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      Ginsenoside Rb1 pretreatment reverses hippocampal changes in BDNF/TrkB mRNA and protein in rats subjected to acute immobilization stress

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          Abstract

          Purpose

          Episodes of acute emotional or physical stress can have significant adverse effects on the hippocampus. Ginsenoside Rb1, the most predominant ginsenoside present in Panax species, has been reported to show a neuroprotective effect. The purpose of this study was to investigate the influence of ginsenoside Rb1 on plasma corticosterone (CORT) and adrenocorticotropic hormone (ACTH) levels and hippocampal brain-derived neurotrophic factor (BDNF) and tyrosine kinase B (TrkB) levels in rats subjected to acute immobilization stress.

          Methods

          Wistar rats were divided into controls treated with saline only (N), rats exposed to stress only (M), and rats pretreated with Rb1 (40 mg.kg (−1)) thirty minutes prior to stress exposure (R). In the model, animals were restrained in a plastic immobilizer for 2 h of acute immobilization stress at room temperature. ELISA was used to determine plasma levels of CORT and ACTH. The effect of Rb1 pretreatment on the expression of BDNF and TrkB was determined by immunofluorescence, real-time PCR, and Western blotting analysis.

          Results

          The R group showed significantly increased plasma CORT and ACTH levels compared to the N and M groups. Acute stress stimulation suppressed BDNF and TrkB protein and mRNA expression in the hippocampus; otherwise, Rb1 pretreatment reversed the decreases.

          Conclusion

          The results from this study demonstrate that Rb1 pretreatment reverses the decreases in hippocampal BDNF/TrkB and increases the plasma levels of CORT and ACTH, indicating a potential neuroprotective effect of Rb1 against acute stress.

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          Most cited references 23

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          Low brain-derived neurotrophic factor (BDNF) levels in serum of depressed patients probably results from lowered platelet BDNF release unrelated to platelet reactivity.

          Recent reports have suggested a role for brain-derived neurotrophic factor (BDNF) in psychiatric disorders. Decreased serum BDNF levels have been reported in major depression, but the cause of this decrease has not yet been investigated. The goal of this study was to assess blood BDNF and a platelet activation index, PF4. Forty-three drug-free patients (27 female, 16 male) diagnosed with major depression and 35 healthy control subjects (18 female, 17 male) were assessed for plasma, serum, and blood BDNF content. Brain-derived neurotrophic factor and PF4 were assayed with enzyme-linked immunosorbent assay methods, and severity of depression was evaluated with the Montgomery-Asberg Depression Rating Scale. Serum and plasma BDNF levels were decreased in depressed patients compared with control subjects. In whole blood, BDNF levels were unaltered in the depressed subjects compared with control subjects. The serum/blood BDNF ratio was lower in patients with major depression. Increased plasma but not serum PF4 levels were observed in depressed subjects compared with control subjects. Our results suggest that an alteration of serum or plasma BDNF is not due to the change in blood BDNF but rather is probably related to mechanisms of BDNF release. Secretion of BDNF seems to be independent of platelet reactivity; other mechanisms are therefore probably involved and need to be elucidated.
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            Trophic factors and neuronal survival.

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              Cancer prevention and therapeutics: Panax ginseng.

               S Helms (2004)
              Panax ginseng has been used as a medicinal plant in China for thousands of years. Current use in Western countries has been diverse, with focused research on cancer therapeutics. P. ginseng apparently mitigates cancer through anti-inflammatory, antioxidant, and apoptotic mechanisms to influence gene expression. Additional mechanisms of investigation include influence on neurotransmission and immunosurveillance. Low toxicity and positive studies in concomitant use with other chemotherapeutic agents is promising. Although there is no conclusive evidence of P. ginseng curing cancer, research has continually found tumor inhibition, especially in the promotion and progression phases.
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                Author and article information

                Journal
                Drug Des Devel Ther
                Drug Des Devel Ther
                DDDT
                dddt
                Drug Design, Development and Therapy
                Dove
                1177-8881
                01 July 2019
                2019
                : 13
                : 2127-2134
                Affiliations
                [1 ] Department of Anesthesiology, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou, Zhejiang 325000, People’s Republic of China
                [2 ] Department of Anesthesiology, The First Affiliated Hospital, College of Medicine, Zhejiang University , Hangzhou, Zhejiang 310003, People’s Republic of China
                [3 ] Department of Gastroenterology and Hepatology, The First Affiliated Hospital of Wenzhou Medical University , Wenzhou, Zhejiang 325000, People’s Republic of China
                [4 ] Department of Anesthesiology, Zhejiang Cancer Hospital , Hangzhou, Zhejiang 310022, People’s Republic of China
                Author notes
                Correspondence: Danyun Jia;Wujun GengDepartment of Anesthesiology, The First Affiliated Hospital of Wenzhou Medical University , Nanbaixiang, Ouhai District, Wenzhou City, Zhejiang Province325000, People’s Republic of ChinaTel/fax +86 577 8858 1162Email 529365150@ 123456qq.com ; gengwujun@ 123456wzhospital.cn
                [*]

                These authors contributed equally to this work

                Article
                201135
                10.2147/DDDT.S201135
                6612975
                © 2019 Kang et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 4, Tables: 1, References: 25, Pages: 8
                Categories
                Original Research

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