Abstract
We investigated the effects of velvet antler polypeptide on cognitive impairment and the underlying mechanisms. Hydrogen peroxide-induced cell injury was used to establish an in vitro model of SH-SY5Y cells. In addition, we established an in vivo mouse model of cognitive impairment using intraperitoneal injections of scopolamine hydrobromide in strain mice. We administered three different doses of velvet antler polypeptide in this mouse model and assessed the influence of velvet antler polypeptide on the morphology of hippocampal neurons, hippocampal neuronal apoptosis, adrenocorticotropic hormone, and corticosterone activities in brain tissue samples, and the molecular and biochemical regulation of B-cell lymphoma-2, B-cell lymphoma-2 Associated X-protein, Cysteine-aspartic acid protease-3, glucocorticoid receptor, mineralocorticoid receptor, and corticotropin-releasing hormone in murine hippocampal neurons. Our data suggest that velvet antler polypeptide decreases glucocorticoid receptor, mineralocorticoid receptor, and corticotropin-releasing hormone levels and regulates the hormones released by the hypothalamic-pituitary-adrenal axis, thus suppressing neuronal apoptosis.
Highlights
With the aging of the world's population, the incidence of neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, and Parkinson's disease is increasing (Jodeiri Farshbaf and Ghaedi, 2017)
Compared to the control group, the total apoptosis rate of the model group was significantly increased (P < 0.05); the total apoptosis rate of the VAP3 group was significantly decreased in comparison to the model group (P < 0.05, Fig. 1B)
Velvet antler polypeptide (VAP) administration inhibited the expression of Caspase-3 and B-cell lymphoma-2 Associated X-protein (Bax) (P < 0.05), and promoted the expression of B-cell lymphoma-2 (Bcl-2) (P < 0.05, Fig. 1C-D)
Summary
With the aging of the world's population, the incidence of neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, and Parkinson's disease is increasing (Jodeiri Farshbaf and Ghaedi, 2017). The HPA axis is an important neuroendocrine system (Spencer and Deak, 2017). Abnormal changes in the levels of hormones released by the HPA axis results in its dysfunction (Paragliola et al, 2017; Spencer and Deak, 2017), leading to its impaired suppression via the hippocampal neurons (Godoy et al, 2018). Decreased function of the hippocampal neurons causes an increased secretion of corticosterone, resulting in the positive feedback of the HPA axis dysfunction (Herman, 2018; Sampedro-Piquero et al, 2018); this leads to further loss of hippocampal function, inducing the development of cognitive impairment (Ahmad et al, 2019; Galts et al, 2019)
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