PMID- 36301028
OWN - NLM
STAT- MEDLINE
DCOM- 20221031
LR  - 20221118
IS  - 2050-4527 (Electronic)
IS  - 2050-4527 (Linking)
VI  - 10
IP  - 11
DP  - 2022 Nov
TI  - Effect of regulating macrophage polarization phenotype on intervertebral disc 
      degeneration.
PG  - e714
LID - 10.1002/iid3.714 [doi]
LID - e714
AB  - BACKGROUND: Macrophages are the only inflammatory cells that can penetrate the 
      closed nucleus pulposus and their polarization plays an important role in 
      intervertebral disc degeneration (IVDD). This paper attempted to investigate the 
      pathogenesis of IVDD by altering the polarization state of macrophages. METHODS: 
      Macrophage RAW264.7 cells were induced by interferongamma (IFN-gamma) and 
      lipopolysaccharide (LPS). The polarization of RAW264.7 cells was estimated by 
      western blot and immunofluorescence. The expressions of inflammatory factors were 
      detected by ELISA. Subsequently, RAW264.7 cells were treated with different 
      concentrations of minocycline (Mino) and sinomenine (Sino), followed by the 
      assessment of cell viability with cell counting kit-8 kit. Then, RAW264.7 cell 
      culture medium was collected for the culture of human nucleus pulposus cells 
      (NPCs). Toluidine blue staining and type II collagen staining were applied to 
      assay the level of type II collagen. The cell apoptosis, oxidative stress, and 
      nitric oxide (NO) level were appraised by TUNEL, oxidative stress kits and NO 
      kit, respectively. Western blot was employed to test the levels of apoptosis- and 
      oxidative stress-related proteins. RESULTS: IFN-gamma and LPS could induce M1 
      polarization of RAW264.7 cells. Mino and Sino could reduce the polarization of 
      RAW264.7 cells toward M1. M1-polarized medium inhibited LPS-induced activity, 
      inflammation, and damage of NPCs, which were enhanced by Mino and Sino in medium. 
      CONCLUSION: M1 polarization of macrophages promoted LPS-induced inflammation and 
      damage of NPCs.
CI  - (c) 2022 The Authors. Immunity, Inflammation and Disease published by John Wiley 
      & Sons Ltd.
FAU - Hou, Xuefeng
AU  - Hou X
AD  - Department of Orthopedics, Binhai County People's Hospital, Jiangsu Province, 
      China.
FAU - Shen, Yucheng
AU  - Shen Y
AD  - Department of Orthopedics, Binhai County People's Hospital, Jiangsu Province, 
      China.
FAU - Sun, Minli
AU  - Sun M
AD  - Department of Geriatrics, Binhai County People's Hospital, Binhai, Jiangsu 
      Province, China.
FAU - Zhang, Bing
AU  - Zhang B
AD  - Department of Orthopedics, Binhai County People's Hospital, Jiangsu Province, 
      China.
FAU - Dai, Jiuming
AU  - Dai J
AD  - Department of Orthopedics, Binhai County People's Hospital, Jiangsu Province, 
      China.
FAU - Chen, Dong
AU  - Chen D
AUID- ORCID: 0000-0001-7163-6696
AD  - Department of Orthopedics, Binhai County People's Hospital, Jiangsu Province, 
      China.
FAU - Liu, Zhidong
AU  - Liu Z
AD  - Department of Orthopedics, Binhai County People's Hospital, Jiangsu Province, 
      China.
LA  - eng
PT  - Journal Article
PL  - England
TA  - Immun Inflamm Dis
JT  - Immunity, inflammation and disease
JID - 101635460
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Collagen Type II)
SB  - IM
MH  - Humans
MH  - *Intervertebral Disc Degeneration/metabolism/pathology
MH  - Lipopolysaccharides/toxicity
MH  - Collagen Type II
MH  - Macrophages/metabolism
MH  - Inflammation/pathology
MH  - Phenotype
PMC - PMC9609449
OTO - NOTNLM
OT  - M1 polarization
OT  - inflammation
OT  - intervertebral disc degeneration
OT  - macrophages
COIS- The authors declare no conflict of interest.
EDAT- 2022/10/28 06:00
MHDA- 2022/11/01 06:00
PMCR- 2022/10/27
CRDT- 2022/10/27 09:43
PHST- 2022/08/22 00:00 [revised]
PHST- 2022/07/19 00:00 [received]
PHST- 2022/08/24 00:00 [accepted]
PHST- 2022/10/28 06:00 [pubmed]
PHST- 2022/11/01 06:00 [medline]
PHST- 2022/10/27 09:43 [entrez]
PHST- 2022/10/27 00:00 [pmc-release]
AID - IID3714 [pii]
AID - 10.1002/iid3.714 [doi]
PST - ppublish
SO  - Immun Inflamm Dis. 2022 Nov;10(11):e714. doi: 10.1002/iid3.714.