高糖危象患者血清瘦素和氧化应激的关系

目的 探讨高糖危象患者血清瘦素水平变化及与氧化应激的关系.方法 选择糖尿病酮症酸中毒和非酮症高血糖患者96例,静脉泵入胰岛素0.1 U·kg1·h1,同时给予补液、对症治疗以及胃肠和静脉营养.检测高糖危象患者治疗前及病情缓解时(72 h)血清瘦素、超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量、总抗氧化能力(TAC)和8-异前列腺素F2α(8-iso-PGF2α)水平.另外选择35例健康体检者作为对照组.结果 高糖危象患者治疗前SOD、TAC和瘦素水平均显著低于健康对照组,而MDA和8-iso-PGF2a均显著高于健康对照组(P均<0.05);高糖危象患者治疗后SOD、TAC和瘦素均显著高于治疗前,而MDA和8-iso-PGF2a均显著低于治疗前(P均<0.05).高糖危象患者治疗前瘦素与MDA呈显著正相关(r=0.38,P<0.05),治疗后瘦素与MDA和8-iso-PGF2a呈显著负相关(r1=-0.35,r2=-0.37,P均<0.05).多元逐步回归分析显示MDA和8-iso-PGF2α均为影响血清瘦素水平的显著因素.结论 高糖危象患者血清瘦素水平明显下降,且与氧化应激有关.     

Type 2 diabetes model TSOD mouse is exposed to oxidative stress at young age

Tsumura Suzuki Obese Diabetes (TSOD) mouse, a model of obese type 2 diabetes, older than around 11 weeks of age develops diabetic phenotypes. Previous studies have indicated that the development of diabetes is partly due to three loci associated with body weight and glucose homeostasis. However, little is known about the initial events triggering the development of the diabetic phenotypes in TSOD mouse. Here, we investigated the alteration of diabetes-related parameters, including the levels of blood glucose and inflammatory cytokines, and the oxidative stress status, in young TSOD mice. TSOD mice at 5 weeks of age showed increases in body weight and plasma total cholesterol level, but not hyperglycemia or impaired glucose tolerance, compared with age-matched control Tsumura Suzuki Non-Obese (TSNO) mice. Plasma tumor necrosis factor (TNF)-α and interleukin (IL)-6 were not detected in TSOD mice at 5 weeks of age. However, plasma total hydroxyoctadecadienoic acid (tHODE), a biomarker of oxidative stress, was increased in TSOD mice relative to TSNO mice at same age. The results demonstrated that young TSOD mice are exposed to oxidative stress before developing the diabetic phenotypes, and suggested that oxidative stress is an initial event triggering the development of diabetes in TSOD mice.     

Aβ25-35致PC12细胞核酸、蛋白质氧化损伤及依达拉奉的保护作用

目的 研究依达拉奉对淀粉样β蛋白25-35（Aβ25-35）诱导的PC12细胞核酸、蛋白质氧化损伤的保护作用。方法 实验对象分为三组：依达拉奉保护组（依达拉奉20μmol／L,Aβ25-35 30 μmol／L）、Aβ25-35干预组（Aβ25-35 30 μmol／L）和正常对照组。采用MTT法测定细胞生存率；慧星法测定DNA单链损伤；ELISA法测定羰基蛋白含量；比色法测定羟自由基（．OH）并计算，OH清除率。结果 与正常对照组相比，Aβ25-35干预组细胞生存率降低。DNA单链损伤明显加重，细胞内羰基蛋白含量升高（P均〈0．001）。依达拉奉保护组与Aβ25-35干预组相比，细胞生存率明显升高，DNA单链损伤明显减轻，细胞内羰基蛋白含量减低（P〈0．001或P〈0．01），但都未达到正常水平。依达拉奉对．OH的有效清除率可高达79．98％。结论 依达拉奉能够通过清除．OH来减轻DNA损伤。并能减少细胞内蛋白质氧化产物的生成，具有神经保护作用。     

大鼠酒精性肝病细胞凋亡与细胞色素P450 2E1和氧化应激的关系

目的 观察酒精性肝病(ALD)大鼠肝组织病理学改变,探讨细胞凋亡与细胞色素P4502E1(CYP2E1)的表达以及与氧化应激的关系.方法 用乙醇灌胃法制备ALD大鼠模型,模型组(37只)给予体积分数为40%的乙醇8 g·kg-1·d-1分两次灌胃,连续8周;对照组(33只)给予等量生理盐水灌胃.实验第8周末,各组选30只大鼠观察肝组织的病理学改变;用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法(TUNEL)检测肝细胞凋亡,用全自动生化仪检测丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)值,用聚合酶链反应(PCR)法测定肝CYP2E1的表达;分别用硫代巴比妥酸法和黄嘌呤氧化酶法测定血清丙二醛(MDA)含量和超氧化物歧化酶(SOD)活性.结果 模型组凋亡的肝细胞明显增多,主要分布在中央静脉周围、点状和灶状坏死区.对照组CYP2E1的c1基因频率为91.65%、c2基因频率为8.35%;模型组c1基因频率为53.35%、c2基因频率为46.65%,差异均有显著性(P均＜0.05).长期摄入乙醇的大鼠血清MDA含量增加,SOD活性下降,与ALD肝细胞凋亡程度有相关性(rMDA=0.644,rSOD=-0.511,P均＜0.05),且MDA与SOD两指标间呈负相关(r=-0.582,P＜0.05).结论 长期摄入乙醇可引起大鼠ALD及肝功能损伤,肝细胞凋亡明显增加.CYP2E1基因PstⅠ及RsaⅠ限制性片段长度多态性与ALD有关,其中c2基因可能与大鼠ALD的发生有关.MDA含量和SOD活性在ALD的肝细胞凋亡过程及脂质过氧化反应中发挥重要作用.     

神经生长因子撤退诱导神经元样PC12细胞凋亡及HRK/MCL-1基因表达变化

目的:探讨神经生长因子(NGF)撤退对已分化神经元样PC12细胞的影响.方法:建立NGF诱导PC12细胞交感神经元样分化模型,观察NGF撤退后,神经元样PC12细胞形态学及超微结构的变化情况,检测凋亡相关基因HRK/MCL-1的表达变化情况.结果:神经元样PC12细胞在NGF撤退后,可观察到显著的细胞凋亡样特征性改变,并随着NGF撒退时间的延长,凋亡率不断增加,同时随着NGF撤退时间的延长,促凋亡基因HRK的表达不断增高.而抑凋亡基因MCL-1在撤退24 h内表达水平下降明显,撤退24 h后变化不显著.结论:NGF撒退确实能诱导已分化的神经元样PC12细胞出现典型的神经元细胞凋亡现象,该现象与凋亡相关基因HRK/MCL-1的表达变化有密切关系.     

高糖危象患者血清瘦素和氧化应激的关系

Objective To investigate the relationship between the levels of serum leptin and oxidative stress in patients with hyperglycemia crisis. Methods A total of 96 patients with diabetic ketoaeidosis (DKA) and nonketotic hyperglycemia (NKH) were treated on a low-dose insulin protocol using intravenous infusion of insulin with the established rate of 0.1U·kg-1·h-1,with the patients on intravenous fluids and receiving nutrition by mouth and vein. The levels of serum leptin, 8-iso-prostaglandin F2α (8-iso-PGF2α, the activities of superoxide dismutase (SOD), total antioxidant capacity (TAC) and the contents of malondialdehyde (MDA) in 96 patients with hyperglycemia crisis on admission and after insulin therapy with resolution of hyperglycemia and ketoacidosis (72 hours) were measured. Another 35 healthy individuals served as normal control. Results The activities of SOD, TAC and the levels of leptin before treatment were lower in patients with hyperglycemia crisis than in normal controls, and the levels of MDA and 8-iso-PGF2a were more markedly elevated than those in normal controls (all P<0. 05). The activities of SOD, TAC and the levels of leptin in patients after treatment were significantly higher than those in patients before treatment, and the levels of MDA and 8-iso-PGF2a. were significantly lower than those in patients on admission (all P<0. 05). There was significant positive correlation between leptin and MDA in patients before treatment (r=0. 38, P<0. 05), and the level of leptin was negatively correlated with MDA and 8-iso-PGF2a in patients after treatment (r1 = - 0. 35, r2= - 0. 37, both P < 0. 05). In stepwise regression analysis, MDA and 8-iso-PGF2α showed a significant association with leptin. Conclusion The levels of leptin are significantly lowered in patients with hyperglycemia crisis. Oxidative stress may participate in determining the leptin level in hyperglycemia crisis.     

高糖危象患者血清瘦素和氧化应激的关系

Objective To investigate the relationship between the levels of serum leptin and oxidative stress in patients with hyperglycemia crisis. Methods A total of 96 patients with diabetic ketoaeidosis (DKA) and nonketotic hyperglycemia (NKH) were treated on a low-dose insulin protocol using intravenous infusion of insulin with the established rate of 0.1U·kg-1·h-1,with the patients on intravenous fluids and receiving nutrition by mouth and vein. The levels of serum leptin, 8-iso-prostaglandin F2α (8-iso-PGF2α, the activities of superoxide dismutase (SOD), total antioxidant capacity (TAC) and the contents of malondialdehyde (MDA) in 96 patients with hyperglycemia crisis on admission and after insulin therapy with resolution of hyperglycemia and ketoacidosis (72 hours) were measured. Another 35 healthy individuals served as normal control. Results The activities of SOD, TAC and the levels of leptin before treatment were lower in patients with hyperglycemia crisis than in normal controls, and the levels of MDA and 8-iso-PGF2a were more markedly elevated than those in normal controls (all P<0. 05). The activities of SOD, TAC and the levels of leptin in patients after treatment were significantly higher than those in patients before treatment, and the levels of MDA and 8-iso-PGF2a. were significantly lower than those in patients on admission (all P<0. 05). There was significant positive correlation between leptin and MDA in patients before treatment (r=0. 38, P<0. 05), and the level of leptin was negatively correlated with MDA and 8-iso-PGF2a in patients after treatment (r1 = - 0. 35, r2= - 0. 37, both P < 0. 05). In stepwise regression analysis, MDA and 8-iso-PGF2α showed a significant association with leptin. Conclusion The levels of leptin are significantly lowered in patients with hyperglycemia crisis. Oxidative stress may participate in determining the leptin level in hyperglycemia crisis.     

高糖危象患者血清瘦素和氧化应激的关系

Objective To investigate the relationship between the levels of serum leptin and oxidative stress in patients with hyperglycemia crisis. Methods A total of 96 patients with diabetic ketoaeidosis (DKA) and nonketotic hyperglycemia (NKH) were treated on a low-dose insulin protocol using intravenous infusion of insulin with the established rate of 0.1U·kg-1·h-1,with the patients on intravenous fluids and receiving nutrition by mouth and vein. The levels of serum leptin, 8-iso-prostaglandin F2α (8-iso-PGF2α, the activities of superoxide dismutase (SOD), total antioxidant capacity (TAC) and the contents of malondialdehyde (MDA) in 96 patients with hyperglycemia crisis on admission and after insulin therapy with resolution of hyperglycemia and ketoacidosis (72 hours) were measured. Another 35 healthy individuals served as normal control. Results The activities of SOD, TAC and the levels of leptin before treatment were lower in patients with hyperglycemia crisis than in normal controls, and the levels of MDA and 8-iso-PGF2a were more markedly elevated than those in normal controls (all P<0. 05). The activities of SOD, TAC and the levels of leptin in patients after treatment were significantly higher than those in patients before treatment, and the levels of MDA and 8-iso-PGF2a. were significantly lower than those in patients on admission (all P<0. 05). There was significant positive correlation between leptin and MDA in patients before treatment (r=0. 38, P<0. 05), and the level of leptin was negatively correlated with MDA and 8-iso-PGF2a in patients after treatment (r1 = - 0. 35, r2= - 0. 37, both P < 0. 05). In stepwise regression analysis, MDA and 8-iso-PGF2α showed a significant association with leptin. Conclusion The levels of leptin are significantly lowered in patients with hyperglycemia crisis. Oxidative stress may participate in determining the leptin level in hyperglycemia crisis.     

高糖危象患者血清瘦素和氧化应激的关系

Objective To investigate the relationship between the levels of serum leptin and oxidative stress in patients with hyperglycemia crisis. Methods A total of 96 patients with diabetic ketoaeidosis (DKA) and nonketotic hyperglycemia (NKH) were treated on a low-dose insulin protocol using intravenous infusion of insulin with the established rate of 0.1U·kg-1·h-1,with the patients on intravenous fluids and receiving nutrition by mouth and vein. The levels of serum leptin, 8-iso-prostaglandin F2α (8-iso-PGF2α, the activities of superoxide dismutase (SOD), total antioxidant capacity (TAC) and the contents of malondialdehyde (MDA) in 96 patients with hyperglycemia crisis on admission and after insulin therapy with resolution of hyperglycemia and ketoacidosis (72 hours) were measured. Another 35 healthy individuals served as normal control. Results The activities of SOD, TAC and the levels of leptin before treatment were lower in patients with hyperglycemia crisis than in normal controls, and the levels of MDA and 8-iso-PGF2a were more markedly elevated than those in normal controls (all P<0. 05). The activities of SOD, TAC and the levels of leptin in patients after treatment were significantly higher than those in patients before treatment, and the levels of MDA and 8-iso-PGF2a. were significantly lower than those in patients on admission (all P<0. 05). There was significant positive correlation between leptin and MDA in patients before treatment (r=0. 38, P<0. 05), and the level of leptin was negatively correlated with MDA and 8-iso-PGF2a in patients after treatment (r1 = - 0. 35, r2= - 0. 37, both P < 0. 05). In stepwise regression analysis, MDA and 8-iso-PGF2α showed a significant association with leptin. Conclusion The levels of leptin are significantly lowered in patients with hyperglycemia crisis. Oxidative stress may participate in determining the leptin level in hyperglycemia crisis.     

高糖危象患者血清瘦素和氧化应激的关系

Objective To investigate the relationship between the levels of serum leptin and oxidative stress in patients with hyperglycemia crisis. Methods A total of 96 patients with diabetic ketoaeidosis (DKA) and nonketotic hyperglycemia (NKH) were treated on a low-dose insulin protocol using intravenous infusion of insulin with the established rate of 0.1U·kg-1·h-1,with the patients on intravenous fluids and receiving nutrition by mouth and vein. The levels of serum leptin, 8-iso-prostaglandin F2α (8-iso-PGF2α, the activities of superoxide dismutase (SOD), total antioxidant capacity (TAC) and the contents of malondialdehyde (MDA) in 96 patients with hyperglycemia crisis on admission and after insulin therapy with resolution of hyperglycemia and ketoacidosis (72 hours) were measured. Another 35 healthy individuals served as normal control. Results The activities of SOD, TAC and the levels of leptin before treatment were lower in patients with hyperglycemia crisis than in normal controls, and the levels of MDA and 8-iso-PGF2a were more markedly elevated than those in normal controls (all P<0. 05). The activities of SOD, TAC and the levels of leptin in patients after treatment were significantly higher than those in patients before treatment, and the levels of MDA and 8-iso-PGF2a. were significantly lower than those in patients on admission (all P<0. 05). There was significant positive correlation between leptin and MDA in patients before treatment (r=0. 38, P<0. 05), and the level of leptin was negatively correlated with MDA and 8-iso-PGF2a in patients after treatment (r1 = - 0. 35, r2= - 0. 37, both P < 0. 05). In stepwise regression analysis, MDA and 8-iso-PGF2α showed a significant association with leptin. Conclusion The levels of leptin are significantly lowered in patients with hyperglycemia crisis. Oxidative stress may participate in determining the leptin level in hyperglycemia crisis.     

高糖危象患者血清瘦素和氧化应激的关系

Objective To investigate the relationship between the levels of serum leptin and oxidative stress in patients with hyperglycemia crisis. Methods A total of 96 patients with diabetic ketoaeidosis (DKA) and nonketotic hyperglycemia (NKH) were treated on a low-dose insulin protocol using intravenous infusion of insulin with the established rate of 0.1U·kg-1·h-1,with the patients on intravenous fluids and receiving nutrition by mouth and vein. The levels of serum leptin, 8-iso-prostaglandin F2α (8-iso-PGF2α, the activities of superoxide dismutase (SOD), total antioxidant capacity (TAC) and the contents of malondialdehyde (MDA) in 96 patients with hyperglycemia crisis on admission and after insulin therapy with resolution of hyperglycemia and ketoacidosis (72 hours) were measured. Another 35 healthy individuals served as normal control. Results The activities of SOD, TAC and the levels of leptin before treatment were lower in patients with hyperglycemia crisis than in normal controls, and the levels of MDA and 8-iso-PGF2a were more markedly elevated than those in normal controls (all P<0. 05). The activities of SOD, TAC and the levels of leptin in patients after treatment were significantly higher than those in patients before treatment, and the levels of MDA and 8-iso-PGF2a. were significantly lower than those in patients on admission (all P<0. 05). There was significant positive correlation between leptin and MDA in patients before treatment (r=0. 38, P<0. 05), and the level of leptin was negatively correlated with MDA and 8-iso-PGF2a in patients after treatment (r1 = - 0. 35, r2= - 0. 37, both P < 0. 05). In stepwise regression analysis, MDA and 8-iso-PGF2α showed a significant association with leptin. Conclusion The levels of leptin are significantly lowered in patients with hyperglycemia crisis. Oxidative stress may participate in determining the leptin level in hyperglycemia crisis.     

高糖危象患者血清瘦素和氧化应激的关系

Objective To investigate the relationship between the levels of serum leptin and oxidative stress in patients with hyperglycemia crisis. Methods A total of 96 patients with diabetic ketoaeidosis (DKA) and nonketotic hyperglycemia (NKH) were treated on a low-dose insulin protocol using intravenous infusion of insulin with the established rate of 0.1U·kg-1·h-1,with the patients on intravenous fluids and receiving nutrition by mouth and vein. The levels of serum leptin, 8-iso-prostaglandin F2α (8-iso-PGF2α, the activities of superoxide dismutase (SOD), total antioxidant capacity (TAC) and the contents of malondialdehyde (MDA) in 96 patients with hyperglycemia crisis on admission and after insulin therapy with resolution of hyperglycemia and ketoacidosis (72 hours) were measured. Another 35 healthy individuals served as normal control. Results The activities of SOD, TAC and the levels of leptin before treatment were lower in patients with hyperglycemia crisis than in normal controls, and the levels of MDA and 8-iso-PGF2a were more markedly elevated than those in normal controls (all P<0. 05). The activities of SOD, TAC and the levels of leptin in patients after treatment were significantly higher than those in patients before treatment, and the levels of MDA and 8-iso-PGF2a. were significantly lower than those in patients on admission (all P<0. 05). There was significant positive correlation between leptin and MDA in patients before treatment (r=0. 38, P<0. 05), and the level of leptin was negatively correlated with MDA and 8-iso-PGF2a in patients after treatment (r1 = - 0. 35, r2= - 0. 37, both P < 0. 05). In stepwise regression analysis, MDA and 8-iso-PGF2α showed a significant association with leptin. Conclusion The levels of leptin are significantly lowered in patients with hyperglycemia crisis. Oxidative stress may participate in determining the leptin level in hyperglycemia crisis.     

Aegle marmelos fruit extract attenuates isoproterenol-induced oxidative stress in rats

Myocardial infarction is a major public health concern and the leading cause of death throughout the world. The present study investigates the ability of Aegle marmelos fruit extract to prevent pathological changes and oxidative stress after isoproterenol induced myocardial infarction in rats. In vitro studies showed that Aegle marmelos fruit extract possesses antioxidant activity. Administration of isoproterenol (85 mg/kg body weight) to rats resulted in significantly elevated plasma transaminases, lactate dehydrogenase and creatine kinase, however, cardiac tissue analyses showed decreased activity of the above enzymes compared to experimental control rats. Further, isoproterenol administration significantly increased plasma and cardiac tissue thiobarbituric acid reactive substances and lowered the activities of cardiac tissue superoxide dismutase, catalase, reduced glutathione, glutathione peroxidase and glutathione-S-transferase when compared to control groups. Pretreatment with Aegle marmelos fruit extract at a dose of 150 mg/kg body weight for a period of 45 days significantly prevented the observed alterations. Our data suggest that Aegle marmelos fruit extract exerts its protective effect by decreasing thiobarbituric acid reactive substances and elevating antioxidants status in isoproterenol treated rats. Both biochemical and histopathological results in the isoproterenol-induced myocardial infarction model emphasize the beneficial action of Aegle marmelos fruit extract as a cardioprotective agent.     

高糖危象患者血清瘦素和氧化应激的关系

Objective To investigate the relationship between the levels of serum leptin and oxidative stress in patients with hyperglycemia crisis. Methods A total of 96 patients with diabetic ketoaeidosis (DKA) and nonketotic hyperglycemia (NKH) were treated on a low-dose insulin protocol using intravenous infusion of insulin with the established rate of 0.1U·kg-1·h-1,with the patients on intravenous fluids and receiving nutrition by mouth and vein. The levels of serum leptin, 8-iso-prostaglandin F2α (8-iso-PGF2α, the activities of superoxide dismutase (SOD), total antioxidant capacity (TAC) and the contents of malondialdehyde (MDA) in 96 patients with hyperglycemia crisis on admission and after insulin therapy with resolution of hyperglycemia and ketoacidosis (72 hours) were measured. Another 35 healthy individuals served as normal control. Results The activities of SOD, TAC and the levels of leptin before treatment were lower in patients with hyperglycemia crisis than in normal controls, and the levels of MDA and 8-iso-PGF2a were more markedly elevated than those in normal controls (all P<0. 05). The activities of SOD, TAC and the levels of leptin in patients after treatment were significantly higher than those in patients before treatment, and the levels of MDA and 8-iso-PGF2a. were significantly lower than those in patients on admission (all P<0. 05). There was significant positive correlation between leptin and MDA in patients before treatment (r=0. 38, P<0. 05), and the level of leptin was negatively correlated with MDA and 8-iso-PGF2a in patients after treatment (r1 = - 0. 35, r2= - 0. 37, both P < 0. 05). In stepwise regression analysis, MDA and 8-iso-PGF2α showed a significant association with leptin. Conclusion The levels of leptin are significantly lowered in patients with hyperglycemia crisis. Oxidative stress may participate in determining the leptin level in hyperglycemia crisis.     

高糖危象患者血清瘦素和氧化应激的关系

Objective To investigate the relationship between the levels of serum leptin and oxidative stress in patients with hyperglycemia crisis. Methods A total of 96 patients with diabetic ketoaeidosis (DKA) and nonketotic hyperglycemia (NKH) were treated on a low-dose insulin protocol using intravenous infusion of insulin with the established rate of 0.1U·kg-1·h-1,with the patients on intravenous fluids and receiving nutrition by mouth and vein. The levels of serum leptin, 8-iso-prostaglandin F2α (8-iso-PGF2α, the activities of superoxide dismutase (SOD), total antioxidant capacity (TAC) and the contents of malondialdehyde (MDA) in 96 patients with hyperglycemia crisis on admission and after insulin therapy with resolution of hyperglycemia and ketoacidosis (72 hours) were measured. Another 35 healthy individuals served as normal control. Results The activities of SOD, TAC and the levels of leptin before treatment were lower in patients with hyperglycemia crisis than in normal controls, and the levels of MDA and 8-iso-PGF2a were more markedly elevated than those in normal controls (all P<0. 05). The activities of SOD, TAC and the levels of leptin in patients after treatment were significantly higher than those in patients before treatment, and the levels of MDA and 8-iso-PGF2a. were significantly lower than those in patients on admission (all P<0. 05). There was significant positive correlation between leptin and MDA in patients before treatment (r=0. 38, P<0. 05), and the level of leptin was negatively correlated with MDA and 8-iso-PGF2a in patients after treatment (r1 = - 0. 35, r2= - 0. 37, both P < 0. 05). In stepwise regression analysis, MDA and 8-iso-PGF2α showed a significant association with leptin. Conclusion The levels of leptin are significantly lowered in patients with hyperglycemia crisis. Oxidative stress may participate in determining the leptin level in hyperglycemia crisis.     

高糖危象患者血清瘦素和氧化应激的关系

Objective To investigate the relationship between the levels of serum leptin and oxidative stress in patients with hyperglycemia crisis. Methods A total of 96 patients with diabetic ketoaeidosis (DKA) and nonketotic hyperglycemia (NKH) were treated on a low-dose insulin protocol using intravenous infusion of insulin with the established rate of 0.1U·kg-1·h-1,with the patients on intravenous fluids and receiving nutrition by mouth and vein. The levels of serum leptin, 8-iso-prostaglandin F2α (8-iso-PGF2α, the activities of superoxide dismutase (SOD), total antioxidant capacity (TAC) and the contents of malondialdehyde (MDA) in 96 patients with hyperglycemia crisis on admission and after insulin therapy with resolution of hyperglycemia and ketoacidosis (72 hours) were measured. Another 35 healthy individuals served as normal control. Results The activities of SOD, TAC and the levels of leptin before treatment were lower in patients with hyperglycemia crisis than in normal controls, and the levels of MDA and 8-iso-PGF2a were more markedly elevated than those in normal controls (all P<0. 05). The activities of SOD, TAC and the levels of leptin in patients after treatment were significantly higher than those in patients before treatment, and the levels of MDA and 8-iso-PGF2a. were significantly lower than those in patients on admission (all P<0. 05). There was significant positive correlation between leptin and MDA in patients before treatment (r=0. 38, P<0. 05), and the level of leptin was negatively correlated with MDA and 8-iso-PGF2a in patients after treatment (r1 = - 0. 35, r2= - 0. 37, both P < 0. 05). In stepwise regression analysis, MDA and 8-iso-PGF2α showed a significant association with leptin. Conclusion The levels of leptin are significantly lowered in patients with hyperglycemia crisis. Oxidative stress may participate in determining the leptin level in hyperglycemia crisis.     

应激状态下肠上皮细胞凋亡水平的变化及其机制

目的探讨在氧化应激状态下肠上皮细胞凋亡水平的变化以及凋亡异常发生的分子机制。方法使用过氧化氢(H2O2)处理培养的HT-29细胞模拟机体活性氧(ROS)损伤肠上皮细胞的体内状况,采用四甲基偶氮唑盐(MTT)微量酶反应比色法进行细胞生存力的检测;采用流式细胞术进行细胞凋亡的检测;采用蛋白质免疫印迹法(Westernblot)检测凋亡相关蛋白的表达。结果H2O2可降低HT-29细胞生存率,且呈现剂量依赖性和时间依赖性(P均<0.05);与空白对照组相比,随着H2O2浓度的增高,细胞凋亡率增加(P均<0.05),随着作用时间的延长,细胞凋亡率也增加(P<0.05);以不同浓度H2O2刺激HT-29细胞24h后发现,与空白对照组相比,Bax的表达随着H2O2浓度的增高而增加,Bcl-2的表达随着H2O2浓度的增高而降低。以500μmol/L,浓度的H2O2刺激HT-29细胞发现,Bax表达随着H2O2作用时间延长而增加,Bcl-2表达随着H2O2作用时间延长而降低。结论应激状态下,肠上皮细胞氧化应激水平与其凋亡程度相关,凋亡调控蛋白Bcl-2/Bax比值失调可能是肠上皮细胞凋亡过度的机制之一。     

Aliskiren attenuates myocardial apoptosis and oxidative stress in chronic murine model of cardiomyopathy

Doxorubicin (DXR) is one of the most effective antineoplastic agents. However, the optimal clinical use of this agent is limited because of marked cardiomyopathy and congestive heart failure. Renin angiotensin system (RAS) plays an important role in the development of cardiac hypertrophy, reperfusion injury and congestive heart failure. Aliskiren (ALK) is a direct inhibitor of renin and does not affect other systems involved in cardiovascular regulation. This study was designed to explore the possible protective effects of ALK (30 and 100 mg/kg, per oral [p.o.] respectively for 42 days) in chronic model of DXR (1.25 mg/kg, intraperitoneally (i.p.) sixteen equal cumulative doses) induced cardiomyopathy in rats. DXR treatment significantly (P < 0.01) increased the activities of serum creatine kinase (CK-MB), lactate dehydrogenase (LDH), cardiomyocyte caspase-3 and catalase (CAT). ALK (100 mg/kg) treatment prevented the animals significantly (P < 0.01) from rise in the above indices. Furthermore ALK (100 mg/kg) significantly restores the DXR-induced decrease in antioxidant defense, reduced glutathione (GSH) and superoxide dismutase (SOD). Transmission electron microscopic studies showed that DXR caused apoptosis in myocardium, manifested as condensation of chromatin network at the margins and rupture of nuclear membrane which was well protected by ALK (100 mg/kg) treatment. The present study indicates that ALK protected rats from DXR-induced cardiomyopathy.