RESUMO
Traumatic brain injury (TBI) is a complex process resulting into structural brain damage and functional deficits as a result of an external mechanical force. This study aimed to investigate the possible ameliorative effect of Raphia hookeri ethanol extract (RHEE) on induced acute traumatic brain injury in rats. The choice of the plant was based on its reported anti-oxidative property. Thirty-six female Wistar rats were divided into six groups of six animals each. I: CONTROL - distilled water orally; II: RHEE - 100 mg/kg RHEE; III: Sharp trauma brain injury (STBI); IV: STBI+RHEE; V: Blunt trauma brain injury (BTBI); VI: BTBI+RHEE. Brain injury was inflicted using modified weight drop technique on experimental day 1 while RHEE was given orally by gavage for 7 days post-injury. Blood was collected serially 24hrs, 72hrs and 7 days post-trauma for full blood count and differentials of the white blood cells. On day nine, rats were euthanized and brain harvested for biochemical and histological analyses. Trauma significantly (p<0.05) reduced the relative brain weight of rats compared with the control. Lymphocyte count increased while neutrophils reduced in all traumatized rats compared with control group. Both BTBI and STBI significantly (p<0.05) elevated MDA and significantly (p<0.05) reduced the level of GSH, the activities of SOD and CAT enzymes compared with control group. Histologically, the extent of haemorrhage into the subarachnoid and brain parenchyma in STBI and BTBI groups was reduced in the BTBI+RHEE and STBI+RHEE groups. Administration of RHEE reduced oxidative damage and ameliorated neuronal damage in sharp and blunt brain injuries.
Assuntos
Lesões Encefálicas Traumáticas/tratamento farmacológico , Frutas , Neurônios/efeitos dos fármacos , Estresse Oxidativo/efeitos dos fármacos , Extratos Vegetais/uso terapêutico , Estresse Mecânico , Animais , Encéfalo/efeitos dos fármacos , Encéfalo/metabolismo , Encéfalo/patologia , Lesões Encefálicas Traumáticas/metabolismo , Lesões Encefálicas Traumáticas/patologia , Etanol/uso terapêutico , Feminino , Neurônios/metabolismo , Neurônios/patologia , Estresse Oxidativo/fisiologia , Extratos Vegetais/isolamento & purificação , Extratos Vegetais/farmacologia , Ratos , Ratos WistarRESUMO
Cisplatin (CIS), a known anticancer drug, has side effects initiated by oxidative damage which hinders its use.Raffia hookeri pulp extract (RHPE), reported to possess antioxidant activity should mitigate cisplatin toxicity. The presentstudy examined the potential of RHPE to reduce brain damage in rats exposed to cisplatin. Forty eight female rats (150 g -220 g) were randomized into four groups (n = 12) viz: Group 1 served as control received distilled water daily, Group 2received 100 mg/kg body weight of RHPE, Group 3 received CIS (7.5 mg/kg body weight, intraperitoneally) as single dose,Group 4 received 100 mg/kg body weight of CIS+RHPE. The RHPE was given orally via gavage for 14 days while the singledose of cisplatin was administered on the eighth day of experiment. Behavioral tests namely: transitions, rearings, groomingsand forelimb grip strength were carried out on 15th day of the experiment after which rats were euthanized followed byhistology and histomorphometry. Cisplatin significantly (p<0.05) reduced the percentage body weight changes, transitions,rearings, groomings and forelimb grip strength compared with the control group, whereas treatment with CIS+RHPEsignificantly (p<0.05) increased these parameters compared with Cisplatin treatment. Cisplatin also caused histologicalalterations of Purkinje neurons, pyramidal neurons of Cornu ammonis3, granule cells and cerebral cortex neurons. Itsignificantly (p<0.05) reduced the diameter of Purkinje (9.1±0.59 µm) compared with control (14.41±0.31 µm) andpyramidal neurons (11.32±0.05 µm) compared with control (17.03±0.54 µm). Rats in the CIS+RHPE had their histologyconsiderably improved compared with those of cisplatin. In conclusion, RHPE reversed the behavioural changes anddemonstrated neuroprotection against CIS-induced behavioural changes and microanatomical alterations of cerebellar,hippocampal and cerebral neurons.