Effect of cholestasis and NeuroAid treatment on the expression of Bax, Bcl-2, Pgc-1α and Tfam genes involved in apoptosis and mitochondrial biogenesis in the striatum of male rats.
Animals
Apoptosis
/ drug effects
Cholestasis
/ drug therapy
Corpus Striatum
/ drug effects
Drugs, Chinese Herbal
/ pharmacology
Gene Expression
Male
Organelle Biogenesis
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
/ biosynthesis
Proto-Oncogene Proteins c-bcl-2
/ biosynthesis
Rats
Rats, Wistar
Transcription Factors
/ biosynthesis
Treatment Outcome
bcl-2-Associated X Protein
/ biosynthesis
Bax
Bcl-2
Cholestasis
NeuroAid
Pgc-1α
Tfam
Journal
Metabolic brain disease
ISSN: 1573-7365
Titre abrégé: Metab Brain Dis
Pays: United States
ID NLM: 8610370
Informations de publication
Date de publication:
01 2020
01 2020
Historique:
received:
17
04
2019
accepted:
16
10
2019
pubmed:
28
11
2019
medline:
30
1
2021
entrez:
28
11
2019
Statut:
ppublish
Résumé
Cholestasis means impaired bile synthesis or secretion. In fact, it is a bile flow reduction following Bile Duct Ligation (BDL). Cholestasis has a main role in necrosis and apoptosis. Apoptosis is a form of programmed cell death that has intrinsic and extrinsic pathways. The intrinsic pathway is mediated by Bcl-2 (B cell lymphoma-2) proteins which integrate death and survival signals. Bcl-2 has anti-apoptotic and Bax has pro-apoptotic effects. Also, striatum is one of the brain regions that has high expressions of Bcl-2 proteins. Moreover, Tfam and Pgc-1α are involved in mitochondrial biogenesis. On the other hand, NeuroAid, is a drug that has neuroprotective and anti-apoptosis effects. In this study, using quantitative PCR, we measured the expression of all these genes in the striatum of male rats following BDL and NeuroAid administration. Results showed, BDL increased the expression of Bax and Tfam and decreased the expression of Bcl-2. NeuroAid restored the effect of BDL on the expression of Bax, while did not alter the effect of BDL on Bcl-2. In addition, it increased the expression of Tfam that was previously elevated by BDL and raised the expression of Tfam in normal rats. Both BDL and NeuroAid, had no effect on Pgc-1α. In conclusion, cholestasis increased the expression of Bax and decreased the expression of Bcl-2, and this effect may have related to enhanced susceptibility of mitochondrial pathways following oxidative stress. Tfam expression was increased following cholestasis and this effect may have related to cellular compensatory mechanisms against high accumulation of free radicals or mitochondrial biogenesis failure. Furthermore, NeuroAid may play a role against apoptosis and can be used to increase mitochondrial biogenesis.
Identifiants
pubmed: 31773435
doi: 10.1007/s11011-019-00508-y
pii: 10.1007/s11011-019-00508-y
doi:
Substances chimiques
Bax protein, rat
0
Bcl2 protein, rat
0
Drugs, Chinese Herbal
0
Neuroaid
0
Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha
0
Ppargc1a protein, rat
0
Proto-Oncogene Proteins c-bcl-2
0
Tfam protein, rat
0
Transcription Factors
0
bcl-2-Associated X Protein
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
183-192Références
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