脂质过氧化对人内皮细胞的损伤及抗氧化剂的保护作用

以氢过氧化估烯作为培养人内皮细胞脂质过氧化反应的引发剂，以亚硒酸钠、维生素E、超氧化物歧化酶作为抗氧剂，应用光镜、脂质过氧化物测定及放射免疫分析等方法观察了抗氧剂对脂质过氧化损伤的内皮细胞形态结构和功能的保护作用。结果表明：氢过氧化枯烯激发和促进了内皮细胞的脂质过氧化反应；而硒、维生素E、超氧化物歧化酶使细胞脂质过氧化物含量减少，由过氧化作用造成的细胞收缩、生物膜系统的损伤程度减轻，对细胞前列腺素（PGI2）合成的抑制作用减弱。提示：上述抗氧剂可能通过对内皮细胞的保护作用，阻止动脉粥样硬化病变的形成和发展。     

褪黑激素对线粒体膜脂质过氧化损伤的保护作用

褪黑激素对线粒体膜脂质过氧化损伤的保护作用李明阳田侠侯京武＊赵保路＊忻文娟＊（空军总医院老年病科，北京１０００３６）褪黑激素（Ｍｅｌａｔｏｎｉｎ）是体内主要由松果体分泌的一种激素，有研究报道褪黑激素具有很强的抗氧化作用，能有效地清除羟自由基及烷过氧自...     

大蒜素对血管内皮细胞脂质过氧化损伤的保护作用

目的 :观察大蒜素对培养的人脐静脉内皮细胞 (HUVEC)脂质过氧化损伤的保护作用。方法 :将HUVEC分成空白组、对照组和实验组 ,实验组分别用终浓度为 5 μg/ml、10 μg/ml、2 0 μg/ml、5 0 μg/ml的大蒜素培养液预处理后 ,再加入浓度为 0 .0 6mmol/L的联胺 37℃孵育 2h ,用扫描电镜观察细胞的形态 ,同时测定细胞培养液中一氧化氮 (NO)、丙二醛 (MDA)和超氧化物歧化酶 (SOD)的含量。结果 :对照组HUVEC明显受损 ,MDA含量增加 (P <0 .0 1) ,NO、SOD减少 (均为P <0 .0 1) ;实验组与对照组比较 ,HUVEC损伤明显减轻 ,MDA含量降低 (P <0 .0 1) ,NO增加 (P <0 .0 1)、SOD增加 (P <0 .0 1) ,且呈剂量依赖性。结论 :大蒜素对HUVEC脂质过氧化损害具有保护作用。     

脂质过氧化对培养人内皮细胞的损伤作用

Lipid peroxidation (LPO) was initiated and facilitated in cultured human endothelial cells (ECs) by treating the cells with diamidel first. The concentration of lipid peroxide in the cells and medium increased with the increase of diamide concentration. Under SEM and TEM, 0.05 x 10(-4) M diamide might induce ultrastructural changes. The prominent changes were contraction, plasma membrane blebbing, and rounding, swelling and dilatation of mitochondria. Vacuolization appeared in cells at 4.0 x 10(-4) M diamide, A decrease of prostacyclin synthesis in these cells accompanied the morphologic changes. The results showed that ECs are sensitive to LPO, suggesting that LPO may play an important role in atherogenesis.     

高压氧对大鼠脂质过氧化的作用

高压氧疗法(Hyperbaric Oxygen TheraPy,HBO)是一种新兴的治疗方法,临床广泛用于多种疾病的治疗。但其有效治疗剂量与中毒剂量非常接近,临床使用HBO对其压力、暴露时间均须严格控制,否则易造成氧中毒。而脂质过氧化反应是其中重要的发生环节之一,因此,我们对HBO不同压力、暴露时间吸入纯氧或空气的大鼠血液、心脑组织脂质过氧化反应     

吸入一氧化氮对犬烟雾吸入性损伤脂质过氧化损害的影响

吸入一氧化氮（ＮＯ）已成为世界的一个医学研究热点，就我们所知，在国内外尚未见到吸入ＮＯ对脂质过氧化损害的报告，为评价其效果，我们观察了吸入４５×１０－６（４５ｐｐｍ）ＮＯ在犬烟雾吸入性损伤对体内氧化与抗氧化方面的影响。材料与方法（一）动物与分组：雄性...     

脂质过氧化对人血管内皮细胞NO合成的影响及维生素E的作用

一、材料与方法1.细胞培养 :人脐静脉内皮细胞 (ＨＵＶＥＣ)培养采用本实验室改进的Ｊａｆｆｅ培养法。经免疫荧光检测第Ⅷ因子相关抗原阳性 ,鉴定为血管内皮细胞。2 .实验分组 :分 8组 ,第 1组为正常对照组 ;第 2组为氢过氧化枯烯 0 0 1ｍｍｏｌ/Ｌ ;第 3组为氢过氧化枯烯 0 0 5ｍｍｏｌ/Ｌ ;第 4组为氢过氧化枯烯 0 10ｍｍｏｌ/Ｌ ;第 5组为氢过氧化枯烯 0 5 0ｍｍｏｌ/Ｌ ;第 6组为氢过氧化枯烯 1 0 0ｍｍｏｌ/Ｌ ;第 7组为氢过氧化枯烯 0 5 0ｍｍｏｌ/Ｌ +维生素Ｅ(ＶｉｔＥ) 5 0ｍｇ/Ｌ ;第 8组为氢过氧化枯烯 1 0 0ｍｍｏｌ/Ｌ +…     

内皮细胞脂质过氧化损伤对单核细胞粘附的影响

以巯基氧化剂联胺作用于培养人血管内皮细胞，引发细胞过氧化脂质蓄积与质过氧化损伤，研究内皮细胞脂质过氧化损伤对人血单核细胞粘附的影响，结果发现，内皮细胞脂质过氧化损伤使单核细胞对内皮细胞的粘附增加，单核细胞主要粘附于受损伤的内皮细胞表面和间隙，提示单核细胞对内皮细胞粘附增加，是内皮细胞脂质过氧化损伤促进和加重动脉粥样硬化病变形成的一个重要机制。     

脂质过氧化作用对单核巨噬细胞系统功能的影响

过氧化脂质对组织细胞有广泛的损害作用。我们用枯烯过氧化氢作为脂质过氧化的诱导剂,研究了脂质过氧化对巨噬细胞和网状内皮系统功能的影响。实验结果表明枯烯过氧化氢诱导的脂质过氧化作用可使巨噬细胞吞噬、消化功能以及产生白介素-1的能力下降,并可损害网状内皮系统的功能。     

黄芩茎叶总黄酮预处理对缺血再灌注心肌脂质过氧化损伤的保护作用

目的：探讨黄芩茎叶总黄酮(SSTF)预处理对缺血再灌注心肌脂质过氧化损伤的保护作用。方法：雄性大鼠分为SSTF预处理组、缺血再灌组和假手术组,缺血再灌术前给SSTF组大鼠SSTF(50、100、200mg·kg~1·d~(-1))灌胃,制备缺血再灌模型,分别测定心肌组织超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量,血清乳酸脱氢酶(LDH)、肌酸激酶(CK)水平。结果：SSTF预处理可不同程度显著降低缺血再灌注引起的MDA含量,提高SOD活性,降低LDH、CK水平。结论：SSTF预处理能通过保护心肌抗氧化酶的活性,抵制脂质过氧化反应,减轻自由基对心肌的损害,对缺血再灌注心肌产生保护作用。     

Protective influence of diphenyl-p-phenylenediamine on hydrazine induced lipid peroxidation and hepatic injury

Previous studies have demonstrated the ability of water soluble and/or lipid soluble antioxidants to reduce the toxicity as well as the biochemical, functional, and pathological changes induced by a variety of hepatotoxic agents. To further determine the ability of diphenyl-p-phenylenediamine (DPPD) to modify chemical induced hepatic injury, the influence of DPPD on hydrazine-induced hepatic toxicity was assessed. The administration of hydrazine to rats significantly increased liver triglycerides. Significant inhibition of triglyceride accumulation occurred in the DPPD-treated group. Hydrazine also caused an increase in hepatic lipid peroxidation as reflected by malonaldehyde (MDA) formation. The enhancement in MDA formation was prevented by DPPD treatment. In contrast to the profound hepatic necrosis observed following hydrazine, livers from DPPD treated rats which received hydrazine showed only mild architectural alterations. The hypoglycemia and retention of BSP which developed upon hydrazine administration was not modified by DPPD. The ability of the lipid soluble antioxidant, DPPD, to significantly inhibit hydrazine-induced fatty infiltration, necrosis, and lipid peroxidation further accents the potential of employment of appropriate antioxidants in the prevention of chemical-induced hepatic injury.     

Protective effect of scutellaria baicalensis stem-leaf total flavonoid on the injury of microvascular architecture and lipid peroxidation induced by cerebral ischemia reperfusion in rats

目的:探讨黄芩茎叶总黄酮(SSTF)预处理对脑局灶性缺血再灌注大脑皮质的保护作用及其机制.方法:线栓法制备局灶性脑缺血再灌注模型,造模成功后24 h测脑梗死体积,单宁酸-氯化铁媒染法显示大脑皮质微血管,并用Mivnt图像分析系统对皮质微血管密度(MVD)及微血管面积密度(MVA)进行定量分析;检测脑皮质组织中超氧化物歧化酶(SOD)活力、丙二醛(MDA)含量.结果:SSTF预处理可改善术后大鼠的MVD和MVA;降低因缺血再灌注引起的脑皮质组织MDA含量增加,提高SOD活力.结论:SSTF预处理可改善脑皮质微血管形态结构,抵制脂质化过氧化反应,减轻自由基损害,对缺血再灌注损伤脑组织具有保护作用.     

Protective effect of melatonin and pinoline on nitric oxide-induced lipid and protein peroxidation in rat brain homogenates

Nitric oxide (NO) is a physiological neurotransmitter, a mediator of the excitatory neurotransmitter glutamate pathways that regulates several neuroendocrine functions, but excessive NO is toxic by itself and it interacts with superoxide radical (O(2)(-)) to form the peroxynitrite anion (ONOO(-)). Using rat brain homogenates, we investigated the effects of melatonin and pinoline in preventing the level of lipid peroxidation (LPO) and carbonyl contents in proteins induced by nitric oxide (NO) which was released by the addition of sodium nitroprusside (SNP). Lipid and protein peroxidation were estimated by quantifying malondialdehyde (MDA) and 4-hydroxyalkenal (4-HDA) concentrations and carbonyl contents, respectively. SNP increased MDA+4-HDA and carbonyl contents production in brain homogenates in a time and concentration dependent manner. Both, melatonin and pinoline reduced NO-induced LPO and carbonyl contents in a dose-dependent manner in concentrations from 0.03 to 3 mM and 1 to 300 microM, respectively. Under the in vitro conditions of this experiment, both antioxidants were more efficient in limiting SNP protein oxidation than lipid damage.     

The effect of Fe2+/ascorbate induced lipid peroxidation on the beta-adrenoceptor of sarcolemmal membranes

Inflammation Research -     

The effect of glycosaminoglycans and proteoglycans on lipid peroxidation

Recent investigations show that glycosaminoglycans (GAGs) and proteoglycans (PGs) have the ability to affect lipid peroxidation, one the best characterized forms of free radical mediated biological damage. A protective effect of these extracellular matrix (ECM) components has been demonstrated in various experimental systems, including fatty acids and liposomes, where oxidation was induced by transition metals, including copper and iron. The effect was specific and dependent on the type and structural features of GAGs and PGs. The mechanism of peroxidation inhibition was likely to be dependent, at least to a large extent, on the sequestration of transition metals by GAG chains. Thus, it is conceivable that GAGs in the ECM and in the pericellular space may contribute to protecting cells against free radical damage. It is of particular interest that in certain tissues (cornea and aorta) aging was associated with a decrease of content of the GAGs which were most effective as anti-oxidant. This suggests that age-induced modifications of ECM composition in certain tissues may increase the susceptibility to oxidative stress. The investigation on the effect of GAGs on lipoprotein oxidation led to apparently conflicting results. An interesting reconciliation is possible, according to which GAGs exerted their protective effect under experimental conditions not compatible with the formation of lipoprotein-GAG complexes; rather, lipoproteins exhibited increased susceptibility to metal-catalyzed oxidation (MCO), possibly due to structural modifications of the particle after binding to GAGs or PGs. This process is likely to occur in the intimal matrix of arteries.     

Enhancement of nitroglycerin induced blood vessel relaxation in chronic renal failure model rats

This study was designed to investigate the alternation of blood vessel relaxation in chronic renal failure (CRF) induced by adenine or partial-nephrectomy. The aorta was employed as the blood vessel material. CRF aorta relaxation in both adenine and partial nephrectomy induced rats increased when treated with glyceryl trinitrate (GTN). In the CRF animals, cGMP levels increased with the severity of CRF status. Aorta cytosolic glutathione S-transferase micro (GSTmicro) activity and enzyme contents increased with CRF. The effect of GTN on aortic vasorelaxation in both CRF statuses completely disappeared by the treatment with sodium nitoprusside. The effects of GTN were observed equally in both adenine- and partial nephrectomy-induced CRF rats. We concluded that alterations of aortic vasorelaxation by GTN in adenine- and partial nephrectomy-induced renal failure rats were caused by the enhancement of nitrogen monoxide production on the aortic blood vessel mediated by the induced GSTmicro in the aorta. This GSTmicro induction is peculiar to CRF since different CRF induction procedures produce the same results.     

川芎嗪对内毒素脂多糖诱导的体外血脑屏障模型通透性增高的保护作用及其机制

目的:探讨川芎嗪对内毒素脂多糖(LPS)诱导的体外血脑屏障模型通透性增高的保护作用及其调控机制。方法:利用脑微血管内皮细胞与星型胶质细胞共培养建立体外大鼠血脑屏障模型,随机分为正常对照组、川芎嗪对照组、LPS干预组和川芎嗪治疗组。采用γ计数仪检测~(125)I-BSA通透量观察体外血脑屏障模型通透性的改变,Western印迹法检测紧密连接蛋白(zonula occludens-1,ZO-1)表达量的变化。结果:LPS使体外血脑屏障模型对~(125)I-BSA的通透量明显增加,脑微血管内皮细胞ZO-1蛋白表达下降,川芎嗪治疗组能明显拮抗LPS的上述作用。结论:川芎嗪对LPS诱导的体外血脑屏障通透性增高具有保护作用,其机制与它能影响血脑屏障紧密连接蛋白ZO-1表达有关。