Glycyrrhizic acid renders robust neuroprotection in rodent model of vascular dementia by controlling oxidative stress and curtailing cytochrome-c release.

Nutritional Neuroscience
Yogeshkanna SathyamoorthyRameshkumar Radhakrishnan

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 defici...Continue Reading

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