腹腔镜子宫肌瘤剜除术对人体蛋白质氧化、脂质过氧化影响的研究

目的探讨腹腔镜手术对子宫肌瘤患者体内蛋白质氧化、脂质过氧化的影响。方法将40例子宫肌瘤患者随机分为腹腔镜组和开腹组两组,每组20例。测定两组患者腹腔镜手术前、手术结束时(气腹解除后5min)及术后24h血浆晚期氧化蛋白产物(AOPP)、丙二醛、血浆谷胱甘肽过氧化物酶(GPx)活性和血浆总抗氧化能力(AOA)的水平,以及开腹手术术前、手术结束(缝合腹壁时)及术后24h的水平。结果(1)腹腔镜组手术结束时血浆AOPP、丙二醛水平高于术前[(69±13)μmol/Lvs(50±9)μmol/L,P<001;(252±055)μmol/Lvs(185±019)μmol/L,P<001],血浆GPx活性、AOA水平低于术前[(029±009)U/mlvs(062±027)U/ml,P<001;(090±024)mmol/Lvs(141±039)mmol/L,P<001];术后24h血浆AOPP、丙二醛、GPx与术前比较差异无统计学意义[(50±10)μmol/L,P>005;(205±068)μmol/L,P>005;(052±006)U/ml,P>005],但AOA水平仍低[(100±031)mmol/L,P<001]。(2)开腹组手术结束时血浆AOPP、丙二醛含量比术前略有升高[(53±100μmol/Lvs(52±70)μmol/L,P>005;(209±051)μmol/Lvs(183±064)μmol/L,P>005],GPx活性、AOA水平比术前略有下降[(051±017)U/mlvs(057±021)U/ml,P>005;(120±046)mmol/Lvs133±037,P>005];术后24h血浆AOPP、丙二醛与术前相比升高[     

Protective effects of melatonin and vitamin E in brain damage due to gamma radiation

Gamma radiation is known to cause serious damage in the brain, and many agents have been used for neuroprotection. In this study, lipid peroxidation levels and histopathological changes in brain tissues of whole-body irradiated rats with likely radiation injury were compared to those with melatonin and vitamin E protection. Forty rats in four equal groups were used. The control group received neither radiation nor medication. The remaining groups received doses of 720 cGy in two equal fractions 12 h apart. The second group received radiation but no medication, the third received radiation plus 100 mg/kg per day of vitamin E i.p., and the fourth received radiation plus 100 mg/kg per day of melatonin i.p. over 5 days. On the 10th postoperative day, all the rats were decapitated and specimens from parietal cortices were analyzed for tissue malondialdehyde (MDA) levels and histopathological changes. Increases in MDA were relatively well prevented by melatonin treatment but less so with vitamin E therapy. On histopathological examination, melatonin significantly reduced the rates of edema, necrosis, and neuronal degeneration, whereas vitamin E reduced only necrosis. Neither substance was capable of preventing vasodilatation. In conclusion, melatonin may be useful in preventing the pathological changes of secondary brain damage as a result of free oxygen radicals generated by irradiation.     

Clinical importance of erythrocyte malondialdehyde levels as a marker for cognitive deterioration in patients with dementia of Alzheimer type: a repeated study in 5-year interval

OBJECTIVES: The aim of the present study was to determine the effects of aging and dementia of the Alzheimer type (DAT) on lipid peroxidation and antioxidant enzyme activities. DESIGN AND METHODS: Twenty-six patients with DAT were included in the present study. Group I: 26 patients diagnosed as DAT and studied 5 yr ago. Group II: This group consisted of the same patients as Group I at the present time. Activities of CuZn superoxide dismutase (CuZn SOD) and glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) concentrations of these 26 subjects were measured and mini mental state examination (MMSE), brief psychiatric rating scale (BPRS), Hamilton depression rating scale (HDRS) were applied. RESULTS: The results revealed that 26 dementia patients had worsened cognitive symptoms and significantly increased CuZn SOD and MDA levels and decreased GSH-Px levels after 5 yr. Significant correlation was found between age and CuZn SOD (r: +0.406, p: 0.034), and between MMSE and MDA (r: -0.411, p: 0.032). CONCLUSIONS: We can conclude that MDA, CuZn SOD, and GSH-Px were significantly affected in the patients with Alzheimer disease. The most striking finding of this study is the significant correlation between MMSE and MDA in patients with DAT.     

Malondialdehyde and Nitric Oxide Levels in the Plasma of Patients with Advanced Laryngeal Cancer

Purpose. We investigated alterations in plasma nitrite, nitrate, total nitric oxide (NO), and malondialdehyde (MDA) levels in patients with advanced stage laryngeal cancer.Methods. We measured the levels of MDA and total NO^–₂, as well as the NO^–₃ marker for NO generation, in 25 patients with advanced laryngeal cancer and 15 healthy control subjects.Results. The levels of plasma MDA, NO, and NO^–₃ were significantly higher in the patients with laryngeal cancer than in the healthy controls (P 0.001 for all). On the other hand, although plasma NO^–₂ was increased in the patient group, the statistical difference was not significant (P 0.05). Moreover, the MDA and NO levels did not differ significantly between patients with stage III and stage IV laryngeal cancer.Conclusion. These findings demonstrate that oxidative stress is increased in patients with advanced laryngeal cancer.     

活血化瘀系列方对脑缺血再灌注损伤的保护作用及机制研究

目的 :探讨活血化瘀系列方 (活血汤、活血益气汤、活血养阴汤 )对大鼠脑缺血再灌注损伤的保护作用及其机制。方法 :采用大脑中动脉阻断法制备大鼠脑缺血再灌注模型 ,缺血 6 0 min,再灌注 3d。观察药物对脑缺血再灌注引起的神经功能缺损症状及病理损伤的影响 ,检测脑组织一氧化氮合酶 (NOS)、超氧化物歧化酶 (SOD)活性的变化和丙二醛 (MDA)含量的变化 ,免疫印迹分析 NMDA受体亚单位蛋白 NR1和内皮型 NOS(e NOS)的表达。结果 :活血化瘀系列方及尼莫地平能显著改善神经功能缺失症状 ,减小梗死体积和脑水肿面积 ,减少神经元损伤 (P<0 .0 5 ) ,组间没有显著性差异 ;活血化瘀系列方和尼莫地平不同程度降低脑组织内 NOS活性和 MDA含量 ,抑制NR1表达 ,增加 SOD的活性 ,但对 e NOS的表达均无明显影响。结论 :活血化瘀系列方对大鼠脑缺血再灌注损伤有保护作用 ,其机制可能与降低脑组织内 NOS活性 ,降低 NR1的表达 ,减少 MDA含量和增加 SOD活性有关。     

雌激素改善皮瓣组织损伤的实验性研究

目的:研究不同剂量雌激素对皮瓣组织损伤及存活面积的影响,并探讨其可能的作用机制.方法:新西兰白兔30只,随机分为A、B、O三组,O组为对照组.在兔背作超长型皮瓣1个,皮瓣蒂部注射雌激素,三组间剂量不同.术后分别检测皮瓣MDA(丙二醛)、NEU(中性粒细胞)计数、皮瓣存活面积S等指标.结果:①A组、B组皮瓣存活面积较O组增加,MDA、NEU较O组减低.②皮瓣存活面积S与血清MDA含量、皮瓣NEU计数之间呈负相关.结论:①雌激素注射处理可降低皮瓣MDA含量、减少NEU浸润.②雌激素注射可增加皮瓣存活面积.其机制与雌激素减轻皮瓣损伤有关.     

Retention of ovaries and oxidative stress of surgery.

OBJECTIVE: Surgical menopause results in severe menopausal symptoms due to the sudden withdrawal of estrogen. This study evaluated the impact of surgical menopause on oxidant and antioxidant status. METHODS: Thirty eight women who underwent total hysterectomy with or without bilateral salpingo-oophorectomy were included. Oxidant status was assessed by measuring plasma levels of malondialdehyde (MDA) and antioxidant status by assessing glutathione (GSH) and estrogen levels. RESULTS: The levels of MDA were increased in all women, and GSH levels were significantly decreased in women who underwent hysterectomy alone but significantly increased in those who also had oophorectomy. Estrogen levels were increased if the ovaries were retained even in postmenopausal women, while they were decreased in the women who underwent oophorectomy. CONCLUSION: Oxidative stress of surgery, as assessed by increased MDA levels, occurred in all women. After oophorectomy, estrogen levels decreased and GSH levels increased in both premenopausal and postmenopausal women. The ovaries may therefore respond to oxidative stress of surgery by increasing estrogen production, estrogen being a better antioxidant than GSH.     

丁基苯酞对缺血脑组织中MDA形成及超氧阴离子自由基产生的抑制作用

局灶性脑缺血6小时再灌注1小时后,缺血脑组织中脂质过氧化产物丙二醛（MDA）的含量明显增加,表明再灌注导致了脂质过氧化损伤,丁基苯酞（dl-NBP,20mg.kg^-1.ip)可显著降低缺血皮层组织在MDA的含量。进一步研究表明,dl-NPB,d-NBP和l-NBP皆可抑制黄嘌呤－黄嘌呤氧化酶反应系统中超氧阴离子自由基的形成,此作用可能与其抑制了黄嘌呤氧化酶活性有关。     

银杏叶提取物体外对铜离子诱导的人血清低密度脂蛋白氧化修饰的抑制作用(英文)

本文在体外对EGb761能否抑制钢离子诱导的人血清低密度脂蛋白氧化修饰进行了研究。低密度脂蛋白（LDL）用EGb76140,80,160mg·L(-1)‘预处理1h,然后用CuSO410μmol·(-1)氧化修饰10h。结果表明LDL被钢离子氧化修饰后低密度脂蛋白中维生素E（VE）被耗竭,丙二醛（MDA）及自身荧光物质（LF）含量升高,载脂蛋白B（apoB）的电泳迁移速率加快。EGb761剂量依赖性地抑制VE的含量降低和MDA及自身荧光物质的含量升高,载脂蛋白B的电泳迁移速率依次减慢。可见在体EGb761能抑制钢离子诱导的人血清低密度脂蛋白氧化修饰。     

Protective effect of ischemic postconditioning on lung ischemia-reperfusion injury in rats and the role of heme oxygenase-1

To investigate the effect of ischemic postconditioning (IPO) on acute lung ischemia-reperfusion (I/R) injury and the protein expression of haeme oxygenase-1 (H0-1), a cytoprotective defense against oxidative injury. Methods: After being anesthetized with chloralhy-drate, forty-eight healthy SD rats were randomly divided into 6 groups (8 in each): sham operation group (S group); I/R group: left lung hilum was clamped for 40 minutes followed by 105 minutes of reperfusion; IPO group: left lung hilum was clamped for40 minutes and postconditioned by 3 cycles of 30 seconds of reperfusion and 30 seconds of reocclusion; Hemin (HM)+ I/R group: hemin, an inducer of HO- 1 was injected intraperitoneally at 40 μmol.kg-1·day-1 for two con-secutive days prior to 40 minutes clamping of left lung hilum; ZnPPIX+IPO group: zinc protoporphyrin Ⅸ, an inhibitor of HO-1 was injected intraperitoneally at 20 mg·kg-1 24 hours prior to 40 minutes clamping of left lung hilum; and HM+S group: HM was administered as in the HM+I/R group without inducing lung I/R. Arterial partial pressure of oxygen (PaO2) and malondialdehyde (MDA) content in serum were assessed. The left lung was removed for determination of wet/dry lung weight ratio and expression of HO-1 protein by immuno-his-tochemical technique and for light microscopic examination. Results: The PaO2 was significantly lower in all the experimental groups compared with sham group (90 mm Hg ±11 mm Hg). However, the values ofPaO2 in IPO (81 mm Hg ±7 mm Hg) and HM+I/R (80 mm Hg±9 mm Hg) were higher than that in I/R (63 mm Hg±9 mm Hg) and ZnPPIX+IPO (65 mm Hg±8 mm Hg) groups (P<0.01). The protein expression of HO-1 in lung tissue was significantly increased in I/R group compared with S group (P<0.01). While the HO-1 protein expression was higher in IPO and HM+I/R groups as compared with I/R group (P<0.05, P<0.01). The lung wet/ dry (W/D) weight ratio and MDA content in serum were significantly increased in I/R group as compared with S or HM+S groups (P<0.01), accompanied by severe lung tissue histological damage, which was attenuated either by IPO or by HM pretreatment (P<0.01, IPO or HM+I/R vs. I/R). The protective effect of IPO was abolished by ZnPPIX. Condusion: Ischemic postconditioning can attenuate the lung ischemia-reperfusion injury through upregulating the protein expression of HO-1 that leads to reduced post-ischemic oxidative damage.