Does inhibition of angiotensin function cause neuroprotection in diffuse traumatic brain injury?
Does inhibition of angiotensin function cause neuroprotection in diffuse traumatic brain injury?
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DOI：
10.22038/ijbms.2018.26586.6512
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发表时间：
2018-06-01
影响因子：
2.2
通讯作者：
Khosravi, Sepehr
中科院分区：
文献类型：
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作者：
Khaksari, Mohammad;Rajizadeh, Mohammad Amin;Khosravi, Sepehr
目的：神经保护作用是在抑制血管紧张素II型1受体（AT1R）后产生的。因此，本研究的目的是研究坎地沙坦在弥漫性创伤性脑损伤（TBI）中的AT1R阻塞。材料与方法：雄性大鼠分为假手术组、脑外伤组、载药组和坎地沙坦组。坎地沙坦（0.3 mg/kg）或对照物在tbi后30分钟给予IP。分别于脑外伤后24小时和5小时测定脑水和埃文斯蓝含量。颅内压（ICP）和神经系统预后分别于创伤后1、1、4和24小时进行评估。氧化指数[丙二醛（MDA）]在TBI后24小时测定。结果：与假手术组比较，脑外伤组和载药组脑水、埃文斯蓝含量、MDA和ICP水平升高。坎地沙坦降低了脑外伤引起的脑水和埃文斯蓝含量，并增加了ICP和MDA。在TBI后24小时，坎地沙坦给药后神经系统评分提高。结论：AT1R阻塞可能通过降低ICP，降低脂质过氧化、脑水肿和血脑屏障（BBB）通透性，从而改善神经系统预后，具有神经保护作用。
Objective(s): Neuroprotection is created following the inhibition of angiotensin II type 1 receptor (AT1R). Therefore, the purpose of this research was examining AT1R blockage by candesartan in diffuse traumatic brain injury (TBI).Materials and Methods: Male rats were assigned into sham, TBI, vehicle, and candesartan groups. Candesartan (0.3 mg/kg) or vehicle was administered IP, 30 min post-TBI. Brain water and Evans blue contents were determined, 24 and 5 hr after TBI, respectively. Intracranial pressure (ICP) and neurologic outcome were evaluated at -1, 1, 4 and 24 hr after TBI. Oxidant index [malondialdehyde (MDA)] was determined 24 hr after TBI.Results: Brain water and Evans blue contents, and MDA and ICP levels increased in TBI and vehicle groups in comparison with the sham group. Candesartan attenuated the TBI-induced brain water and Evans blue contents, and ICP and MDA enhancement. The neurologic score enhanced following candesartan administration, 24 hr after TBI.Conclusion: The blockage of AT1R may be neuroprotective by decreasing ICP associated with the reduction of lipid peroxidation, brain edema, and blood-brain barrier (BBB) permeability, which led to the improvement of neurologic outcome.