The Therapeutic Effect of Silymarin and Silibinin on Depression and Anxiety Disorders and Possible Mechanism in the Brain: A Systematic Review.
Silymarin
anxiety
depression
neurogenesis
silibinin
systematic review
Journal
Central nervous system agents in medicinal chemistry
ISSN: 1875-6166
Titre abrégé: Cent Nerv Syst Agents Med Chem
Pays: United Arab Emirates
ID NLM: 101269163
Informations de publication
Date de publication:
2023
2023
Historique:
received:
04
05
2023
revised:
05
07
2023
accepted:
18
07
2023
medline:
26
9
2023
pubmed:
24
8
2023
entrez:
24
8
2023
Statut:
ppublish
Résumé
Depression and anxiety are the most common mental disorders worldwide. We aimed to review silymarin and silibinin effects and underlying mechanisms in the central nervous system (CNS) for depression and anxiety treatment. The research protocol was prepared based on following the PRISMA statement. An extensive search was done in essential databases such as PubMed, Cochrane Library, Web of Science (ISI), Embase, and Scopus. Considering the study inclusion and exclusion criteria, 17 studies were finally included. The desired information was extracted from the studies and recorded in Excel, and the consequences and mechanisms were reviewed. Silymarin and silibinin upregulated brain-derived neurotrophic factor (BDNF) and improved neural stem cells (NSCs) proliferation in the cortex and hippocampus. They also increased neurochemical serotonin (5-HT), dopamine (DA), and norepinephrine (NE) levels. Silymarin and silibinin reduced malondialdehyde (MDA) formation and increased glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities. In addition, silymarin and silibinin reduced interleukin (IL)-6, IL-1β, and IL-12β, reducing tumor necrosis factor α (TNF-α) induced neuroinflammation. Silymarin and silibinin exert anti-depression and anxiolytic effects by regulating neurotransmitters, endocrine, neurogenesis, and immunologic systems. Therefore, as natural and complementary medicines, they can be used to reduce the symptoms of depression and anxiety; However, more clinical studies are needed in this field.
Sections du résumé
BACKGROUND
BACKGROUND
Depression and anxiety are the most common mental disorders worldwide.
OBJECTIVE
OBJECTIVE
We aimed to review silymarin and silibinin effects and underlying mechanisms in the central nervous system (CNS) for depression and anxiety treatment.
METHODS
METHODS
The research protocol was prepared based on following the PRISMA statement. An extensive search was done in essential databases such as PubMed, Cochrane Library, Web of Science (ISI), Embase, and Scopus. Considering the study inclusion and exclusion criteria, 17 studies were finally included. The desired information was extracted from the studies and recorded in Excel, and the consequences and mechanisms were reviewed.
RESULTS
RESULTS
Silymarin and silibinin upregulated brain-derived neurotrophic factor (BDNF) and improved neural stem cells (NSCs) proliferation in the cortex and hippocampus. They also increased neurochemical serotonin (5-HT), dopamine (DA), and norepinephrine (NE) levels. Silymarin and silibinin reduced malondialdehyde (MDA) formation and increased glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) activities. In addition, silymarin and silibinin reduced interleukin (IL)-6, IL-1β, and IL-12β, reducing tumor necrosis factor α (TNF-α) induced neuroinflammation.
CONCLUSION
CONCLUSIONS
Silymarin and silibinin exert anti-depression and anxiolytic effects by regulating neurotransmitters, endocrine, neurogenesis, and immunologic systems. Therefore, as natural and complementary medicines, they can be used to reduce the symptoms of depression and anxiety; However, more clinical studies are needed in this field.
Identifiants
pubmed: 37612866
pii: CNSAMC-EPUB-133969
doi: 10.2174/1871524923666230823094403
doi:
Substances chimiques
Silymarin
0
Silybin
4RKY41TBTF
Antioxidants
0
Glutathione
GAN16C9B8O
Types de publication
Systematic Review
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
86-94Informations de copyright
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