目的:研究大豆异黄酮对D半乳糖致衰老大鼠抗氧化能力的影响。方法:用D半乳糖注射Wistar雄性大鼠5个月,建立衰老模型。对致衰老模型组、大豆异黄酮组肝脏、心脏和前列腺丙二醛(MDA)含量、超氧化物歧化酶(SOD)、谷胱甘肽过氧化酶(GSHPx)活性进行测定及比较。结果:低、中、高不同剂量大豆异黄酮灌喂组与模型组大鼠相比,各脏器MDA含量(μmol/L)(心脏:695±093,562±112,435±112比802±111;肝脏:815±085,647±120,515±112比935±135;前列腺:715±092,558±115,423±125比833±124)均有降低,差异有统计学意义(Plt;005),而SOD酶活性(nmol/L)(心脏:4732±308,5518±428,6120±368比3225±370;肝脏:18121±506,19015±706,19720±570比17213±512;前列腺:4156±301,4607±421,5015±335比3374±305)和GSHPx酶活性(nmol/L)(心脏:905±096,1111±245,1313±146比713±151;肝脏:902±105,1150±223,1362±192比698±160;前列腺:435±085,613±102,747±155比312±106)有升高,差异同样具有统计学意义(Plt;005);大豆异黄酮摄入量越高,MDA含量越低,而SOD、GSHPx酶活性越高。结论:摄入适量大豆异黄酮可有效增强大鼠机体抗氧化能力,从而延缓D半乳糖诱发的大鼠衰老。
目的:探讨甲状腺功能亢进症(甲亢)患者血浆对氧磷酯酶1(PON1)活性变化以及与其它氧化应激指标的关系。方法:分别测定50名对照组和78例甲亢组空腹血浆中游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)、促甲状腺激素(TSH)、PON1活性、超氧化物歧化酶(SOD)、丙二醛(MAD)、氧化低密度脂蛋白(ox-LDL)及血脂含量,并进行相关性分析。 结果:甲亢患者血浆PON1活性(139 ±64)kU/L,ox-LDL(598.3±58.6)μg/L,MDA(15.11±3.26) μmol/L及SOD(80.2±25.3)NU/mL。对照组上述指标分别为:PON1(168 ±70)kU/L,ox-LDL (446.2±62.2) μg/L,MDA (10.02±3.00) μmol/L,SOD(92.9±26.9)NU/mL。血浆PON1和SOD活性显著低于对照组(Plt;0.01),ox-LDL和MDA水平显著高于对照组(Plt;0.01)。甲亢患者血浆PON1活性与SOD呈正相关(r=0. 381,Plt; 0.05),与ox-LDL、MDA呈负相关(r=-0. 411,r=-0. 445,Plt; 0.01)。 结论:甲亢患者血浆PON1活性显著降低,可能与氧化应激增强有关。
Objective To investigate the influence of chronic alcohol ingestion on the severity of acute lung injury (ALI) induced by oleic acid and lipopolysaccharide (LPS).Methods Thirty-two SD rats were randomly administrated with alcohol or water for 6 weeks，then instilled with oleic acid and LPS to induce ALI or with normal saline as control.Thus the rats were randomly divided into two injury groups [ethanol group and water group] and two control groups [ethanol group and water group] (n=8 in each group). PaO2,Wet to dry lung weight ratio (W/D)，levels of γ-glutamylcysteinylglycine (GSH) and malonaldehyde (MDA) in the lung tissue were measured.Results Compared to corresponding control groups，the PaO2 and GSH significantly decreased，and the lung W/D and MDA level were significantly increased in the injury groups (all Plt;0.05).In the injury groups，the changes of above parameters were more significant in the alcohol group than thoe in the water group (all Plt;0.05)，except the lung W/D with no significant difference.Conclusion Chronic ethanol ingestion was relevalent to oxidation/ antioxidation imbalance and more severe lung injury in rats with severe septic after trauma,which suggests that chronic alcohol abuse could increase the severity of acute lung injury.
Objective To study the effects of malondialdehyde (MDA), superoxide dismutase (SOD) and tumor necrosis factor-α (TNF-α) on brain tissue in rats with pancreatic encephalopathy (PE). Methods Thirty-six Wistar rats were randomly divided into control group (n=6) and PE model group (n=30). In control group, rats were injected with normal saline by internal carotid artery (0.1 ml/100 g) and were killed on the first day after the injection. In PE model group, rats were injected with phospholipases A2 (0.1 ml/100 g, 1 000 U/0.1 ml) by internal carotid artery, to establish animal model of PE in rat and 10 rats were killed on day 1, 3, 7 respectively after the injection. The changes of water content in the brain were measured. Leucocytes aggregation and margination in the microvessels, and the changes of cerebral cells and nerve fibers were observed. The levels of MDA, TNF-α and the activity of SOD were tested in the brain homogenate in rats. Results In PE model group, water contents of brain increased; The phenomena of leucocytes accumulation and margination, cellular edema of neurons and demyelination of nerve fibers became more obvious; The levels of MDA and TNF-α increased significantly than those in the control group, while the activity of SOD reduced (P＜0．05， P＜0.01)． Conclusion Inthe rat model of PE, MDA, SOD, and TNF-α play important roles on the occurrence and development of brain injury.
Objective：To observe the histochemical changes of retinal photochemical damage in rats. Methods：The changes of retinal ultrastructure were observed.The concentration of malondaldehyde(MDA) was tested and the activity the histochemical change of cytochrome oxidase (CCO) and (Mg ++ -ATPasw) were evaluated on the retnal photochemical damage in SD rats. Results：At the 6th hour after light exposure,the swelling appwared at the nuclei of photoreceptor,the mitochondria of inner segment.The apical microvilli of RPE disappeared and lysosomes increased in RPE.On the 6th day after light exposure,the changes became more obvious.While on the 14th day after light expose the nuclei of photoreceptors and the inner segments renewed but the arrangement of the disk was lose;and the microvilli appeared of the disk was lose;and the microvilli appeared at the tip of RPE.The Activity of CCO and Mg ++ -ATPase decreased and MDA increased in retina at the 6th hour and on the 6th day and they recovered on the 14th day after light exposure. Conclusion：Lipd peroxidation that broke the cell membrane system of photoreceptor which induced changes of the cell ultrastru cture abd the activity of enzyme might relate to pathogenesis in retinal photochemical damage. (Chin J Ocul Fundus Dis,1998,14:38-40)
ObjectiveTo study the effect of rotenone on rat substantia nigra dopamine (DA) in the nervous system and oxidative stress parameters (malondialdehyde and glutathione), the influence of rotenone on DA neurons toxic effect and its pathogenesis. MethodsThis study applied back subcutaneous injection of rotenone in rats [1.0 mg/(kg·d)], and used immunocytochemistry technique to detect changes in the expression of tyrosine kinase (TH) in 10 rats of the control group and 10 rats of the experimental group. Spectrophotometry was used to detect the change of oxidative stress parameters in rats (malondialdehyde and glutathione). ResultsDA neurons in rats had various degrees of damage. The TH immune response strength of rats in the substantia nigra and striatum decreased significantly. The number of immune response nigra TH positive neurons was significantly less in the experimental group than in the control group (P< 0.01). Spectrophotometer method was used to detect the midbrain nigra of glutathione, which was significantly less in the experimental group than in the control group (P<0.01). Malondialdehyde in the experimental group was significantly higher (P<0.01). ConclusionRotenone has obvious neurotoxicity, and can lead to the damage of DA neurons and obvious oxidative stress injury in rats, which provides an experimental basis for the pathogenesis of Parkinson's disease, and at the same time provides new targets for the treatment.
Objective To explore the effect of oxygen inhalation on the retinae of newborn rats and its mechanism.Methods We mimicked the retinopathy of prematurity(ROP) by putting the newborn rats in high concentrated oxygen. One-day old rats were put into the oxygen box with the oxygen concentration of 80% for continuous 7 days; then in air condition for 7 days. The arterial blood oxygen pressure, retinal superoxide dismutase (SOD), and malondialdehyde (MDA) of the rats (1,2,4,7,8,9,11,14 days old) were examined. The diameter of retinal vessels′main branch and the coverage rate of peripheral vessels were measured in 7- and 14-day-old rats by ink perfusion. The retinal neovascularization of rats (8,9,11, 14 days old) were observed by HE staining. The rats of the same age fed in air condition were in the control group.Results The differential pressures of blood oxygen of rats (1,2,4,7 days old) in study group were significantly higher than those in the control group (P＜0.01), while the differential pressures of blood oxygen of rats (8,9,11,14 days old) in study group were lower than those in the control group (P＞0.05). The contents of SOD of the retinae in the rats ( 1,2,4,7,8 days old) were significantly lower than those in the control group(P＜0.01, P＜0.05 ), while the contents of MDA were significantly higher than those in the control group (P＜0.01,P＜0.05). The diameter of retinal vessels′main branch in 7-day rats was 75% of the control group, and the coverage rate of peripheral vessels was 22% of the control group; and was 61% and 73% respectively in 14-day-old rats. The neovascularization could be seen in 16.7% of the rats in the study group and nought in the control group.Conclusion The damage of free radical of the retina in high concentrated oxygen and hypoxia situation after oxygen supply may be one of the most important mechanism of ROP. (Chin J Ocul Fundus Dis，2003，19：269-332)
Objective To observe the levels of malonaldehyde (MDA) , interleukin-8 (IL-8) and tumor necrosis factor-α(TNF-α) in lung tissues of subjects with or without chronic obstructive pulmonary disease (COPD) , and investigate their roles in the the pathogenesis of COPD. Methods The content of MDA, IL-8 and TNF-αin lung tissues of smokers with COPD (n=9) , ex-smokers with COPD (n=8) , non-smokers with COPD (n=7) , healthy smokers (n=9) , healthy ex-smokers (n=8) and healthy nonsmokers (n=6) was measured with enzyme-linked immunosorbent assay ( ELISA) and corrected by creatinine. Results The levels of MDA, IL-8 and TNF-α in lung tissues of the COPD patients were significantly higher than those in the healthy subjects (Plt;0.05) , which were also significantly higher in the smokers when compared with the non-smokers (Plt;0.05) , whether suffering from COPD or not. In the COPD patients, not the levels of IL-8 but MDA and TNF-αin lung tissues of the smokers were significantly higher than those in the ex-smokers (Plt;0.05) ; whereas in the healthy cases, no statistical significance was revealed between the smokers and the ex-smokers on the levels of MDA and IL-8 in lung tissues except TNF-α( Pgt;0.05) . Conclusion The abnormal increase of MDA, IL-8 and TNF-αin lung tissues caused by chronic smoking may play an important role in the the pathogenesis of COPD.
【Abstract】 Objective To investigate the protective role of recombinant human growth hormone (rhGH )in ischemic reperfusion injury of rat liver and its mechanism. Methods One hundred Male rats were randomly divided into two groups: the rhGH group and the control group. In the rhGH group, rhGH were injected （0.2U/100g weight） to rats seven days before the ischemic reperfusion injury, and in the control group, normal saline was injected instead. Serum levels of ALT， TNF-α and IL-1α were tested. Hepatic tissue was sectioned for to detect the level of EC and MDA, the expression of NF-κB and ICAM-1 mRNA on SEC. Ultrastructural characteristics histopathological characteristics were determined also. Results Serum levels of ALT, TNF-α, IL-1α and the contents of MDA in the control group were significantly higher than those in the rhGH group （P＜0.05）. Comparied with control group, rhGH also decreased NF-κB activation, and reduced the expression of ICAM-1 mRNA of SEC in the liver cells （P＜0.05）. Electronic microscopic revealed that the hepatic sinusoidal endothelial cells and the hepatocellular mitochondria were injured in the control group. Pretreatment with the rhGH was able to significantly improved the pathological changes. Conclusion rhGH might confer the protection to ischemic reperfusion injury of rat liver through reducing the expression of NF-κB to down-regulate cytokine (IL-1α,TNF-α), MDA and inhibition the expression of ICAM-1 mRNA.