β-Carotene: A Natural Compound Improves Cognitive Impairment and Oxidative Stress in a Mouse Model of Streptozotocin-Induced Alzheimer’s Disease

Abstract

Alzheimer’s disease (AD) is a neurodegenerative disease characterized by a cascade of changes in cognitive, behavioral, and social activities. Several areas of the brain are involved in the regulation of memory. Of most importance are the amygdala and hippocampus. Antioxidant therapy is used for the palliative treatment of different degenerative diseases like diabetes, cirrhosis, and Parkinson’s, etc. The objective of this study was to assess the effectiveness of exogenous antioxidants, in particular, β carotene (1.02 and 2.05 mg/kg) against intracerebroventricular injected streptozotocin-induced memory impairment in mice. Streptozotocin (3 mg/kg, i.c.v) was administered in two separate doses (on 1st and 3rd days of treatment) for neurodegeneration. Fifty Albino mice (male) were selected in the protocol, and they were classified into five groups (Group I—control, Group II—disease, Group III—standard, Group IV–V—β-carotene-treated) to investigate the cognitive enhancement effect of selected antioxidants. The cognitive performance was observed following the elevated plus-maze, passive avoidance, and open field paradigms. Acetylcholine esterase, β-amyloid protein, and biochemical markers of oxidative stress such as glutathione peroxidase, superoxide dismutase, and catalase were analyzed in brain homogenates. In silico activity against acetylcholinesterase (AChE) was determined by the molecular modeling of β-carotene. β-carotene at a dose of 2.05 mg/kg was found to attenuate the deleterious effects of streptozotocin-induced behavioral and biochemical impairments, including the inhibition of acetylcholinesterase activity. The in silico studies confirmed the binding capacity of β-carotene with the acetylcholinesterase enzyme. The administration of β-carotene attenuated streptozotocin-induced cognitive deficit via its anti-oxidative effects, inhibition of acetylcholinesterase, and the reduction of amyloid β-protein fragments. These results suggest that β-carotene could be useful for the treatment of neurodegenerative diseases such as Alzheimer’s disease.

The Effects of Resveratrol, Caffeine, β‐Carotene, and Epigallocatechin Gallate (EGCG) on Amyloid‐β25--35 Aggregation in Synthetic Brain Membranes

“…Resveratrol was shown to improve memory performance and facilitate memory formation in mice, [46,47] and -carotene supplementation improved cognitive impairment and oxidative stress. [48,49] Both EGCG and caffeine were also reported to reduce cognitive impairment and prevent memory decline. [50,51] Resveratrol is most commonly found in the skin of grapes, and is often consumed in the form of red wine.…”

Appraisal of anti‐Parkinson activity of rhinacanthin‐C in haloperidol‐induced parkinsonism in mice: A mechanistic approach

“…PD was induced by intraperitoneal administration of haloperidol (1 mg/Kg) in all mice for 25 days except normal control group, 30 min after oral administration of standard drug and testing compounds (Hira et al, 2019). RC solution was prepared by dissolving it in vegetable oil in required concentrations of 5 mg/Kg, 10 mg/Kg, and 20 mg/Kg.…”

“…When both eyes of the mice went down into the hole, it is considered as one dip. The mean of the total number of head dips was used for expressing results (Hira et al, 2019).…”

Anti-Apoptotic Effects of Carotenoids in Neurodegeneration

“…The ability of β-carotene to work against lipid peroxidation and decrease oxidative stress makes it an important factor in brain-related diseases. [118]. Lower levels of β-carotene in the cerebral cortex are associated with traumatic brain injury [119].…”

“…Unlike vitamin A, which can produce oxidative stress with excess treatment, β-carotene does not show pro-oxidant activity in the brain, and it has been thus suggested as a safer antioxidant [ 116 ]. Treatment with β-carotene improves retention of intracellular antioxidants such as glutathione and superoxide dismutase during neurotoxicity [ 118 , 120 ]. β-carotene increases protein levels of nuclear Nrf2 and upregulates downstream targets containing antioxidant response elements (ARE) such as NAD(P)H quinone dehydrogenase and heme oxygenase-1 [ 120 ].…”