PMID- 34965184
OWN - NLM
STAT- MEDLINE
DCOM- 20220222
LR  - 20231105
IS  - 2165-5987 (Electronic)
IS  - 2165-5979 (Print)
IS  - 2165-5979 (Linking)
VI  - 13
IP  - 1
DP  - 2022 Jan
TI  - The protective effects of S14G-humanin (HNG) against mono-sodium urate (MSU) 
      crystals- induced gouty arthritis.
PG  - 345-356
LID - 10.1080/21655979.2021.2001911 [doi]
AB  - Gout is a common and complex form of arthritis that has brought great 
      inconveniences to the normal lives of patients. It is reported that oxidative 
      stress and nod-like receptor family protein 3 (NLRP3) inflammasome-mediated 
      inflammatory reactions are involved in the pathogenesis of gout arthritis. 
      S14G-humanin (S14G-HNG) is a modified peptide of HNG with higher inhibitory 
      activity on the accumulation and deposition of Abeta. Recently, S14G-HNG has been 
      reported to exert great anti-inflammatory effects. The present study proposed to 
      explore the possible therapeutic property of S14G-HNG against gout arthritis. An 
      animal model was established by stimulation with mono-sodium urate (MSU) 
      crystals, followed by treatment with colchicine and S14G-HNG, respectively. The 
      elevated Gait score promoted synovitis score and activated myeloperoxidase (MPO) 
      observed in MSU crystals-treated mice were significantly reversed by colchicine 
      and S14G-HNG. Bone marrow-derived macrophages (BMDMs) were isolated from mice and 
      stimulated with MSU crystals, followed by being treated with 25 and 50 muM 
      S14G-HNG. The increased mitochondrial reactive oxygen species (ROS) and 
      Malondialdehyde (MDA) levels, upregulated NADPH oxidase-4 (NOX-4), activated 
      NLRP3 inflammasome, and elevated production of inflammatory factors in MSU 
      crystals-treated BMDMs were dramatically reversed by S14G-HNG, accompanied by the 
      upregulation of sirtuin type-1 (SIRT1). Lastly, the protective effects of 
      S14G-HNG against MSU crystals-induced NLRP3 inflammasome activation were 
      significantly abolished by the knockdown of SIRT1. In conclusion, our data reveal 
      that S14G-HNG could possess potential benefits against MSU crystals-induced gout 
      arthritis, with colchicine displaying a better effect.
FAU - Zhang, Jihui
AU  - Zhang J
AUID- ORCID: 0000-0002-6236-2547
AD  - Department of Rheumatism and Immunology, The Second Affiliated Hospital of Harbin 
      Medical University, Harbin City, Heilongjiang Province, China.
FAU - Lei, Hongwei
AU  - Lei H
AD  - Department of Rheumatism and Immunology, The Second Affiliated Hospital of Harbin 
      Medical University, Harbin City, Heilongjiang Province, China.
FAU - Li, Xiu
AU  - Li X
AD  - Department of Rheumatism and Immunology, The Second Affiliated Hospital of Harbin 
      Medical University, Harbin City, Heilongjiang Province, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Bioengineered
JT  - Bioengineered
JID - 101581063
RN  - 0 (Gly(14)-Humanin)
RN  - 0 (NLR Family, Pyrin Domain-Containing 3 Protein)
RN  - 0 (Nlrp3 protein, mouse)
RN  - 0 (Peptides)
RN  - 0 (Reactive Oxygen Species)
RN  - 268B43MJ25 (Uric Acid)
RN  - 4Y8F71G49Q (Malondialdehyde)
RN  - EC 1.11.1.7 (Peroxidase)
RN  - EC 1.6.3.- (NADPH Oxidase 4)
RN  - EC 1.6.3.- (Nox4 protein, mouse)
RN  - SML2Y3J35T (Colchicine)
SB  - IM
MH  - Animals
MH  - Arthritis, Gouty/chemically induced/*drug therapy/metabolism
MH  - Cells, Cultured
MH  - Colchicine/*administration & dosage/pharmacology
MH  - Disease Models, Animal
MH  - Macrophages/*cytology/drug effects/metabolism
MH  - Malondialdehyde/metabolism
MH  - Mice
MH  - NADPH Oxidase 4/metabolism
MH  - NLR Family, Pyrin Domain-Containing 3 Protein/metabolism
MH  - Peptides/*administration & dosage/pharmacology
MH  - Peroxidase/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Treatment Outcome
MH  - Uric Acid/*adverse effects
PMC - PMC8805931
OTO - NOTNLM
OT  - NLRP3 inflammasome
OT  - NOX-4
OT  - ROSs
OT  - S14G-HNG
OT  - SIRT1
OT  - gout arthritis
COIS- No potential conflict of interest was reported by the author(s).
EDAT- 2021/12/30 06:00
MHDA- 2022/02/23 06:00
PMCR- 2021/12/29
CRDT- 2021/12/29 17:11
PHST- 2021/12/29 17:11 [entrez]
PHST- 2021/12/30 06:00 [pubmed]
PHST- 2022/02/23 06:00 [medline]
PHST- 2021/12/29 00:00 [pmc-release]
AID - 2001911 [pii]
AID - 10.1080/21655979.2021.2001911 [doi]
PST - ppublish
SO  - Bioengineered. 2022 Jan;13(1):345-356. doi: 10.1080/21655979.2021.2001911.