈0．01）;L-精氨酸治疗组MDA水平[（308．73±37．48）nmol／L]和LDH水平[（2065．35±347．46）U／L1与ISO组MDA含量[（389．63±42．85）nmol／L]和LDH水平[（3582．89±364．51）U／L）]比较均降低,差异有统计学意义（P〈0．05或P〈0．01）。结论早期给予L-精氨酸可以通过增加NO含量,减少MDA和LDH水平．减少心肌问质胶原沉积进而抑制病理性心肌肥大。     

大豆异黄酮对高脂血症大鼠体内SOD、GSH-Px活力及MDA含量的影响

目的研究大豆异黄酮(SI)对高脂血症大鼠体内SOD、GSH-Px活力及MDA含量的影响。方法50只Wister大鼠随机分为5组,分别接受基础饲料,高脂饲料及高脂饲料分别添加大豆异黄酮30mg/kg,90mg/kg和270mg/kg处理,实验6周。结果与正常对照组比较,高脂血症大鼠脑组织SOD活力,肝脑组织GSH-Px活力都有明显降低(P<0.01),肝脑组织中的MDA含量则升高;而添加SI的高脂血症大鼠体内SOD,GSH-Px活力有不同程度升高(P<0.05～P<0.01),而以低中剂量的SI作用显著(P<0.01),肝脑组织中的MDA含量降低。结论适宜剂量的SI对高脂血症大鼠体内SOD、GSH-Px活力有明显升高作用,而对MDA含量有明显降低作用。