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Updated: Apr 17, 2026

A Rat Model of Middle Cerebral Artery Occlusion/Reperfusion Without Damaging the Anatomical Structure of Cerebral Vessels
Published on: May 17, 2024
Effects of Tannic Acid on the Ischemic Brain Tissue of Rats
Halil Murat Sen1, Adile Ozkan, Mustafa Guven
1Department of Neurology, Faculty of Medicine, Canakkale Onsekiz Mart University, Terzioğlu Kampüsü, Canakkale, Turkey, hmuratsen@gmail.com.
Abstract:
Many studies of brain ischemia have shown the role played by massive ischemia-induced production of reactive oxygen species, the main mechanism of neuronal death. However, currently, there is no treatment choice to prevent cell death triggered by reactive oxygen species. In our study, we researched the effects of tannic acid, an antioxidant, on the ischemic tissue of rats with induced middle cerebral artery occlusion. The animals were divided into three groups of eight animals. The sham group were only administered 10 % ethanol intraperitoneally, the second group had middle cerebral artery occlusion induced and were given 10 % ethanol intraperitoneally, while the third group had middle cerebral artery occlusion with 10 mg/kg dose tannic acid dissolved in 10 % ethanol administered within half an hour intraperitoneally. The rats were sacrificed 24 h later, and brain tissue was examined biochemically and histopathologically. Biochemical evaluation of brain tissue found that comparing the ischemic group with no treatment with the tannic acid-treated ischemia group; the superoxide dismutase (SOD) levels were higher, malondialdehyde (MDA) levels were lower, and nuclear respiratory factor-1 (NRF-1) was higher in the tannic acid-treated group. Histopathological examination showed that the histopathological results of the tannic acid group were better than the group not given tannic acid. Biochemical and histopathological results showed that tannic acid administration had an antioxidant effect on the negative effects of ischemia in brain tissue.
Insights
Tannic acid, an antioxidant, demonstrated protective effects against brain ischemia in rats. Treatment with tannic acid improved biochemical markers and reduced neuronal damage, offering a potential therapeutic strategy for ischemic conditions.
Area of Science:
- Neuroscience
- Biochemistry
- Pharmacology
Background:
- Brain ischemia triggers massive reactive oxygen species production, a primary cause of neuronal death.
- Current treatments lack the ability to prevent reactive oxygen species-induced cell death.
- Antioxidants are being investigated as potential neuroprotective agents against ischemic damage.
Purpose of the Study:
- To investigate the neuroprotective effects of tannic acid, a known antioxidant, in a rat model of middle cerebral artery occlusion (MCAO).
- To evaluate the impact of tannic acid on biochemical and histopathological changes in ischemic brain tissue.
Main Methods:
- Rats underwent induced middle cerebral artery occlusion and were divided into sham, ischemic (vehicle-treated), and ischemic (tannic acid-treated) groups.
- Tannic acid (10 mg/kg) was administered intraperitoneally within 30 minutes of MCAO induction.
- Brain tissues were analyzed biochemically for superoxide dismutase (SOD), malondialdehyde (MDA), and nuclear respiratory factor-1 (NRF-1) levels, and histopathologically 24 hours post-occlusion.
Main Results:
- Tannic acid treatment significantly increased SOD and NRF-1 levels compared to the untreated ischemic group.
- Malondialdehyde (MDA) levels were significantly lower in the tannic acid-treated group.
- Histopathological examination revealed improved tissue integrity in rats treated with tannic acid.
Conclusions:
- Tannic acid exhibits significant antioxidant effects, mitigating the detrimental impacts of ischemia on brain tissue.
- These findings suggest tannic acid holds promise as a therapeutic agent for preventing neuronal death in ischemic stroke.
- Further research is warranted to explore the clinical applicability of tannic acid in managing brain ischemia.

