Abstract
Aging is an ultimate reality that everyone has to face. D-galactose (D-gal) has been used extensively to develop aging model. Trace elements such as selenium (Se) have been used as a potential antioxidant for neuro-protection. The present work aims to develop therapeutic agents such as Se for the treatment of aging-induced neurological ailments such as anxiety, depression, and memory impairment. For this purpose, mice were treated with D-gal at a dose of 300 mg/ml/kg and various doses of Se (0.175 and 0.35mg/ml/kg) for 28 days. Behavioral tests were monitored after treatment days. After the behavioral assessment, mice were decapitated and their brains were collected. Hippocampi were removed from the brain for biochemical, neurochemical, and histopathological analysis. The present findings of behavioral analysis showed that D-gal-induced anxiety- and depression-like symptoms were inhibited by both doses of Se. D-gal-induced memory alteration was also prevented by repeated doses of Se (0.175 and 0.35mg/ml/kg). Biochemical analysis showed that D-gal-induced increase of oxidative stress and inflammatory markers and decrease of antioxidant enzymes and total protein contents in the hippocampus were prevented by Se administration. An increase in the activity of acetylcholinesterase was also diminished by Se. The neurochemical assessment showed that D-gal-induced increased serotonin metabolism and decreased acetylcholine levels in the hippocampus were restored by repeated treatment of Se. Histopathological estimations also exhibited; normalization of D-gal induced neurodegenerative changes. It is concluded that D-gal-induced dysfunction in mice hippocampus caused anxiety, depression, memory impairment, oxidative stress, neuro-inflammation, and histological alterations that were mitigated by Se via its antioxidant potential, anti-inflammatory property, and modulating capability of serotonergic and cholinergic functions.
Highlights
Aging is a gradual functional impairment at the organismal and cellular levels (Wagner et al 2016) These physiological dysfunctions are attributed to increased genomic instability, altered metabolism, and the loss of regenerative potential (Baker et al 2016)
It was observed that repeated treatment with D-gal at a dose of 300 mg/ml/kg produced behavioural deficits that were similar to anxiety and depression-like behaviour, and memory impairment as well
Results of the present study showed that D-gal prolonged immobility time in FST suggesting depression-like behaviour (Figure 3) with decreased serotonin metabolism (Figure 8)
Summary
Aging is a gradual functional impairment at the organismal and cellular levels (Wagner et al 2016) These physiological dysfunctions are attributed to increased genomic instability, altered metabolism, and the loss of regenerative potential (Baker et al 2016). The process of aging is associated with a variety of disorders that cause tissue homeostasis imbalance, memory, and learning impairments (Bonfili et al 2020) depression, and anxiety-like behavior (Samad et al 2019). Extensive evidence shows that aging is progressed by oxidative stress which is induced by a discrepancy between reactive oxygen species formation and antioxidant system (Cabello-Verrugio et al 2016). Extensive studies show that the accumulation of Dgal alters the antioxidant system and speed up the process of aging (Du et al 2019). Excessive D-gal may cause rapid reactive oxygen species formation which hinders the cellular antioxidant defense system and (Samad et al 2019)
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