PMID- 34855756
OWN - NLM
STAT- MEDLINE
DCOM- 20220110
LR  - 20220110
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 16
IP  - 12
DP  - 2021
TI  - A green-lipped mussel reduces pain behavior and chondrocyte inflammation and 
      attenuated experimental osteoarthritis progression.
PG  - e0259130
LID - 10.1371/journal.pone.0259130 [doi]
LID - e0259130
AB  - The green-lipped mussel (GLM) contains novel omega-3 polyunsaturated fatty acids, 
      which exhibit anti-inflammatory and joint-protecting properties. Osteoarthritis 
      (OA) is a degenerative joint disease characterized by a progressive loss of 
      cartilage; oxidative stress plays a role in the pathogenesis of OA. The 
      objectives of this study were to investigate the in vivo effects of the GLM on 
      pain severity and cartilage degeneration using an experimental rat OA model, and 
      to explore the mode of action of GLM. OA was induced in rats by intra-articular 
      injection of monosodium iodoacetate (MIA) into the knee. Oral GLM was initiated 
      on the day after 3dyas of MIA injection. Limb nociception was assessed by 
      measuring the paw withdrawal latency and threshold. Samples were analyzed both 
      macroscopically and histologically. Immunohistochemistry was used to investigate 
      the expression of interleukin-1beta (IL-1beta), IL-6, nitrotyrosine, and inducible 
      nitric oxide synthase (iNOS) in knee joints. Also, the GLM was applied to OA 
      chondrocyte, and the expression on catabolic marker and necroptosis factor were 
      evaluated by real-time polymerase chain reaction. Administration of the GLM 
      improved pain levels by preventing cartilage damage and inflammation. GLM 
      significantly attenuated the expression levels of mRNAs encoding matrix 
      metalloproteinase-3 (MMP-3), MMP-13, and ADAMTS5 in IL-1beta-stimulated human OA 
      chondrocytes. GLM decreased the expression levels of the necroptosis mediators 
      RIPK1, RIPK3, and the mixed lineage kinase domain-like protein (MLKL) in 
      IL-1beta-stimulated human OA chondrocytes. Thus, GLM reduced pain and cartilage 
      degeneration in rats with experimentally induced OA. The chondroprotective 
      properties of GLM included suppression of oxidative damage and inhibition of 
      catabolic factors implicated in the pathogenesis of OA cartilage damage. We 
      suggest that GLM may usefully treat human OA.
FAU - Jhun, JooYeon
AU  - Jhun J
AD  - The Rheumatism Research Center, Catholic Research Institute of Medical Science, 
      The Catholic University of Korea, Seoul, South Korea.
FAU - Na, Hyun Sik
AU  - Na HS
AD  - The Rheumatism Research Center, Catholic Research Institute of Medical Science, 
      The Catholic University of Korea, Seoul, South Korea.
FAU - Cho, Keun-Hyung
AU  - Cho KH
AD  - The Rheumatism Research Center, Catholic Research Institute of Medical Science, 
      The Catholic University of Korea, Seoul, South Korea.
FAU - Kim, Jiyoung
AU  - Kim J
AD  - The Rheumatism Research Center, Catholic Research Institute of Medical Science, 
      The Catholic University of Korea, Seoul, South Korea.
FAU - Moon, Young-Mee
AU  - Moon YM
AD  - The Rheumatism Research Center, Catholic Research Institute of Medical Science, 
      The Catholic University of Korea, Seoul, South Korea.
FAU - Lee, Seung Yoon
AU  - Lee SY
AD  - The Rheumatism Research Center, Catholic Research Institute of Medical Science, 
      The Catholic University of Korea, Seoul, South Korea.
FAU - Lee, Jeong Su
AU  - Lee JS
AD  - The Rheumatism Research Center, Catholic Research Institute of Medical Science, 
      The Catholic University of Korea, Seoul, South Korea.
FAU - Lee, A Ram
AU  - Lee AR
AD  - The Rheumatism Research Center, Catholic Research Institute of Medical Science, 
      The Catholic University of Korea, Seoul, South Korea.
FAU - Kim, Seok Jung
AU  - Kim SJ
AD  - Department of Orthopedic Surgery, Uijeongbu St. Mary's Hospital, College of 
      Medicine, The Catholic University of Korea, Seoul, Republic of Korea.
FAU - Cho, Mi-La
AU  - Cho ML
AUID- ORCID: 0000-0001-5715-3989
AD  - The Rheumatism Research Center, Catholic Research Institute of Medical Science, 
      The Catholic University of Korea, Seoul, South Korea.
FAU - Park, Sung-Hwan
AU  - Park SH
AD  - Division of Rheumatology, Department of Internal Medicine, Seoul St. Mary's 
      Hospital, College of Medicine, The Catholic University of Korea, Seoul, Republic 
      of Korea.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20211202
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Fatty Acids, Omega-3)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Bivalvia/*metabolism
MH  - Fatty Acids, Omega-3/*pharmacology
MH  - Inflammation/*drug therapy
MH  - Male
MH  - Osteoarthritis/*drug therapy
MH  - Pain/*drug therapy
MH  - Rats
MH  - Rats, Wistar
PMC - PMC8638931
COIS- The authors have declared that no competing interests exist.
EDAT- 2021/12/03 06:00
MHDA- 2022/01/11 06:00
PMCR- 2021/12/02
CRDT- 2021/12/02 17:27
PHST- 2021/03/08 00:00 [received]
PHST- 2021/10/14 00:00 [accepted]
PHST- 2021/12/02 17:27 [entrez]
PHST- 2021/12/03 06:00 [pubmed]
PHST- 2022/01/11 06:00 [medline]
PHST- 2021/12/02 00:00 [pmc-release]
AID - PONE-D-21-07398 [pii]
AID - 10.1371/journal.pone.0259130 [doi]
PST - epublish
SO  - PLoS One. 2021 Dec 2;16(12):e0259130. doi: 10.1371/journal.pone.0259130. 
      eCollection 2021.