Glycyrrhizic acid renders robust neuroprotection in rodent model of vascular dementia by controlling oxidative stress and curtailing cytochrome-c release. (1st December 2020)

• Record Type: Journal Article
• Authors: Sathyamoorthy, Yogeshkanna; Kaliappan, Kathiravan; Nambi, Pradeepkumar; Radhakrishnan, Rameshkumar
• Is Part Of: Nutritional neuroscience. Volume 23:Number 12(2020)
• Page Start: 955
• Page End: 970
• Publication Date: 2020-12-01
• Subjects: Chronic cerebral hypoperfusion -- glycyrrhizic acid -- neural protection -- cognitive behaviour; Neuropharmacology -- Periodicals; Diet -- Periodicals; Diet therapy -- Periodicals; Nutrition -- Periodicals; 615.78
• DOI: 10.1080/1028415X.2019.1580935
• Languages: English
• ISSNs: 1028-415X

Abstract

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.