Khaksari, Mohammad, Rajizadeh, Mohammad Amin, Bejeshk, Mohammad Abbas, Soltani, Zahra, Motamedi, Sina, Moramdi, Fatemeh, Islami, Masoud, Shafa, Shahriyar, Khosravi, Sepehr. (1397). Does inhibition of angiotensin function cause neuroprotection in diffuse traumatic brain injury?. , 21(6), 615-620. doi: 10.22038/ijbms.2018.26586.6512
Mohammad Khaksari; Mohammad Amin Rajizadeh; Mohammad Abbas Bejeshk; Zahra Soltani; Sina Motamedi; Fatemeh Moramdi; Masoud Islami; Shahriyar Shafa; Sepehr Khosravi. "Does inhibition of angiotensin function cause neuroprotection in diffuse traumatic brain injury?". , 21, 6, 1397, 615-620. doi: 10.22038/ijbms.2018.26586.6512
Khaksari, Mohammad, Rajizadeh, Mohammad Amin, Bejeshk, Mohammad Abbas, Soltani, Zahra, Motamedi, Sina, Moramdi, Fatemeh, Islami, Masoud, Shafa, Shahriyar, Khosravi, Sepehr. (1397). 'Does inhibition of angiotensin function cause neuroprotection in diffuse traumatic brain injury?', , 21(6), pp. 615-620. doi: 10.22038/ijbms.2018.26586.6512
Khaksari, Mohammad, Rajizadeh, Mohammad Amin, Bejeshk, Mohammad Abbas, Soltani, Zahra, Motamedi, Sina, Moramdi, Fatemeh, Islami, Masoud, Shafa, Shahriyar, Khosravi, Sepehr. Does inhibition of angiotensin function cause neuroprotection in diffuse traumatic brain injury?. , 1397; 21(6): 615-620. doi: 10.22038/ijbms.2018.26586.6512

Does inhibition of angiotensin function cause neuroprotection in diffuse traumatic brain injury?

Iranian Journal of Basic Medical Sciences
مقاله 10، دوره 21، شماره 6، شهریور 2018، صفحه 615-620    اصل مقاله (455.37 K)
نوع مقاله: Original Article
شناسه دیجیتال (DOI): 10.22038/ijbms.2018.26586.6512
نویسندگان
Mohammad Khaksari1؛ Mohammad Amin Rajizadeh2؛ Mohammad Abbas Bejeshk3؛ Zahra Soltani* 2؛ Sina Motamedi2؛ Fatemeh Moramdi4؛ Masoud Islami2؛ Shahriyar Shafa2؛ Sepehr Khosravi2
1Endocrinology and Metabolism Research Center, Institute of Basic and Clinical Physiology Sciences, Kerman University of Medical Sciences, Kerman, Iran
2Neuroscience Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran
3Physiology Research Center, Institute of Neuropharmacology, Afzalipour Faculty of Medical Sciences, Kerman University of Medical Sciences, Kerman, Iran
4Pharmaceutics Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran
چکیده
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.
کلیدواژه‌ها
Angiotensin II receptor؛ Blood-brain barrier؛ Brain edema؛ Brain injury؛ Candesartan؛ Intracranial pressure؛ Lipid Peroxidation
مراجع
آمار
تعداد مشاهده مقاله: 1,563
تعداد دریافت فایل اصل مقاله: 863