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| Ascorbic acid alleviates hydrocephalus and protects blood-brain barrier via inhibiting oxidative stress in a rat model of intracerebral hemorrhage |
| YAN Lin1, LIAO Yuxiang2,3, AN Zhihan2,3, LIAO Xinbin2,3, ZHANG Zhiping2,3, XIAO Gelei2,3 |
1. Department of Neurosurgery, Hunan Brain Hospital/The Second People's Hospital of Hunan Province, Changsha 410007, China;
2. Department of Neurosurgery, Xiangya Hospital, Central South University, Changsha 410008, China;
3. Diagnosis and Treatment Center for Hydrocephalus, Xiangya Hospital, Central South University, Changsha 410008, China |
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Abstract Objective To observe the effects of ascorbic acid (AA) on oxidative stress and blood-brain barrier (BBB) in rats with intracerebral hemorrhage (ICH), and on post-hemorrhagic hydrocephalus (PHH) formation in rats with ICH. Methods A rat model of PHH after ICH was developed through autologous blood infusion. To observe the effect of AA on the PHH condition of ICH rats, to observe the effect of AA on the nerve damage condition of ICH rats, to detect the expression of oxidative stress-related markers, and to detect the expression of BBB-related marker proteins. Results Compared with the ICH group, rats in the ICH-AA group had a smaller ventricular volume, a lesser degree of brain tissue damage, alleviated neuronal damage, lower brain water content, lower neurological function scores mNSS, decreased iNOS and MDA expression, increased SOD expression, up-regulated SVCT2 expression, decreased MMP-2 expression, and increased occludin, claudin-5, and ZO-1 expression. Compared with the PHH group, the ventricular volume of rats in the PHH-AA group was slightly reduced, the degree of brain tissue damage was basically the same, neuronal damage was not alleviated, but the brain water content was reduced, neurological function scores of mNSS were improved, iNOS and MDA expression was reduced, SOD expression was increased, SVCT2 expression was up-regulated, MMP-2 expression was reduced, and the expression of occludin, claudin-5, and ZO-1 expression was slightly increased. Conclusion AA inhibited the degree of oxidative stress and protected the BBB in ICH rats, alleviated the formation of PHH, and played a neuroprotective role in the early stage of ICH; whereas, after the formation of PHH, AA only partially inhibited the degree of oxidative stress but did not have any reparative effect on the BBB that had been damaged, and could not treat PHH, but could play a neuroprotective role.
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Received: 22 July 2023
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2023, Vol. 20 
