ArticleAmerican journal of translational research2025
TIGAR alleviates cognitive impairment in rats with chronic cerebral hypoperfusion by suppressing oxidative stress and pyroptosis.
Article in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- Metabolomics Analysis Revealed That SXZ Ameliorates Cognitive Impairment in Naturally Aged Rats by Promoting Glutathione Metabolism and Inhibiting the Ferroptosis Pathway.CNS neuroscience & therapeutics · 2026Article
- Neuromodulation Techniques in Chronic Cerebral Hypoperfusion: Mechanisms and Therapeutic Advances.CNS neuroscience & therapeutics · 2026Review
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6 authors.
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Abstract
backgroundIt is postulated that oxidative stress and pyroptosis, which are induced by chronic cerebral hypoperfusion (CCH), contribute to the pathogenesis of vascular cognitive impairment (VCI). The protective role of TIGAR in neurologic illnesses has been the subject of extensive examination, yet its role in models of CCH-induced cognitive impairment remains unexplored. The objective of this study was to ascertain whether TIGAR is a neuroprotective agent in rats with CCH that reduces oxidative stress and pyroptosis.
methodsA CCH model was established in rats through the use of bilateral common carotid artery occlusion (BCCAO). The effects of TIGAR on cognitive function and anxiety-depressive behaviors in rats with CCH were examined. To this end, the Y-maze and open field tests were employed. Nissl and hematoxylin-eosin (H&E) staining were used to assess histologic changes in the CA1 area of the hippocampus. Hippocampal glutathione (GSH) activity, malondialdehyde (MDA) content, and NADPH/NADP+ ratio were measured using the WST-8 colorimetric method to assess oxidative stress. The expression of TIGAR and pyroptosis-related proteins was assessed by western blotting.
resultsA model of CCH-induced cognitive impairment was successfully established. Four weeks after BCCAO, cerebral blood flow returned to normal in the rats, and cognitive impairment and anxiety-depression-like behavior developed. In rats with CCH, MDA levels increased, GSH activity and NADPH/NADP+ ratio decreased, and pyroptosis-related protein expression increased. The pathologic findings indicated that there was an exacerbation of neuronal injury in the CA1 area of the hippocampus and that the cells were loosely arranged. In rats with CCH, overexpression of TIGAR reduced pyroptosis-associated protein expression while increasing MDA content, GSH activity, and NADPH/NADP+ ratio. It promoted neuronal cell survival, and improved cognitive function and anxiety-depression-like behavior.
conclusionOverexpression of TIGAR reduced CCH-induced oxidative stress and pyroptosis and ameliorated cognitive dysfunction and anxiety-depression-like behavior in rats. These findings suggest that TIGAR counteracts oxidative stress and prevents pyroptosis, making it a promising target for the treatment of VCI.
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