牛磺酸对大鼠实验性脂肪肝的防治作用

牛磺酸能减轻肝脏脂质过氧化损伤，对酒精性脂肪肝有良好的防治作用。非酒精性脂肪肝（NAFL）的病理改变与酒精性脂肪肝有颇多相似之处，本实验观察牛磺酸对NAFL的影响，旨在为临床应用提供依据。     

染料木素对异丙肾上腺素所致大鼠心肌肥厚的保护作用

目的观察染料木素（GEN）对异丙肾上腺素所致大鼠心肌肥厚的保护作用及其对心肌组织抗氧化能力的影响。方法雄性SD大鼠48只,随机分为对照组,心肌肥厚模型组,溶剂组,低、中、高剂量GEN组。造模成功后第2天开始给予不同浓度的GEN、二甲基亚砜或生理盐水,连续14 d,末次给药后禁食12 h,取心脏称左心室质量,计算左心室质量参数,比色法测定心肌组织超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活性及丙二醛（MDA）含量,酶法测定血清及心肌组织乳酸脱氢酶（LDH）和肌酸激酶（CK）活性。结果心肌肥厚模型组左心室质量参数升高,心肌组织SOD和GSH-Px活性降低、MDA含量升高,血清LDH和CK活性升高,而心肌组织LDH和CK活性降低。GEN治疗组与心肌肥厚模型组相比各项指标均明显改善（P〈0.05）。结论 GEN可通过提高SOD和GSH-Px活性,提高心肌组织抗氧化能力,减少心肌酶的释放,从而起抗心肌肥厚作用。     

外源性硫化氢对大鼠全脑缺血-再灌注损伤的保护作用

目的研究外源性硫化氢对大鼠全脑缺血-再灌注损伤的保护作用及机制。方法健康雄性SD大鼠18只,随机分为假手术组(6只)及等渗盐水组(6只)、NaHS干预组(6只)。采用改良Pulsinelli四血管闭塞法制备大鼠全脑缺血-再灌注模型,在大鼠缺血-再灌注后,NaHS干预组立即腹腔注射NaHS(25μmol/kg),等渗盐水组立即腹腔注射等量等渗盐水,均1次/d,共注射7 d。假手术组仅暴露血管,不作其他处理。测定大鼠海马组织中超氧化物歧化酶(SOD)和丙二醛(MDA)的含量,通过硫堇染色观察海马CA1区神经元密度。结果①等渗盐水组[(133±12)kU/g]和NaHS干预组[(229±21)kU/g]的SOD水平低于假手术组[(297±24)kU/g],等渗盐水组的SOD水平低于NaHS干预组,差异均有统计学意义P<0.01)。②等渗盐水组[(55.4±6.2)μmol/g]和NaHS干预组[(22.5±7.9)μmol/g]的MDA水平高于假手术组[(6.1±1.3)μmol/g],等渗盐水组的MDA水平高于NaHS干预组,差异均有统计学意义P<0.01)。③等渗盐水组[(88±15)个/mm2]和NaHS干预组[(156±19)个/mm2]的神经元密度低于假手术组[(237±25)个/mm2],等渗盐水组的神经元密度低于NaHS干预组,差异均有统计学意义P<0.01)。结论外源性硫化氢对大鼠脑缺血-再灌注损伤具有保护作用。其机制可能与提高抗氧化酶活性、抗脂质过氧化损伤有关。     

促红细胞生成素的心肌保护作用

促红细胞生成素（EPO）主要由肾脏皮质髓质交界处的肾小管旁细胞分泌，是一种刺激骨髓造血的糖蛋白类激素，主要作用为促红系祖细胞分化及分裂为成熟红细胞，已广泛用于治疗慢性肾衰、恶性肿瘤、自身免疫性疾病伴发性贫血、骨髓增生异常综合征等疾病所致的贫血。近年来的研究已经证明，不仅肾小管周围间质细胞可以分泌EPO，     

老年大鼠肝中脂质过氧化作用与不饱和脂肪酸和抗氧酶

体内脂质过氧化程度随增龄而增加,而底物不饱和脂肪酸是否也随之变化？我们以老年和青年ＳＤ大鼠为实验对象,测定肝ＳＯＤ和ＣＡＴ活性以及ＭＤＡ的同时,检测了多不饱和脂肪酸（ＰＵＦＡ）的变化,拟探讨脂质过氧化的原因,为研究衰老机制提供实验依据。１　材料和方法１．１　实验动物　Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ健康大鼠,由河北省实验动物中心提供,老年大鼠２０月龄,青年大鼠３月龄,雌雄各半。１．２　试剂　ＳＯＤ试剂盒和ＭＤＡ试剂盒由南京建成生物工程研究所生产,标准脂肪酸,脂肪酸甲酯为Ｓｉｇｍａ公司产品,其他试剂均…     

促红细胞生成素与心肌保护

促红细胞生成素(erythropoietin,EPO)不只局限于治疗贫血.研究表明EPO及其受体在心血管系统有广泛表达,并参与心肌保护,可能与其抗凋亡机制及磷酸肌酸-3激酶、丝裂原活化蛋白激酶等信号通路介导相关.这将在以后为预防和治疗心肌缺血-再灌注损伤提供一条新的途径.     

姜黄素对紫外线氧化损伤人角质形成细胞的保护作用

目的 研究中波紫外线(UVB)照射所致人角质形成细胞的氧化损伤以及姜黄素(curcumin,Cur)对其损伤的抗氧化防护效果.方法 在角质形成细胞培养的基础上,实验组经30 mJ/cm2 UVB照射后,加入不同剂量的Cur(1.25 ～5.0 μg/ml),继续培养18 h,采用生物化学法测定细胞超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)和乳酸脱氢酶(LDH)活性及丙二醛(MDA)和活性氧(ROS)含量.结果 人角质形成细胞经UVB照射后加入Cur,与UVB照射组比较,ROS和MDA含量明显降低(P＜0.05),并显示Cur剂量-效应关系;而SOD和GSH-Px显著增高(P＜0.05),LDH活性显著降低(P＜0.05),均显示其剂量-效应关系.结论 Cur能增加细胞内抗氧化酶活性,抑制脂质过氧化反应,具有对UVB照射所致人角质形成细胞的氧化损伤防护作用.     

山莨菪碱对毒蕈所致大鼠急性肾损伤的保护作用

随机将１７４只大鼠分为Ⅰ、Ⅱ、Ⅲ组，每组５８只动物。Ⅰ组：用等渗盐水灌胃；Ⅱ组：用毒蕈匀浆液灌胃；Ⅲ组：毒蕈匀浆液灌胃同时腹腔注射山莨菪碱注射液，观察肾脏生化和形态学改变。Ⅱ组灌胃后６ｈ肾皮质自由基有关指标出现明显变化，肾近曲和远曲小管出现超微结构病变，２４ｈ后出现光镜下病变，尿钠、钾排泄增加，尿渗透压降低。Ⅲ组灌胃后１２ｈ肾皮质匀浆自由基有关指标出现异常变化，肾近曲和远曲小管出现超微结构病变，晚     

重组人促红细胞生成素对瓣膜置换术患者心肌保护作用

目的:探讨重组人促红细胞生成素(rHuEPO)预处理对体外循环下行二尖瓣置换术患者的心肌保护作用及其可能的机制.方法:选择择期在体外循环下行二尖瓣置换术的风湿性心脏病患者30例,随机分为实验组和对照组.实验组患者从术前3 d 起,皮下注射rHuEPO 200 IU/kg,1次/d.2组其他处理条件相同.于术前及术后3 d测定血常规.于术前,主动脉开放后2 h、6 h、12 h及24 h测定血清心肌酶谱及肌钙蛋白I(cTnI)的水平.结果:术前、术后血常规无显著变化.实验组在主动脉开放后各时间点血清心肌酶谱及肌钙蛋白水平显著低于对照组,差异具有统计学意义( P＜0.05).结论:rHuEPO预处理 (皮下注射)能减轻二尖瓣置换术患者的血清心肌酶及肌钙蛋白表达,具有显著的保护心肌作用.     

粉防己碱对大鼠顿抑心肌脂质过氧化的作用

本实验探讨了粉防已碱(Tetrandrine,Tet)对心肌顿抑(MS)时心肌丙二醛(MDA)含量的影响.结果:对照组MDA为116.3±11.2nmol/g蛋白,心肌缺血15min时MDA含量仅轻度升高(P>0.05),而缺血15min+再灌注2h(MS)时则增加 2.4倍(P<0.01).心肌缺血前20min分别腹腔内给予Tet 64.2和96.3μmol/kg能显著减轻MS时MDA含量的升高,改善心功能.左室dp/dt_(max)与心肌MDA含量呈明显负相关(r=-0.89,P<0.01).结果表明:心肌脂质过氧化增强与MS的发生有关,Tet通过减轻心肌脂质过氧化对MS具有保护作用.     

冠脑益嗪对大鼠心肌缺血/再灌注损伤保护作用的机制

目的 :观察冠脑益嗪对大鼠心肌缺血 /再灌注损伤的影响 ,探讨其保护作用的机制。方法 :采用在体大鼠心肌缺血 /再灌注模型 ,于结扎冠状动脉前 3m in iv冠脑益嗪 ,观察在心肌缺血 /再灌注状态下心电图、心肌丙二醛（MDA）、超氧化物歧化酶 （SOD）、Ca2 +、游离脂肪酸 （FFA）及血清中肌酸激酶 （CK）、乳酸脱氢酶 （L DH）的变化。结果 :冠脑益嗪能显著降低缺血 /再灌注损伤引起的室性心律失常发生率 ,缩短持续时间 ;升高 SOD活性 ,减少 MDA生成 ;减少 Ca2 +在心肌组织内的聚积 ;亦能明显降低心肌 CK、L DH和 FFA的释放。结论 :冠脑益嗪对大鼠心肌缺血 /再灌注损伤的保护作用可能与保护氧自由基清除酶的活性 ,防止膜脂质过氧化及阻断钙内流有关     

左旋精氨酸对犬实验性冬眠心肌的保护作用

目的 :观察左旋精氨酸对冬眠心肌功能、代谢与结构的影响。方法 :30只犬短期冬眠心肌模型随机分为 3组 :A组 （n=14）灌注生理盐水 ;B组 （n=8）灌注左旋精氨酸 ;C组 （n=8）灌注 L- MNNA。结果 :3组间左心室舒张末期压、血乳酸、ATP含量及电镜下结构改变差异显著。左旋精氨酸组明显优于其他两组。结论 :左旋精氨酸可改善冬眠心肌、代谢与功能结构。     

Protective effects of melatonin against caustic esophageal burn injury in rats

Abstract:  Caustic ingestion is one of the most life-threatening events in the pediatric age group, which requires the immediate management and subsequent treatment of its most significant complication, i.e. alterations in esophageal structure. We investigated whether melatonin could reduce the esophageal burn damage induced by sodium hydroxide. It was assumed that melatonin could be effective because of its function as a direct free radical scavenger, its antioxidative actions and its ability to diminish tissue hydroxyproline (HP) levels. Esophageal burns were induced in male rats by the administration of 10% sodium hydroxide. Lipid peroxidation (LPO) products were then measured at the following times: 0, 1, 6, 24, 48 and 72 hr after treatment. Tissue HP concentrations in the injured area were assessed at 14 days after the administration of sodium hydroxide. The groups received either systemic melatonin or normal saline. There were two, non-ischemic, sham control groups treated with or without melatonin. LPO products, malondialdehyde (MDA) and 4-hydroxyalkenal (4-HDA), increased immediately after the administration of sodium hydroxide; this indicates the participation of free radicals in the development of damage. Melatonin diminished the oxidative response and the amount of HP in the late phase of the lesion. Melatonin reduced oxidative damage in the early phase of the esophageal burns induced by sodium hydroxide.     

Stabilizing effect of antioxidants and inhibitors of prostaglandin synthesis on after-contractions in Ca2+-overloaded myocardium

Summary Ca²⁺ overload followed by after-contractions was induced by perfusion of mammalian papillary muscles with O–K ₀ ⁺ , high Ca²⁺ solution. The effect of lipotrophic agents (dexamethasone, indomethacin) or free radical scavengers (-tocopherol, reduced glutathione, synthetic antioxidant) was tested at different stages of Ca²⁺ overloading processes. All the agents tested proved to be effective in attenuating the after-contractions. Activation of lipid peroxidation has been suggested as one of the possible molecular events underlying mechanical destabilization of Ca²⁺-overloaded myocardium.     

Experimental study of alternations in erythrocyte membrane lipid peroxidation and fluidity induced by high-cholesterol diet in rabbits

Background Animal models of hyperlipidemia were established by feeding rabbits with high-cholesterol diet, and the changes in structure and function of cell membrane in rabbits were also reduced by hyperlipidemia. Thus, the alternations in erythrocyte membrane lipid peroxidation （EMLP） and fluidity in rabbits induced by high-cholesterol diet were researched by us. Methods Fourteen rabbits were subjected to high-cholesterol diet （cholesterol 2 g/d） and the other 14 rabbits to common diet everyday for consecutive two months, plasma total cholesterol （TC）, and blood lipids as well as EMLP and fluidity were measured before and after the feeding. Results Compared with the feeding before, levels of TC and low density lipoprotein- cholesterol （LDL-C） were significantly raised, those of erythrocyte membrane low density lipoprotein- cholesterol （MLDL-C）, membrane conjugated diene （MCD）, erythrocyte malonaldehyde （RMDA） were significantly increased, while those of erythrocyte superoxide dismutase （R-SOD）, membrane fluidity （M-Flu） and membrane high density lipoprotein-cholesterol （MHDL-C） were significantly decreased in experimental group, and there were no changes in control group. Conclusions High-cholesterol diet induces lipid peroxidation and lower fluidity of erythrocyte membrane.     

促血小板生成素对小鼠药物性心肌损伤的保护作用

目的研究促血小板生成素（thrombopoietin,TPO）的心肌保护作用。方法小鼠分为对照组、多柔比星组、TPO组。多柔比星组及TPO组小鼠第1天予多柔比星20 mg/kg经腹腔注射;TPO组小鼠予TPO 15μg/kg,共3次经腹腔注射。第1天（多柔比星注射前）和第5天予小鼠做超声心动图检查;第5天取小鼠心肌组织行苏木素伊红染色,显微镜下评价心肌组织损伤程度。比较第1～8天内多柔比星组和TPO组存活率。结果与第0天相比,第5天多柔比星组的心率、每分钟心输出量、左心室短轴缩短率明显下降,差异有统计学意义（P〈0.05）;镜下见小鼠心肌组织明显损伤,说明药物性心肌损伤的模型能成功建立。相对多柔比星组,TPO组心率、每分钟心输出量、左心室短轴缩短率明显改善,差异有统计学意义（P〈0.05）。TPO组镜下评分示心肌损伤显著降低,8 d内的生存率明显高于多柔比星组,差异有统计学意义（P〈0.05）。结论 TPO对损伤心肌有保护作用。     

山莨菪碱对兔缺血再灌注后心室肌细胞L-钙离子通道电流的影响

目的研究山莨菪碱对兔在体缺血再灌注后心室肌细胞L-钙离子通道电流的影响,探讨山莨菪碱抗再灌注心律失常的细胞学离子机制。方法 45只新西兰大耳白兔按随机数字表法随机分为3组:缺血再灌注动物模型组(I-R组,结扎冠状动脉左前降支30min后再开放120min);山莨菪碱治疗组(Ani组,手术前1min给予动物耳缘静脉注射山莨菪碱5mg/kg);假手术对照组(只开胸不结扎血管)。采用酶解的方法分离缺血部位心室肌外膜单个心室肌细胞,应用全细胞膜片钳技术记录L-钙离子通道电流。结果 (1)I-R组、Ani组室性心动过速和心室颤动发生率均比对照组高,差异有统计学意义(P0.05);Ani组室性心动过速和心室颤动发生率明显低于I-R组,差异有统计学意义(26.7%(4/15)vs.40%(6/15),P0.05;6.7%(1/15)vs.26.7%(4/15),P0.05)。与对照组比较,I-R组心律失常评分升高,差异有统计学意义[(3.6±0.8)分vs.(1.1±0.3)分,P0.01];Ani组心律失常评分差异无统计学意义[(2.6±0.7)分vs.(1.1±0.3)分,P0.05]。(2)I-R组电流密度峰值(0mV)较对照组显著升高,差异有统计学意义[(-4.34±0.92)pA/pFvs.(-3.13±1.22)pA/pF,P0.05];Ani组电流密度峰值较I-R组明显下降,差异有统计学意义[(-3.25±0.79)pA/pFvs.(-4.34±0.92)pA/pF,P0.05]。Ani组电流密度峰值与对照组比较,差异无统计学意义[(-3.25±0.79)pA/pFvs.(-3.13±1.22)pA/pF,P0.05]。结论山莨菪碱可逆转缺血再灌注心室肌细胞的电重构,这可能是其降低心律失常发生率的细胞学离子机制。     

Protective effect of melatonin against alpha-naphthylisothiocyanate-induced liver injury in rats

The protective effect of melatonin against alpha-naphthylisothiocyanate (ANIT)-induced liver injury with cholestasis was examined in rats injected once with the toxicant (75 mg/kg body weight (BW)). In rats injected with ANIT alone, liver injury with cholestasis did not occur 12 hr after the injection but appeared at 24 hr, judging from the serum levels of marker enzymes and components. When melatonin (10 or 100 mg/kg BW) was orally administered to the ANIT-injected rats at 12 hr after the injection, the administered indoleamine dose-dependently prevented the formation of liver injury with cholestasis. In rats injected with ANIT alone, serum lipid peroxide (LPO) concentration increased 24 hr after the injection, while liver LPO concentration increased 12 hr after the injection and further increased at 24 hr. Myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration, in the liver of the ANIT-injected rats increased 12 hr after the injection and further increased at 24 hr. The oral administration of melatonin (10 or 100 mg/kg BW) to the ANIT-injected rats attenuated the increases in serum and liver LPO concentrations and liver MPO activity found at 24 hr after the injection in a dose-dependent manner. These results indicate that orally administered melatonin at pharmacological doses protects against ANIT-induced liver injury with cholestasis in rats, and suggest that this protective effect of melatonin could be due to its antioxidant action and its inhibitory action against neutrophil infiltration in the liver of ANIT-injected rats.