| Hypertension is the most important risk factor for cerebrovascular disease. In China it was reported that 80% of cerebral vascular diseases and hypertension, of which 86% of cerebral hemorrhage and cerebral infarction 71% have history of hypertension. But no symptoms of hypertension, the chance of cerebral vascular disease is 4 times the normal blood pressure, also found that both systolic or diastolic blood pressure increased the risk of brain disease are large. The mechanism of hypertension caused by cerebrovascular disease, cerebral arteriosclerosis mainly to accelerate the occurrence of cerebrovascular ischemia, degeneration, hardening, resulting in brain tissue blood supply, inadequate support for the occurrence of apoptosis provided the conditions in the area of cell death is physiological, active, reversible death, have called programmed cell death or apoptosis (programmed cell death, PCD). While for the treatment of high blood pressure, how to effectively inhibit apoptosis become a hot research topic.The experiment proved to significantly reduce blood pressure at spontaneously hypertensive rats (SHR) blood pressure, with the dose-effect relationship. However, on its hypertension disease caused apoptosis of brain research have not yet been reported. In this study, by RT-PCR and Western Blotting method on blood pressure in spontaneously hypertensive rats at induced gene expression of cerebral cortex were detected. To explore the antihypertensive NO.1 at prevention of hypertension induced apoptosis of neural cells for future clinical application further provides a basis for scientific experiments.Method:A total of 60 males and females half and half in spontaneously hypertensive rats (SHR) and 12 healthy males and females half and half Wistar rats (weight 200±20g), were randomly divided into 6 groups:1, the control group (healthy rats); 2, model group (spontaneously hypertensive rats); 3, positive drug group (captopril 5mg/kg.d); 4, antihypertensive NO.1 at the low dose group (antihypertensive NO.1 0.25g/kg.d); 5, antihypertensive NO.1 at the middle dose group (antihypertensive NO.1 at 0.5g/kg.d); 6, antihypertensive NO.1 at the high dose group (antihypertensive NO.1 at 1g/kg.d). Model group and control group were given the same dose of placebo, and the remaining group of continuous medication for 4 weeks.4w later, the rats in the sudden death, and postmortem brain tissue samples, mainly through RT-PCR and Western Blotting methods were used to antihypertensive NO.1 at the cerebral cortex in spontaneously hypertensive rats Bcl-2, Bax, NF-κB P65, CLC-2 and CLC-3 mRNA expression, and analyzed statistically.Result:1)Antihypertensive NO.1 can significantly reduce blood pressure in spontaneously hypertensive rats blood pressure, and has a dose-effect relationship.2)Antihypertensive NO.1 can lead to hypertensive cerebral cortex cells in pro-apoptotic Bax gene expression decreased significantly, while the anti-apoptotic gene Bcl-2 expression increased significantly.3)Antihypertensive NO.1 can increase the spontaneously hypertensive rat cerebral cortex cells NF-κB P65 gene expression.4)When hypertension in rats, the rats of CLC-2 and the expression of CLC-3 has significantly increased; and to antihypertensive NO.1, the expression of CLC-2 and CLC-3 has significantly decline.Conclusion:1)Antihypertensive NO.1 by lowering the pro-apoptotic gene expression and increased expression of anti-apoptosis gene in spontaneously hypertensive rats of the cerebral cortex play a protective role.2)Antihypertensive NO.1 may be by increasing the expression of NF-κB P65 to reduce neuronal damage that hypertension induced it, brain tissue and thus play a protective role.3)Antihypertensive NO.1 can lead to cerebral cortex in spontaneously hypertensive rats chloride channel family gene expression decreased, suggesting that antihypertensive NO.1 of hypertension may be caused by changes in the cells of the volume decrease of metabolic enhancement, and thus on hypertension-induced cell injury play a protective role.
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