Version 1
: Received: 29 June 2023 / Approved: 3 July 2023 / Online: 3 July 2023 (13:26:33 CEST)
How to cite:
Bhatia, S.; Paramasivam, R.; Zolkefley, M.K.I.; Kandasamy, R.; Raju, M.; Abdullah, J.M. Nitric Oxide Synthase and Oxidative Stress Mediating Secondary Neuronal Damage in Perihaematoma Region of Intracerebellar Hemorrhage of Mice. Preprints2023, 2023070097. https://doi.org/10.20944/preprints202307.0097.v1
Bhatia, S.; Paramasivam, R.; Zolkefley, M.K.I.; Kandasamy, R.; Raju, M.; Abdullah, J.M. Nitric Oxide Synthase and Oxidative Stress Mediating Secondary Neuronal Damage in Perihaematoma Region of Intracerebellar Hemorrhage of Mice. Preprints 2023, 2023070097. https://doi.org/10.20944/preprints202307.0097.v1
Bhatia, S.; Paramasivam, R.; Zolkefley, M.K.I.; Kandasamy, R.; Raju, M.; Abdullah, J.M. Nitric Oxide Synthase and Oxidative Stress Mediating Secondary Neuronal Damage in Perihaematoma Region of Intracerebellar Hemorrhage of Mice. Preprints2023, 2023070097. https://doi.org/10.20944/preprints202307.0097.v1
APA Style
Bhatia, S., Paramasivam, R., Zolkefley, M.K.I., Kandasamy, R., Raju, M., & Abdullah, J.M. (2023). Nitric Oxide Synthase and Oxidative Stress Mediating Secondary Neuronal Damage in Perihaematoma Region of Intracerebellar Hemorrhage of Mice. Preprints. https://doi.org/10.20944/preprints202307.0097.v1
Chicago/Turabian Style
Bhatia, S., Muthu Raju and Jafri Malin Abdullah. 2023 "Nitric Oxide Synthase and Oxidative Stress Mediating Secondary Neuronal Damage in Perihaematoma Region of Intracerebellar Hemorrhage of Mice" Preprints. https://doi.org/10.20944/preprints202307.0097.v1
Abstract
The underlying mechanisms of secondary neuronal damage following intracerebellar hemorrhage are not yet clear. We aimed to study the possible mechanisms in the mediation of secondary neuronal damage following intracerebellar hemorrhage. ICbH was induced by collagenase type VII-S into mice in 2 phases (n=24/phase): 12 in control group, 12 in day 1 group, 12 in day 3 group and another 12 in day 7 group. All mice underwent locomotor assessment and subsequently sacrificed on day 1, day 3 and day 7 respectively. Cerebellum from phase one and phase two were taken to study morphological, immunohistochemistry and oxidative stress respectively. Mice behavior disturbed following ICbH at day 3 and y 7 as compared with control. Besides, NO increased-on day 1 post induction and suppressed on day 3 and 7. Expressions of SOD, CAT, nNOS, GPX1 and COX-2 were significantly raised on day 3. Morphological studies of the perihaematoma region and tissue showed neuronal damage occurred from day 1 onwards, peaked on day 3 and continued day 7. NO and expression of genes be correlating with morphological changes. Briefly, NO and oxidative stress has an important role in the cascade of secondary neuronal damage of the perihematomal region of ICbH.
Medicine and Pharmacology, Neuroscience and Neurology
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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