Retinal ischemia-reperfusion injury(RIRI)is a common cause of visual impairment and blindness.At the cellular level,ischemic and reperfuion retinal injury consists of a self-reinforcing destructive cascade involving o...Retinal ischemia-reperfusion injury(RIRI)is a common cause of visual impairment and blindness.At the cellular level,ischemic and reperfuion retinal injury consists of a self-reinforcing destructive cascade involving oxidative stress initiated by energy failure,inflammatory reaction,calcium influx,increased glutamatergic stimulation and neuronal depolarisation and apoptosis.A number of animal models and analytical techniques have been used to study the retinal ischemia-reperfusion injury,we now understand much better than ever before in the mechanism of RIRI,and an increase in the therapeutic strategies has been developed experimentally to attenuate the detrimental effects of retinal ischemia-reperfusion injury.Thus far,however,success in the laboratory has not been translated to the clinic.Given the increasing understanding of the events involved in ischemia-reperfusion neuronal injury,it is hoped that clinically effective treatments for retinal ischemia-reperfusion injury will soon be available.展开更多
Objective: To explore the effect and mechanism of angiotensin II receptor blockers-Irbesartan on occurrence of ventricular arrhythmias in rats with myocardial ischemia. Methods: Rats with embryonic cardiomyocytes-H9c2...Objective: To explore the effect and mechanism of angiotensin II receptor blockers-Irbesartan on occurrence of ventricular arrhythmias in rats with myocardial ischemia. Methods: Rats with embryonic cardiomyocytes-H9c2 were randomly divided into control group. ischemia group. Irbesartan group and Irbesartan+ischemia group. The cell viability of rats in each group was tested using MTT. Real-time PCR was employed to detect the expression of connexin43 (Cx43) mRNA and western blot to detect the expression of Cx43 and phosphorylated Cx43. SD rats were randomly divided into the sham-operation group (SO). myocardial infarction group (MI). Irbesartan group and MI+ Irbesartan group, with 10 rats in each group. HE staining was employed to observe the change in the pathomorpholouy of left ventricular tissue and TUNEL method to analyze the cell apoptosis in the tissue. The immunofluorescence was adopted to observe the expression and distribution of Cx43 in the left ventricular myocardium and study the change in the expression of Cx43 in the cardiac muscular tissue at mRNA and protein level. Results: The intervention of lrbesartan in the condition of ischemia indicated the significant decrease in the number of necrotic cells. The expression of Cx43 was significantly decreased under the culture of ischemia (P<0.05), but in the presence of Irbesartan, the expression of Cx43 was increased compared with the ischemia group (p<0.01). The results of WB assay showed the similar trend of change at mRNA level. There was the significant difference in the score of ventricular arerythmia between MI group and SO group (P<0.01). The incidence of ventricular tachycardia or ventricular fibrillation was significantly increased compared with the one in SO group (P<0.05). There was the significant difference in the overall score between MI+Irbesartan group and MI group (P<0.05). The expression of Cx43 in the cardiac muscular tissue in MI group was significantly decreased (P<0.01(US) SO group). But the expression of Cx43 was increased after the treatment with Irbesartan. Conclusions: Irbesartan can inhibit the injury of H9c2 cardiomyocytes and the decreased expression of Cx43 that are induced by the ischemic myocardial infarction. Irbesartan can also improve the reconstruction of Cx43 in rats with ischemic myocardium to inhibit the myocardial infarction-induced arrhythmias.展开更多
文摘Retinal ischemia-reperfusion injury(RIRI)is a common cause of visual impairment and blindness.At the cellular level,ischemic and reperfuion retinal injury consists of a self-reinforcing destructive cascade involving oxidative stress initiated by energy failure,inflammatory reaction,calcium influx,increased glutamatergic stimulation and neuronal depolarisation and apoptosis.A number of animal models and analytical techniques have been used to study the retinal ischemia-reperfusion injury,we now understand much better than ever before in the mechanism of RIRI,and an increase in the therapeutic strategies has been developed experimentally to attenuate the detrimental effects of retinal ischemia-reperfusion injury.Thus far,however,success in the laboratory has not been translated to the clinic.Given the increasing understanding of the events involved in ischemia-reperfusion neuronal injury,it is hoped that clinically effective treatments for retinal ischemia-reperfusion injury will soon be available.
基金supported by Research Topic of Department of Health of Jiangxi Province(No.20131074)Natural Science Fund of Jiangxi Province(No:20122BAB205028)
文摘Objective: To explore the effect and mechanism of angiotensin II receptor blockers-Irbesartan on occurrence of ventricular arrhythmias in rats with myocardial ischemia. Methods: Rats with embryonic cardiomyocytes-H9c2 were randomly divided into control group. ischemia group. Irbesartan group and Irbesartan+ischemia group. The cell viability of rats in each group was tested using MTT. Real-time PCR was employed to detect the expression of connexin43 (Cx43) mRNA and western blot to detect the expression of Cx43 and phosphorylated Cx43. SD rats were randomly divided into the sham-operation group (SO). myocardial infarction group (MI). Irbesartan group and MI+ Irbesartan group, with 10 rats in each group. HE staining was employed to observe the change in the pathomorpholouy of left ventricular tissue and TUNEL method to analyze the cell apoptosis in the tissue. The immunofluorescence was adopted to observe the expression and distribution of Cx43 in the left ventricular myocardium and study the change in the expression of Cx43 in the cardiac muscular tissue at mRNA and protein level. Results: The intervention of lrbesartan in the condition of ischemia indicated the significant decrease in the number of necrotic cells. The expression of Cx43 was significantly decreased under the culture of ischemia (P<0.05), but in the presence of Irbesartan, the expression of Cx43 was increased compared with the ischemia group (p<0.01). The results of WB assay showed the similar trend of change at mRNA level. There was the significant difference in the score of ventricular arerythmia between MI group and SO group (P<0.01). The incidence of ventricular tachycardia or ventricular fibrillation was significantly increased compared with the one in SO group (P<0.05). There was the significant difference in the overall score between MI+Irbesartan group and MI group (P<0.05). The expression of Cx43 in the cardiac muscular tissue in MI group was significantly decreased (P<0.01(US) SO group). But the expression of Cx43 was increased after the treatment with Irbesartan. Conclusions: Irbesartan can inhibit the injury of H9c2 cardiomyocytes and the decreased expression of Cx43 that are induced by the ischemic myocardial infarction. Irbesartan can also improve the reconstruction of Cx43 in rats with ischemic myocardium to inhibit the myocardial infarction-induced arrhythmias.
