Objective:To study the correlation of serum homocysteine (Hcy) metabolism with nerve cytokine and apoptosis molecule levels in patients with epilepsy.Methods:Patients with epileptic seizures and non-epileptic seizures...Objective:To study the correlation of serum homocysteine (Hcy) metabolism with nerve cytokine and apoptosis molecule levels in patients with epilepsy.Methods:Patients with epileptic seizures and non-epileptic seizures who were treated in our hospital between January 2014 and December 2016 were selected as epileptic seizure group and non-epileptic seizure group respectively, and healthy volunteers during the same period were as selected as control group. The serum was collected to determine the levels of Hcy metabolism indexes, nerve cytokines and apoptosis molecules.Results:Serum Hcy, BDNF, NGF, NSE, IGF-I, Bax, Caspase-3, MDA and 8-OHdG levels of epileptic seizure group were significantly higher than those of non-epileptic seizure group and control group while VitB12, Fol and Bcl-2 levels were significantly lower than those of non-epileptic seizure group and control group;serum Hcy, VitB12, Fol, BDNF, NGF, NSE, IGF-I, Bcl-2, Bax, Caspase-3, MDA and 8-OHdG levels of non-epileptic seizure group were not significantly different from those of control group;serum Hcy level in patients with epileptic seizure was positively correlated with BDNF, NGF, NSE, IGF-I, Bax, Caspase-3, MDA and 8-OHdG levels, and negatively correlated with Bcl-2 level while VitB12 and Fol levels were negatively correlated with BDNF, NGF, NSE, IGF-I, Bax, Caspase-3, MDA and 8-OHdG levels, and positively correlated with Bcl-2 level.Conclusion:Abnormal serum Hcy metabolism in patients with epileptic seizures can aggravate the neuron injury and apoptosis.展开更多
Objective To evaluate the effects of Carvedilol on cardiopulmonary bypass (CPB)-induced myocardiocyte apoptosis and its effects on regulation of Fas, FasL expression, caspase-3 activity and oxidative stress in the le...Objective To evaluate the effects of Carvedilol on cardiopulmonary bypass (CPB)-induced myocardiocyte apoptosis and its effects on regulation of Fas, FasL expression, caspase-3 activity and oxidative stress in the left ventricle (LV) in this setting.Methods Ten adult dogs undergoing conventional hypothermic CPB were randomly divided into control and Carvedilol treated groups (n=5, respectively). Dogs in Carvedilol treated group received a bolus of Carvedilol (1 mg/kg) intravenously and a maintenance dosage of Carvedilol (3 μg·min -1·kg -1) for 3 hours after the reperfusion of the heart. Dogs in control group received no Carvediolol. LV samples were obtained before, during and 3 hours after CPB. In situ nick end-labeling (TUNEL) technique was used to detect the apoptotic cells. The expressions of Fas and FasL were detected immunohistochemically and quantified by fluorescence activated cell sorting (FACS). The activity of caspase-3 enzyme and malondialdehyde (MDA) level were measured by cleavage of Z-DEVD-AMC substrate and thiobarbituric acid reactive substance (TBARS) method, respectively. Results Before and during CPB, all the parameters were not significantly different intra- or between groups (P>0.05). After CPB, these parameters in both groups were significantly elevated compared with those of before and during CPB (P<0.028, respectively). However, the number of apoptotic cells in Carvedilol treated group was significantly decreased compared with that of the control group (P<0.021). The expressions of Fas and FasL were significantly downregulated by Carvedilol (P<0.001 and 0.003, respectively). The caspase-3 activity and the content of MDA in the Carvedilol treated group was also significantly reduced (P<0.026 and 0.005, respectively). Conclusions Carvedilol significantly reduces CPB-induced cardiomyocyte apoptosis in dog hearts and the reduction of cardiomyocyte apoptosis is associated with downregulation of Fas and FasL expression, inhibition of caspase-3 activity and oxidative stress in LV.展开更多
文摘Objective:To study the correlation of serum homocysteine (Hcy) metabolism with nerve cytokine and apoptosis molecule levels in patients with epilepsy.Methods:Patients with epileptic seizures and non-epileptic seizures who were treated in our hospital between January 2014 and December 2016 were selected as epileptic seizure group and non-epileptic seizure group respectively, and healthy volunteers during the same period were as selected as control group. The serum was collected to determine the levels of Hcy metabolism indexes, nerve cytokines and apoptosis molecules.Results:Serum Hcy, BDNF, NGF, NSE, IGF-I, Bax, Caspase-3, MDA and 8-OHdG levels of epileptic seizure group were significantly higher than those of non-epileptic seizure group and control group while VitB12, Fol and Bcl-2 levels were significantly lower than those of non-epileptic seizure group and control group;serum Hcy, VitB12, Fol, BDNF, NGF, NSE, IGF-I, Bcl-2, Bax, Caspase-3, MDA and 8-OHdG levels of non-epileptic seizure group were not significantly different from those of control group;serum Hcy level in patients with epileptic seizure was positively correlated with BDNF, NGF, NSE, IGF-I, Bax, Caspase-3, MDA and 8-OHdG levels, and negatively correlated with Bcl-2 level while VitB12 and Fol levels were negatively correlated with BDNF, NGF, NSE, IGF-I, Bax, Caspase-3, MDA and 8-OHdG levels, and positively correlated with Bcl-2 level.Conclusion:Abnormal serum Hcy metabolism in patients with epileptic seizures can aggravate the neuron injury and apoptosis.
文摘Objective To evaluate the effects of Carvedilol on cardiopulmonary bypass (CPB)-induced myocardiocyte apoptosis and its effects on regulation of Fas, FasL expression, caspase-3 activity and oxidative stress in the left ventricle (LV) in this setting.Methods Ten adult dogs undergoing conventional hypothermic CPB were randomly divided into control and Carvedilol treated groups (n=5, respectively). Dogs in Carvedilol treated group received a bolus of Carvedilol (1 mg/kg) intravenously and a maintenance dosage of Carvedilol (3 μg·min -1·kg -1) for 3 hours after the reperfusion of the heart. Dogs in control group received no Carvediolol. LV samples were obtained before, during and 3 hours after CPB. In situ nick end-labeling (TUNEL) technique was used to detect the apoptotic cells. The expressions of Fas and FasL were detected immunohistochemically and quantified by fluorescence activated cell sorting (FACS). The activity of caspase-3 enzyme and malondialdehyde (MDA) level were measured by cleavage of Z-DEVD-AMC substrate and thiobarbituric acid reactive substance (TBARS) method, respectively. Results Before and during CPB, all the parameters were not significantly different intra- or between groups (P>0.05). After CPB, these parameters in both groups were significantly elevated compared with those of before and during CPB (P<0.028, respectively). However, the number of apoptotic cells in Carvedilol treated group was significantly decreased compared with that of the control group (P<0.021). The expressions of Fas and FasL were significantly downregulated by Carvedilol (P<0.001 and 0.003, respectively). The caspase-3 activity and the content of MDA in the Carvedilol treated group was also significantly reduced (P<0.026 and 0.005, respectively). Conclusions Carvedilol significantly reduces CPB-induced cardiomyocyte apoptosis in dog hearts and the reduction of cardiomyocyte apoptosis is associated with downregulation of Fas and FasL expression, inhibition of caspase-3 activity and oxidative stress in LV.
