Abstract:The effect and mechanism of resveratrol on depression-like behavior in mice with depression were investigated. A mouse model of depression was established by social isolation combined with chronic unpredictable stress. The mice were randomly divided into the control group, the model group, the low dose group, the medium dose group and the high dose group. The rats in the low, medium and high dose groups were intraperitoneally injected with resveratrol 10, 20 and 30 mg/kg, respectively. The control and model gr… Show more
“…In the development of depressive-like behaviors, the rat models are manifested with reduced NPY expression [17]. Academically, the expression of NPY is evidenced to decline in mice with depression [35]. Consistently, the above-mentioned study findings are as same as the previous literature to some extent.…”
Researches pivoting on histone deacetylases (HDACs) in depression have been excessively conducted, but not much on HDAC1. Therein, the present study is launched to disclose the mechanism of HDAC1/microRNA (miR)-124-5p/neuropeptide Y (NPY) axis in depression. Sprague Dawley rats were stimulated by chronic unpredictable mild stress to establish depression models. Depressed rats were injected with inhibited HDAC1 or suppressed miR-124-5p to explore their roles in body weight, learning and memory abilities, oxidative stress and inflammation in serum and neurotransmitter expression in hippocampal tissues. MiR-124-5p, HDAC1 and NPY expression in the hippocampus were tested. The interactions of miR-124-5p, HDAC1 and NPY expression were also confirmed. Higher miR-124-5p and HDAC1 and lower NPY expression levels were found in the hippocampus of depressed rats. Inhibited miR-124-5p or suppressed HDAC1 attenuated learning and memory abilities and increased body weight of depressed rats. Knockdown of miR-124-5p or inhibition of HDAC1 suppressed oxidative stress and inflammation and promoted neurotransmitter expression of depressed rats. HDAC1 mediated miR-124-5p to regulate NPY. Knockdown of NPY abolished the protective effects of inhibited miR-124-5p on depressed rats. Our study illustrates that suppression of either miR-124-5p or HDAC1 up-regulates NPY to improve memory and learning abilities in depressed mice, which may update the existed knowledge of depression and provide a novel reference for treatment of depression.
“…In the development of depressive-like behaviors, the rat models are manifested with reduced NPY expression [17]. Academically, the expression of NPY is evidenced to decline in mice with depression [35]. Consistently, the above-mentioned study findings are as same as the previous literature to some extent.…”
Researches pivoting on histone deacetylases (HDACs) in depression have been excessively conducted, but not much on HDAC1. Therein, the present study is launched to disclose the mechanism of HDAC1/microRNA (miR)-124-5p/neuropeptide Y (NPY) axis in depression. Sprague Dawley rats were stimulated by chronic unpredictable mild stress to establish depression models. Depressed rats were injected with inhibited HDAC1 or suppressed miR-124-5p to explore their roles in body weight, learning and memory abilities, oxidative stress and inflammation in serum and neurotransmitter expression in hippocampal tissues. MiR-124-5p, HDAC1 and NPY expression in the hippocampus were tested. The interactions of miR-124-5p, HDAC1 and NPY expression were also confirmed. Higher miR-124-5p and HDAC1 and lower NPY expression levels were found in the hippocampus of depressed rats. Inhibited miR-124-5p or suppressed HDAC1 attenuated learning and memory abilities and increased body weight of depressed rats. Knockdown of miR-124-5p or inhibition of HDAC1 suppressed oxidative stress and inflammation and promoted neurotransmitter expression of depressed rats. HDAC1 mediated miR-124-5p to regulate NPY. Knockdown of NPY abolished the protective effects of inhibited miR-124-5p on depressed rats. Our study illustrates that suppression of either miR-124-5p or HDAC1 up-regulates NPY to improve memory and learning abilities in depressed mice, which may update the existed knowledge of depression and provide a novel reference for treatment of depression.
“…Extensive studies show that monoaminergic neurotransmission involving 5-HT, NE and DA exerts major influence on brain circuits by regulating mood, reactivity to psychological stress, self-control, motivation, drive, and cognitive performance [25]. Studies also showed that the levels of DA and 5-HT decreased in the hypothalamic tissue of patients with depression [26]. Folate is necessary for proper biosynthesis of the monoamine neurotransmitters 5-HT, NE and DA [13].…”
Background: Depression is characterized by significant and low mood. Classical antidepressants are still not adequate in treating depression because of undesirable side effects. Folic acid, a member of the vitamin B complex, in considered to be strongly associated with the function and development of the central nervous system. Thus, in this study, we established a model of depression through chronic unpredictable mild stress (CUMS) in rats and assessed the antidepressant effects and mechanisms of folic acid. Methods: Sprague-Dawley rats were randomly divided into four groups: control, chronic unpredictable mild stress (CUMS), CUMS treated with folic acid, and CUMS treated with citalopram. Rats were assessed in terms of weight change, open-field test and sucrose preference. Homocysteine, monoamine neurotransmitters, interleukin-6, brainderived neurotrophic factor (BDNF), β-endorphin levels in the serum and brains of rats were analysed. Results: Folic acid exhibited antidepressant-like effects in open-field and sucrose preference tests. Folic acid treatment effectively increased the levels of monoamine neurotransmitters, BDNF and β-endorphin, interleukin-6 and homocysteine levels were also significantly suppressed by folic acid administration. Conclusions: These findings serve as preclinical evidence that folic acid plays an antidepressant-like role in several pathways involving monoamine neurotransmitters. Thus, folic acid may be used as a potential antidepressant.
“…Resveratrol treatment enhanced neurogenesis, upregulated Sirt1, and inhibited NF-kB activation ameliorating depression-like behaviors [ 89 ]. Moreover, resveratrol was reported to be able to increase neurotransmitters dopamine and serotonin significantly in the prefrontal cortex and NPY expression in the brain suggesting to act as an antagonist for depression treatment [ 90 ].…”
Section: The Pathogenesis Of Mental Disordersmentioning
Mental disorders including depression, anxiety, schizophrenia, autism spectrum disorders, bipolar and etc. have a considerable proportion of global disorder burden. Many nutritional psychiatry investigations have been conducted to evaluate the relationship between several individual nutrients such as herbal compounds with mental health. Resveratrol, a famous polyphenol compound, is known as an antioxidant, anti-inflammatory, anti-apoptotic, and neuroprotective agent regulating the function of brain and improves the behavioral factors associated with learning, anxiety, depression, and memory. In addition, this natural compound can cross the blood–brain barrier representing neurological influences. The pharmacological interest of utilizing resveratrol in mental disorders is due to its anti-inflammatory and antioxidant features. The aim of this paper was to review the studies evaluated the potential effects of resveratrol on mental disorders.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.