| Autor: |
BULAMA, Ibrahim, NASIRU, Suleiman, BILBIS, Suleman Lawal, ABBAS, Abdullahi Yahaya, NASIRU, Jinjiri Ismail, SAIDU, Yusuf, ARIS, Mohamad Moklas Mohamad, NORMA, Mat Taib Che, CHIROMA, Musa Samaila |
| Předmět: |
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| Zdroj: |
Journal of Cellular Neuroscience & Oxidative Stress; 2020, Vol. 12 Issue 1, p922-936, 15p |
| Abstrakt: |
Generation of reactive oxygen species (ROS) during traumatic brain injury (TBI) has been identified as an important factor that is responsible for disease progression and cell death, particularly in secondary injury process. Ascorbic acid (AA) is an exogenous antioxidant that can be used to quench ROS in neurodegeneration. Its antioxidant properties have been reported in some neurodegenerative conditions in rats. In the present study, we examined the neurotherapeutic effects of AA in TBI-induced rats. Three groups of seven rats each were used for this study. Group I was induced with TBI and treated with AA (67,5 mg/kg orally). Group II was traumatized but not treated (TNT), while group III (control) was neither traumatized nor treated (NTNT). Treatment started 30 min after TBI and lasted for 21 days. Morris water maze (MWM), elevated plus maze, and open field test were carried out in the rats. Antioxidant enzymes [(superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx)] and their gene expressions were analyzed. Malondialdehyde level, S100B concentration, and histological studies were also conducted. The treatment with AA improved learning and memory, locomotor function, and decreased anxiety in the treated groups compared to group II. S100B was significantly (p<0.05) lowered in the treated group as compared to the group II rats. Treatment with AA also decreases malondialdehyde level when compared to group II. There were increased activities of SOD, CAT, and GPx activities in the treated group when compared to the control group. These were in agreement with their gene expressions that are highly expressed in the same groups. In conclusion, present data suggest that AA induced neuroprotective effects via down-regulation of lipid peroxidation and up-regulation of antioxidant redox system in the TBI-induced rats. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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