PMID- 31841174
OWN - NLM
STAT- MEDLINE
DCOM- 20201109
LR  - 20201109
IS  - 2284-0729 (Electronic)
IS  - 1128-3602 (Linking)
VI  - 23
IP  - 23
DP  - 2019 Dec
TI  - Effect of IL-1beta on apoptosis of synovial cells in rheumatoid arthritis rats via 
      the NF-kappaB pathway.
PG  - 10211-10217
LID - 19656 [pii]
LID - 10.26355/eurrev_201912_19656 [doi]
AB  - OBJECTIVE: The aim of this study was to investigate the role of interleukin-1beta 
      (IL-1beta) in the apoptosis of synovial cells in rheumatoid arthritis (RA) rats, and 
      to explore the underlying mechanism. MATERIALS AND METHODS: The apoptosis of the 
      synovial cells in RA rats in the IL-1beta group and the control group was analyzed 
      by scoring under an electron microscope. The expressions of cleaved-poly 
      (ADP-ribose) polymerase (PARP), PARP and anti-apoptosis gene products in synovial 
      cells of IL-1beta treated RA rats were explored as well. Meanwhile, the expressions 
      of B-cell lymphoma 2 (Bcl-2), Bcl-xL, and Active-Caspase3 in the synovial cells 
      of RA rats with IL-1beta treatment were evaluated by the Western blotting. To 
      further clarify the relationship between IL-1beta and the nuclear factor 
      kappa-light-chain-enhancer of activated B cells (NF-kappaB) pathway in the synovial 
      cells of RA rats, the expressions of NF-kappaB regulated the gene products of matrix 
      metalloproteinase-3 (MMP-3), MMP-9, cyclooxygenase-2 (Cox-2), and vascular 
      endothelial growth factor (VEGF) in synovial cells of RA rats after that we 
      investigated the treatment with IL-1beta (was investigated). In addition, the 
      expression of NF-kappaB in the synovial cells of RA rats treated with IL-1beta was 
      determined. RESULTS: The results showed that, compared with the control group, 
      IL-1beta treatment significantly increased the number of apoptotic cells. This meant 
      that IL-1beta treatment could promote the apoptosis of the synovial cells (p<0.05). 
      IL-1beta treatment significantly promoted the expression level of cleaved-PARP 
      (p<0.05). However, it remarkably reduced the expressions of Bcl-2 and Bcl-xL 
      (p<0.05). Meanwhile, the level of the active-Caspase3 in the synovial cells of RA 
      rats treated with IL-1beta was significantly enhanced (p<0.01). In comparison with 
      the control group, the IL-1beta group exhibited significantly elevated expressions 
      of NF-kappaB-regulated gene products in the synovial cells of RA rats (p<0.01). 
      Besides, the positive markers of the activated NF-kappaB were detected in the 
      synovial cells of RA rats in the IL-1beta group and the control group. The results 
      demonstrated that they were mainly located in the nucleus of the IL-1beta group. 
      CONCLUSIONS: IL-1beta can promote the apoptosis of the synovial cells in RA rats via 
      the NF-kappaB pathway.
FAU - Guo, J-T
AU  - Guo JT
AD  - Department of Rheumatology and Immunology, People's Hospital of Ningxia Hui 
      Autonomous Region, Ningxia, China. guojiangtao0314@163.com.
FAU - Cao, X-Q
AU  - Cao XQ
FAU - Wu, L-L
AU  - Wu LL
FAU - Ma, X-L
AU  - Ma XL
FAU - Hao, C-F
AU  - Hao CF
FAU - Yang, Y-S
AU  - Yang YS
FAU - Zhang, M-Z
AU  - Zhang MZ
LA  - eng
PT  - Journal Article
PL  - Italy
TA  - Eur Rev Med Pharmacol Sci
JT  - European review for medical and pharmacological sciences
JID - 9717360
RN  - 0 (Bcl2l1 protein, rat)
RN  - 0 (Interleukin-1beta)
RN  - 0 (NF-kappa B)
RN  - 0 (Proto-Oncogene Proteins c-bcl-2)
RN  - 0 (Vascular Endothelial Growth Factor A)
RN  - 0 (bcl-X Protein)
RN  - 9007-81-2 (Freund's Adjuvant)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
RN  - EC 2.4.2.30 (Parp1 protein, rat)
RN  - EC 2.4.2.30 (Poly (ADP-Ribose) Polymerase-1)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.24.- (Matrix Metalloproteinases)
SB  - IM
MH  - Animals
MH  - Apoptosis/drug effects/*physiology
MH  - Arthritis, Rheumatoid/chemically induced/metabolism/*physiopathology
MH  - Caspase 3/biosynthesis
MH  - Cells, Cultured
MH  - Cyclooxygenase 2/biosynthesis
MH  - Freund's Adjuvant
MH  - Interleukin-1beta/pharmacology/*physiology
MH  - Male
MH  - Matrix Metalloproteinases/biosynthesis
MH  - NF-kappa B/metabolism/*physiology
MH  - Poly (ADP-Ribose) Polymerase-1/biosynthesis
MH  - Proto-Oncogene Proteins c-bcl-2/biosynthesis
MH  - Rats
MH  - Signal Transduction/drug effects/physiology
MH  - Synoviocytes/metabolism/*physiology
MH  - Vascular Endothelial Growth Factor A/biosynthesis
MH  - bcl-X Protein/biosynthesis
EDAT- 2019/12/17 06:00
MHDA- 2020/11/11 06:00
CRDT- 2019/12/17 06:00
PHST- 2019/12/17 06:00 [entrez]
PHST- 2019/12/17 06:00 [pubmed]
PHST- 2020/11/11 06:00 [medline]
AID - 19656 [pii]
AID - 10.26355/eurrev_201912_19656 [doi]
PST - ppublish
SO  - Eur Rev Med Pharmacol Sci. 2019 Dec;23(23):10211-10217. doi: 
      10.26355/eurrev_201912_19656.