ReferenceID 1972
Ginsenoside Re Protects against Serotonergic Behaviors Evoked by 2,5-Dimethoxy-4-iodo-amphetamine in Mice via Inhibition of PKCδ-Mediated Mitochondrial Dysfunction
Int J Mol Sci
It has been recognized that serotonin 2A receptor (5-HT2A) agonist 2,5-dimethoxy-4-iodo-amphetamine (DOI) impairs serotonergic homeostasis. However, the mechanism of DOI-induced serotonergic behaviors remains to be explo
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Record Fields
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- Reference Id
- 1972
- Evidence Id
- 18562
- Core Evidence Id
- 18562
- Source Reference Id
- 3969
- Herb2 Reference Id
- HBREF004766
- Subject Paper Key
- HBIN027742_34281274
- Pubmed Id
- 34281274
- Doi
- 10.3390/ijms22137219
- Paper Title
- Ginsenoside Re Protects against Serotonergic Behaviors Evoked by 2,5-Dimethoxy-4-iodo-amphetamine in Mice via Inhibition of PKCδ-Mediated Mitochondrial Dysfunction
- Paper Abstract
- It has been recognized that serotonin 2A receptor (5-HT2A) agonist 2,5-dimethoxy-4-iodo-amphetamine (DOI) impairs serotonergic homeostasis. However, the mechanism of DOI-induced serotonergic behaviors remains to be explored. Moreover, little is known about therapeutic interventions against serotonin syndrome, although evidence suggests that ginseng might possess modulating effects on the serotonin system. As ginsenoside Re (GRe) is well-known as a novel antioxidant in the nervous system, we investigated whether GRe modulates 5-HT2A receptor agonist DOI-induced serotonin impairments. We proposed that protein kinase Cdelta (PKCdelta) mediates serotonergic impairments. Treatment with GRe or 5-HT2A receptor antagonist MDL11939 significantly attenuated DOI-induced serotonergic behaviors (i.e., overall serotonergic syndrome behaviors, head twitch response, hyperthermia) by inhibiting mitochondrial translocation of PKCdelta, reducing mitochondrial glutathione peroxidase activity, mitochondrial dysfunction, and mitochondrial oxidative stress in wild-type mice. These attenuations were in line with those observed upon PKCdelta inhibition (i.e., pharmacologic inhibitor rottlerin or PKCdelta knockout mice). Furthermore, GRe was not further implicated in attenuation mediated by PKCdelta knockout in mice. Our results suggest that PKCdelta is a therapeutic target for GRe against serotonergic behaviors induced by DOI.
- Journal
- Int J Mol Sci
- Publish Year
- 2021
- Experiment Subject
- mouse
- Experiment Type
- Animal Experiment
- Phenotype Related
- Hyperthermia; Serotonin Syndrome; Serotonergic Syndrome
- Paper Title Cn
- Paper Title En
- Ginsenoside Re Protects against Serotonergic Behaviors Evoked by 2,5-Dimethoxy-4-iodo-amphetamine in Mice via Inhibition of PKCδ-Mediated Mitochondrial Dysfunction
- Bilingual Status
- semi_complete