Dehydrocorydaline induced antidepressant-like effect in a chronic unpredictable mild stress mouse model via inhibiting uptake-2 monoamine transporters

Jin, Luhong; Zhou, Sisi; Zhu, Shujie; Lei, Shaowei; Du, Weijuan; Jiang, Huidi; Zeng, Su; Zhou, Hui

doi:10.1016/j.ejphar.2019.172725

Cited by 12 publications

(10 citation statements)

References 37 publications

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“…In our study, DHC inhibited depolarization-evoked glutamate release in a concentration-dependent manner, with concentrations ranging from 50 to 1 µM and IC 50 values of 20.8 µM. Jin et al showed that systemic administration of DHC at a dose of 1.5-3 mg/kg could produce an antidepressant effect in an animal model of depression [13]. Jin et al showed that systemic administration of DHC at a dose of 1.5-3 mg/kg could produce an antidepressant effect in an animal model of depression [13].…”

Section: Discussionsupporting

confidence: 56%

“…While DHC could be detected in various brain regions of rats, how DHC delivers to the brain remains to be further explored [36]. Although DHC has been shown to have antidepressant, analgesic, and antinociceptive effects and exert antioxidative and anti-inflammatory activities in animal models [9,13,37], the precise mechanism of the neuroprotective effect of DHC has not yet been fully elucidated. Previous research has already demonstrated that compounds with potent antioxidative and antiinflammatory activities might offer benefits in neuroprotective effects, as free radicalinduced oxidative damage to the brain has been regarded as an important cause of neuronal death in a variety of neurodegenerative disorders of the CNS [38,39].…”

Section: Discussionmentioning

confidence: 99%

“…In addition, DHC decreases the production of proinflammatory cytokines and possesses anti-inflammatory effects. In addition, DHC can change the content of monoamines in the brain to process antidepressant-like effects [13]. However, the neuroprotective effects of DHC are still unknown.…”

Section: Introductionmentioning

confidence: 99%

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Inhibition of Glutamate Release from Rat Cortical Nerve Terminals by Dehydrocorydaline, an Alkaloid from Corydalis yanhusuo

et al. 2022

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Excessive release of glutamate induces excitotoxicity and causes neuronal damage in several neurodegenerative diseases. Natural products have emerged as potential neuroprotective agents for preventing and treating neurological disorders. Dehydrocorydaline (DHC), an active alkaloid compound isolated from Corydalis yanhusuo, possesses neuroprotective capacity. The present study investigated the effect of DHC on glutamate release using a rat brain cortical synaptosome model. Our results indicate that DHC inhibited 4-aminopyridine (4-AP)-evoked glutamate release and elevated intrasynaptosomal calcium levels. The inhibitory effect of DHC on 4-AP-evoked glutamate release was prevented in the presence of the vesicular transporter inhibitor bafilomycin A1 and the N- and P/Q-type Ca2+ channel blocker ω-conotoxin MVIIC but not the intracellular inhibitor of Ca2+ release dantrolene or the mitochondrial Na+/Ca2+ exchanger inhibitor CGP37157. Moreover, the inhibitory effect of DHC on evoked glutamate release was prevented by the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) inhibitor PD98059. Western blotting data in synaptosomes also showed that DHC significantly decreased the level of ERK1/2 phosphorylation and synaptic vesicle-associated protein synapsin I, the main presynaptic target of ERK. Together, these results suggest that DHC inhibits presynaptic glutamate release from cerebrocortical synaptosomes by suppressing presynaptic voltage-dependent Ca2+ entry and the MAPK/ERK/synapsin I signaling pathway.

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Section: Discussionsupporting

confidence: 56%

Section: Discussionmentioning

confidence: 99%

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Inhibition of Glutamate Release from Rat Cortical Nerve Terminals by Dehydrocorydaline, an Alkaloid from Corydalis yanhusuo

et al. 2022

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“…Deh is an important bioactive component of the Chinese herb Corydalis ambigua . This herb has a wide range of therapeutic effects in a variety of diseases, including cancer associated pain ( Huo et al, 2018 ), depression ( Jin et al, 2019 ), melanoma ( Hu et al, 2019 ), and so on. For example, Deh stimulates MAPK activation of p38 protein and enhances the interaction between MyoD and E protein, thus leading to the activation of MyoD and myoblast differentiation, and enhancing the regeneration ability of injured muscle stem cells ( Yoo et al, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

“…Deh has been reported to have beneficial effects in the treatment of depression and melanoma. For instance, Deh can alter the content of monoamine in brains by limiting uptake-2 monoamine transporters, thus exerting its antidepressant effects ( Jin et al, 2019 ). Additionally, it restrains cell proliferation, migration and invasion by inhibiting the MEK1/2-ERK1/2 signaling pathway in melanoma ( Hu et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

Dehydrocorydaline Protects Against Sepsis-Induced Myocardial Injury Through Modulating the TRAF6/NF-κB Pathway

Zhang

et al. 2021

Front. Pharmacol.

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We aim to investigate the effect and mechanism of dehydrocorydaline (Deh), an alkaloidal component isolated from Rhizoma corydalis, in the treatment of sepsis-mediated myocardial injury. Lipopolysaccharide (LPS) was taken to construct an in-vitro sepsis-myocardial injury models H9C2 cardiomyocytes. The in-vivo model of sepsis in C57BL/6 mice was induced by intraperitoneal injection of Escherichia coli (E. coli). The in-vitro and in-vivo models were treated with Deh in different concentrations, respectively. Hematoxylin-eosin (HE) staining, Masson staining, and immunohistochemistry (IHC) staining were taken to evaluate the histopathological changes of the heart. ELISA was applied to evaluate the levels of inflammatory factors, including IL-6, IL-1β, TNFα, IFNγ, and oxidized factors SOD, GSH-PX in the plasma or culture medium. Western blot was used to measure the expressions of Bax, Bcl2, Caspase3, iNOS, Nrf2, HO-1, TRAF6, NF-κB in heart tissues and cells. The viability of H9C2 cardiomyocytes was detected by the CCK8 method and BrdU assay. The ROS level in the H9C2 cardiomyocytes were determined using immunofluorescence. As a result, Deh treatment improved the survival of sepsis mice, reduced TUNEL-labeled apoptosis of cardiomyocytes. In vitro, Deh enhanced the viability of LPS-induced H9C2 cardiomyocytes and inhibited cell apoptosis. Additionally, Deh showed significant anti-inflammatory and anti-oxidative stress functions via decreasing IL-1β, IL-6, TNFα, and IFNγ levels, mitigating ROS level, up-regulating Nrf2/HO-1, SOD, and GSH-PX expressions dose-dependently. Mechanistically, Deh inhibited TRAF6 expression and the phosphorylation of NF-κB p65. The intervention with a specific inhibitor of TRAF6 (C25-140) or NF-κB inhibitor (BAY 11-7082) markedly repressed the protective effects mediated by Deh. In conclusion, Deh restrains sepsis-induced cardiomyocyte injury by inhibiting the TRAF6/NF-κB pathway.

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Corydaline alleviates Parkinson’s disease by regulating autophagy and GSK-3β phosphorylation

Zhou,

2024

Psychopharmacology

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Dehydrocorydaline induced antidepressant-like effect in a chronic unpredictable mild stress mouse model via inhibiting uptake-2 monoamine transporters

Cited by 12 publications

References 37 publications

Inhibition of Glutamate Release from Rat Cortical Nerve Terminals by Dehydrocorydaline, an Alkaloid from Corydalis yanhusuo

Inhibition of Glutamate Release from Rat Cortical Nerve Terminals by Dehydrocorydaline, an Alkaloid from Corydalis yanhusuo

Dehydrocorydaline Protects Against Sepsis-Induced Myocardial Injury Through Modulating the TRAF6/NF-κB Pathway

Corydaline alleviates Parkinson’s disease by regulating autophagy and GSK-3β phosphorylation

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