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。
【Abstract】Objective To investigate the expressions of TNF-α and superoxide dismutase (SOD) mRNA in myocardium of rats with obstructive jaundice (OJ). Methods The expressions of TNF-α and SOD mRNA were semi-quantitatively analyzed after amplification of cDNA in myocardium of the rats with OJ by RTPCR. Results The expression of TNF-α mRNA increased and that of SOD mRNA decreased in the myocardium of rats with OJ. The level of plasm TNF-α increased and SOD synthesis in myocardium decreased. Conclusion The injury of myocardium in OJ is correlated with increasing expression of TNF-α mRNA and decreasing expression of SOD mRNA.
Perfusion of free flaps from groin of rabbits, after 12 hours of complete ischemia, with superoxide dismutase (SOD), an oxygen free radical scavenger, would significantly increase the survival rate of these flaps from 18.75% to 75% in the control group. Tissue levels of SOD and malonydialdehyde (MDA, an end product of lipoperoxidation) were measured before ischemia, after ischemia but before reperfusion, and 60 minites after reperfusion. In untreated flap, after 12 hours- ischemia, the SOD content of skin decreased significantly as compared with the SOD content before ischemia, and reperfusion further decreased SOD activity, while the concentration of MDA increased after ischemia and further increased after reperfusion. In the treated flaps, the concentration of SOD was not decrease and MADnot increased after reperfusion. There was a negative correlation between the values of SOD and MDA. These findings suggested that free oxygen radicals playedan important role in the free flap ischemia reperfusion injury. SOD could increase the survival of ischemic free-flaps by reducing lipoperoxidation. The results had significant clinical implications with regard to organ preservation and transplantation.
Electron spin resonance (ESR) spectroscopy and spin trapping agent PBN were applied to measure directly the changes of oxygen free redicals (OFR) in gastric mucosa of rats with portal hypertension (PHT) injured by shockreperfusion, and treated with superoxide dismutase (SOD), radix salviae miltiorrhizae (RSM), with concomitant monitoring activity of SOD and pathology of gastric mucosa. Results showed that the amount of OFR increased markedly in gastric mucosa of PHT rats during the shock-reperfusion. The pathological changes were in accordance with alteration of the amount of OFR and the activity of SOD. Gastric mucosa in PHT was more susceptible to shock-reperfusion insult than normal controls. The anti-oxidant SOD, RSM used at early stage exerted mild gastric mucosal insult through different mechanisms.
目的:研究缺氧预处理对老年大鼠子宫及双附件切除术后疲劳是否有改善作用,并通过对比观察超氧化物歧化酶及丙二醛水平的变化,初步探讨缺氧预处理的作用机制。方法:将老年大鼠分为空白对照组、对照组、缺氧预处理三组。空白对照组为假手术组,对照组为子宫及双附件切除术组, 缺氧预处理组为缺氧预处理加子宫及双附件切除术组。对比观察缺氧预处理对大鼠体力活动及血清超氧化物歧化酶和丙二醛水平的影响。结果:空白对照组、对照组、缺氧预处理三组大鼠悬尾不动时间分别为:(21±3)s,(83±10)s,(44±5)s,各组间比较Plt;0.05。三组SOD活性分别为:(131.23±5.31)U/L,(36.12±9.68)U/L,(73.01±9.82)U/L,各组间比较Plt;0.05。三组MDA水平分别为:(9.78±1.26)μmol/L,(29.87±3.13)μmol/L,(15.98±2.21)μmol/L,各组间比较Plt;0.05。结论:缺氧预处理可提高老年大鼠的抗氧化能力,对老年大鼠子宫及双附件切除术后疲劳综合征有明显的改善作用。
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。
To study the variations of l ipid peroxidation products and copper, zinc-superoxide dismutase(CuZn-SOD) in pathological scars (hypertrophic scars and keloids). Methods The specimens were gained from patients of voluntary contributions from May 2005 to August 2005. The tissues of hypertrophic scar (10 cases, aged 16-35 years, the mean course of disease was 2.2 years), keloid (10 cases, aged 17-32 years, the mean course of disease was 8 months) and normal skin (8 cases, aged 16-34 years) were obtained. The content of malonaldehyde (MDA)and CuZn-SOD activity were detected by spectrophotometric method. The expression of CuZn-SOD was evaluated by immunohistochemistry technique. Results The contents of MDA and CuZn-SOD activity were significantly higher in hypertrophic scars[MDA (1.139 0 ± 0.106 7)nmoL/mg prot, CuZn-SOD (31.65 ± 2.21)U/mg prot, (P lt; 0.05)]and keloids[MDA (1.190 0 ± 0.074 8)nmoL/ mg prot, CuZn-SOD (34.36 ± 5.01)U/mg prot (P lt; 0.05)] than those of normal skin tissues [MDA (0.821 3 ± 0.086 4)nmoL/mg prot, CuZn-SOD (20.60 ± 5.56)U/mg prot]. Immunohistochemical studies indicated that the brown particles were CuZn-SOD positive signals, which mainly located cytoplasm in normal skin tissues, hypertrophic scars as well as keloids epidermal keratinocytes and dermal fibroblasts. CuZn-SOD expression evaluation in hypertrophic scars (4.14 ± 0.90, P lt; 0.05) and keloids epidermal keratinocytes (4.43 ± 0.79, P lt; 0.05) markedly increased when compared with normal skin tissues (2.20 ± 0.45). The expression of CuZn-SODin hypertrophic scars (4.00 ± 0.82, P lt; 0.05) and keloids dermal fibroblasts (4.43 ± 0.53, P lt; 0.05) were significantly higher than that of normal skin tissues (1.60 ± 0.89). There were no differences in the content of MDA, CuZn-SOD activity and expression evaluation between hypertrophic scars and keloids (P gt; 0.05). Conclusion In pathological scars, the contents of MDA and CuZn-SOD activity increase and the expressions of CuZn-SOD are enlarged.
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.
Through dog models of common bile duct obstruction (BDO), the contents of liver superoxide dismutase (SOD) and malondialdehyde(MDA) were measured 2,3,4 and 5 weeks after BDO. Results indicated that the hepatic MDA content was increased 2 weeks after BDO as compared with control group (Ｐ＜0.01), the hepatic SOD content was decreased 3 weeks after BDO (Ｐ＜0.05). When bile duct obstructing, these changed were more serious. The results suggest that liver has little ability to eliminate the superoxide free radicals after BDO, whereas the lipid peroxidation products increase. It may be one of the mechanisms of liver damage after BDO.