https://orcid.org/0000-0002-5592-4783
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ABSTRACT
Background: Chronic cerebral hypoperfusion (CCH), a concern for neurocognitive health, is linked to various vascular ailments and other comorbidities. This study primarily aims to explain the mitigating effects of glycyrrhizic acid (GA) on cognitive health challenged by chronic cerebral hypoperfusion.
Methods: Adult male Sprague Dawley rats were allocated into four groups: (i) Sham, (ii) Lesion (2VO), (iii) GA treated (20 mg/kg), and (iv) lithium chloride (Li) treated (40 mg/kg). On 30th postoperative day the rats were tested for cognitive behaviour through a repertoire of tests. Rats were transcardially perfused and the brain samples were obtained for histological assessments. For biochemical assessments, hippocampus isolated from fresh brain was utilized.
Results: The antioxidant propensity of GA curtailed ROS generation by restoring mitochondrial complex I and IV, enzymatic and non-enzymatic antioxidant activity. However, Li group exhibited significantly reduced antioxidant defence, when compared with GA. The strong antioxidant defence had caused considerable restoration of pyramidal neurons, myelin and dendritic spine density in GA treated than Li treated. GA treated rats showed a remarkable amelioration of cognitive deficits when compared with lesion rats. Finally, GA also reduced the cytochrome-c release, thus creating a blockade for further succession of apoptotic events.
Conclusion: The outcome of this study clearly implies that GA shows promising neuroprotection in CCH-induced rats by enhancing the endogenous antioxidants and curtails the apoptosis by reducing cytochrome-c release. GA was also found to be much better than Li through modulation of GSK3β/Nrf2 pathway, in turn, mitigates the adverse consequences of CCH.
Acknowledgement
The financial support by Department of Science and Technology - PURSE programme (Junior research fellowship) and Council of Scientific and Industrial Research Senior research fellowship for the first author is greatly acknowledged.
Disclosure statement
No potential conflict of interest was reported by the authors.
Notes on contributors
Yogeshkanna Sathyamoorthy obtained B.Tech. in Biotechnology, M.S. in Neuroscience (Faculty of Medicine), and is pursuing Ph.D. in Neuroscience-Anatomy, with research interests in experimental cerebrovascular research and translational neuroscience.
Kathiravan Kaliappan obtained B.Sc. in Animal Sciences, M.Sc. in Anatomy (Faculty of Medicine), and is pursuing Ph.D. in Anatomy, with research interests in experimental cerebrovascular research and translational neuroscience.
Pradeepkumar Nambi obtained B.Sc. in Zoology, M.Sc. in Anatomy (Faculty of Medicine), and is pursuing Ph.D. in Anatomy, with research interests in experimental cerebrovascular research and translational neuroscience.
Rameshkumar Radhakrishnan obtained M.Sc. in Anatomy (Faculty of Medicine) and Ph.D. in Anatomy. Presently he is serving as Assistant professor in Anatomy, University of Madras, Taramani campus, Tamil Nadu, India. His research interests are in experimental cerebrovascular research and translational neuroscience, and therapeutics for neurodegenerative diseases using novel cell-based and ethno-pharmacological approaches.