The key role of transcription factors on the innate immunity reaction
- VernacularTitle:Эсийн программчилсан үхэлд транскрипцийн факторуудын үүрэг
- Author:
Ulziisaikhan J
1
;
Gandolgor Ts
1
;
Tsogtsaikhan S
1
;
Yokochi T
2
;
Enkhsaikhan L
1
;
Jambaldorj J
3
,
4
;
Munkhbayar S
4
;
Munkhtuvshin N
4
;
Munkhbat B
4
,
5
;
Bilegtsaikhan Ts
4
,
5
,
6
Author Information
1. Department of Microbiology and Immunology, School of Biomedical Sciences, MNUMS
2. Department of Microbiology and Immunology, Aichi Medical University School of Medicine
3. Department of Molecular Biology and Genetics, School of Biomedical Sciences, MNUMS
4. Central Scientific Research Laboratory, IMS
5. Core Laboratory, Science and Technology Center, MNUMS
6. Department of Biochemistry, School of Biomedical Sciences, MNUMS
- Publication Type:Journal Article
- Keywords:
Valproic acid;
Lipopolysaccharide;
apoptosis;
p53;
p65
- From:
Health Laboratory
2019;10(2):23-33
- CountryMongolia
- Language:Mongolian
-
Abstract:
Background:The effect of lipopolysaccharide (LPS) on valproic acid (VPA)-induced cell death was examined by using mouse RAW 264.7 macrophage cells.
Materials and methods, results:LPS inhibited the activation of caspase 3 and poly (ADP-ribose) polymerase (PARP) and prevented VPA-induced apoptosis. LPS inhibited VPA-induced p53 activation and pifithrin-α as a p53 inhibitor as well as LPS prevented VPA-induced apoptosis. LPS abolished the increase of Bax/Bcl-2 ratio, which is a critical indicator of p53-mediated mitochondrial damage, in response to VPA. The nuclear factor (NF)-κB inhibitors, Bay 11-7082 and parthenolide, abolished the preventive action of LPS on VPA-induced apoptosis. A series of toll-like receptor (TLR) ligands, Pam3CSK4, poly I:C, and CpG DNA as well as LPS prevented VPA-induced apoptosis.
Conclusion:Taken together, LPS was suggested to prevent VPA-induced apoptosis via activation of anti-apoptotic NF-κB and inhibition of pro-apoptotic p53 activation.
- Full text:HL-2019-10(2)-23-33.pdf
