Перейти к основному содержанию
AkademIndex

Продукты

Для разработчиков

AkademBaseОткрытый API экосистемы
Статья

Neuroprotective effects of crude extract of Crataegus songarica on a rat model of traumatic brain injury

Xueliang GaoDepartment of Neurosurgery, Hebei Hospital of Traditional Chinese Medicine, Shijiazhuang, Hebei 050011, ChinaZhao WangDepartment of Neurosurgery, Hebei Hospital of Traditional Chinese Medicine, Shijiazhuang, Hebei 050011, ChinaPeilei Jiaof Pharmacy, University of Benin, Benin City, 300001 NigeriaYapeng Zhaoof Pharmacy, University of Benin, Benin City, 300001 NigeriaKai Wangof Pharmacy, University of Benin, Benin City, 300001 NigeriaPuyang Liof Pharmacy, University of Benin, Benin City, 300001 NigeriaJianye ChengDepartment of Neurosurgery, Hebei Hospital of Traditional Chinese Medicine, Shijiazhuang, Hebei 050011, ChinaLi-Peng QinDepartment of Neurosurgery, Hebei Hospital of Traditional Chinese Medicine, Shijiazhuang, Hebei 050011, ChinaZengbin FuDepartment of Neurosurgery, Hebei Hospital of Traditional Chinese Medicine, Shijiazhuang, Hebei 050011, China
2022en
ABI

Аннотация


 
 
 
 Purpose: To investigate the protective effect of Crataegus songarica extract (CSCE) against traumatic brain injury (TBI) in rats, and the underlying mechanism of action.
 Methods: A rat model of TBI was established via tracheal intubation procedure, and the rats were treated with graded doses of CSCE. Neuronal survival was determined by Nissl staining, while neuronal apoptosis was measured using TUNEL-staining. Neurological impairments were determined based on neurological severity score (NSS).
 Results: Treatment of TBI rats with CSCE enhanced neuronal survival and decreased TUNEL-positive cell fraction in the brain cortex. The treatment prevented elevation of NSS and suppressed mRNA and protein expression levels of IL-6 and TNF-α in brain cortex. Moreover, CSCE treatment prevented TBI-mediated suppression of activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx), and attenuated hydrogen peroxide (H2O2) levels in TBI rat brain cortex. Treatment of TBI rats with CSCE down-regulated NF-κB expression, increased Nrf2 expression and up-regulated mRNA expressions of heme oxygenase 1 (HO-1) and quinine oxidoreductase 1 (NQO-1).
 Conclusion: These results suggest that CSCE prevents TBI-mediated reduction in neuronal survival and inhibits brain cortical neuronal death in rats. It improves NSS and inhibits inflammatory response via activation of Nrf2 pathway and targeting of NF-κB expression. Therefore, CSCE is a potential therapeutic agent for TBI.
 
 
 

Перевод пока недоступен

Идентификаторы

Цитирования и источники

Цитирований: 2Использованных источников: 0