PMID- 38194722
OWN - NLM
STAT- MEDLINE
DCOM- 20240123
LR  - 20240202
IS  - 1945-4589 (Electronic)
IS  - 1945-4589 (Linking)
VI  - 16
IP  - 1
DP  - 2024 Jan 8
TI  - Danggui-Shaoyao-San (DSS) ameliorates the progression of osteoarthritis via 
      suppressing the NF-kappaB signaling pathway: an in vitro and in vivo study combined 
      with bioinformatics analysis.
PG  - 648-664
LID - 10.18632/aging.205410 [doi]
AB  - BACKGROUND: Osteoarthritis (OA) is a common chronic age-related joint disease 
      characterized primarily by inflammation of synovial membrane and degeneration of 
      articular cartilage. Accumulating evidence has demonstrated that 
      Danggui-Shaoyao-San (DSS) exerts significant anti-inflammatory effects, 
      suggesting that it may play an important role in the treatment of knee 
      osteoarthritis (KOA). METHODS: In the present study, DSS was prepared and 
      analyzed by high-performance liquid chromatography (HPLC). Bioinformatics 
      analyses were carried out to uncover the functions and possible molecular 
      mechanisms by which DSS against KOA. Furthermore, the protective effects of DSS 
      on lipopolysaccharide (LPS)-induced rat chondrocytes and cartilage degeneration 
      in a rat OA model were investigated in vivo and in vitro. RESULTS: In total, 114 
      targets of DSS were identified, of which 60 candidate targets were related to 
      KOA. The target enrichment analysis suggested that the NF-kappaB signaling pathway 
      may be an effective mechanism of DSS. In vitro, we found that DSS significantly 
      inhibited LPS-induced upregulation of inducible nitric oxide synthase (iNOS), 
      cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), matrix metalloproteinase-3 
      (MMP3), and matrix metalloproteinase-13 (MMP13). Meanwhile, the degradation of 
      collagen II was also reversed by DSS. Mechanistically, DSS dramatically 
      suppressed LPS-induced activation of the nuclear factor kappa B (NF-kappaB) signaling 
      pathway. In vivo, DSS treatment prevented cartilage degeneration in a rat OA 
      model. CONCLUSIONS: DSS could ameliorate the progression of OA through 
      suppressing the NF-kappaB signaling pathway. Our findings indicate that DSS may be a 
      promising therapeutic approach for the treatment of KOA.
FAU - Chen, Shuai
AU  - Chen S
AD  - Guangzhou University of Chinese Medicine, Guangzhou 510405, Guangdong, China.
AD  - Guangzhou Hospital of Integrated Traditional and Western Medicine, Guangzhou 
      510800, Guangdong, China.
AD  - Lingnan Medical Research Center of Guangzhou University of Chinese Medicine, 
      Guangzhou 510405, Guangdong, China.
FAU - Kang, Pan
AU  - Kang P
AD  - Guangzhou University of Chinese Medicine, Guangzhou 510405, Guangdong, China.
AD  - Lingnan Medical Research Center of Guangzhou University of Chinese Medicine, 
      Guangzhou 510405, Guangdong, China.
FAU - Zhao, Zhuanglin
AU  - Zhao Z
AD  - Guangzhou University of Chinese Medicine, Guangzhou 510405, Guangdong, China.
AD  - Guangzhou Hospital of Integrated Traditional and Western Medicine, Guangzhou 
      510800, Guangdong, China.
FAU - Zhang, Hongyi
AU  - Zhang H
AD  - Guangzhou Hospital of Integrated Traditional and Western Medicine, Guangzhou 
      510800, Guangdong, China.
FAU - Li, Jianliang
AU  - Li J
AD  - Guangzhou University of Chinese Medicine, Guangzhou 510405, Guangdong, China.
AD  - Lingnan Medical Research Center of Guangzhou University of Chinese Medicine, 
      Guangzhou 510405, Guangdong, China.
FAU - Xu, Kun
AU  - Xu K
AD  - Shi’s Center of Orthopedics and Traumatology, Shuguang Hospital Affiliated 
      to Shanghai University of Traditional Chinese Medicine, Shanghai 200120, China.
FAU - Gong, Dawei
AU  - Gong D
AD  - Guangzhou University of Chinese Medicine, Guangzhou 510405, Guangdong, China.
AD  - Lingnan Medical Research Center of Guangzhou University of Chinese Medicine, 
      Guangzhou 510405, Guangdong, China.
FAU - Jiao, Feng
AU  - Jiao F
AD  - Guangzhou Hospital of Integrated Traditional and Western Medicine, Guangzhou 
      510800, Guangdong, China.
FAU - Wang, Haibin
AU  - Wang H
AD  - Guangzhou University of Chinese Medicine, Guangzhou 510405, Guangdong, China.
AD  - Department of Orthopedics, The First Affiliated Hospital of Guangzhou University 
      of Chinese Medicine, Guangzhou 510405, Guangdong, China.
FAU - Zhang, Meng
AU  - Zhang M
AD  - Henan Provincial People’s Hospital, Zhengzhou University People’s 
      Hospital, Zhengzhou 450003, Henan, China.
LA  - eng
PT  - Journal Article
DEP - 20240108
PL  - United States
TA  - Aging (Albany NY)
JT  - Aging
JID - 101508617
RN  - 0 (NF-kappa B)
RN  - 0 (danggui-shaoyao-san)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Drugs, Chinese Herbal)
SB  - IM
MH  - Rats
MH  - Animals
MH  - *NF-kappa B/metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Anti-Inflammatory Agents/pharmacology
MH  - Signal Transduction
MH  - Inflammation/metabolism
MH  - *Osteoarthritis, Knee/drug therapy/metabolism
MH  - Chondrocytes/metabolism
MH  - *Drugs, Chinese Herbal
PMC - PMC10817397
OTO - NOTNLM
OT  - Danggui-Shaoyao-San
OT  - NF-kappaB
OT  - bioinformatics
OT  - inflammation
OT  - osteoarthritis
COIS- CONFLICTS OF INTEREST: The authors declare that they have no conflicts of 
      interest.
EDAT- 2024/01/10 00:42
MHDA- 2024/01/23 06:43
PMCR- 2024/01/15
CRDT- 2024/01/09 18:05
PHST- 2023/05/01 00:00 [received]
PHST- 2023/11/29 00:00 [accepted]
PHST- 2024/01/23 06:43 [medline]
PHST- 2024/01/10 00:42 [pubmed]
PHST- 2024/01/09 18:05 [entrez]
PHST- 2024/01/15 00:00 [pmc-release]
AID - 205410 [pii]
AID - 10.18632/aging.205410 [doi]
PST - ppublish
SO  - Aging (Albany NY). 2024 Jan 8;16(1):648-664. doi: 10.18632/aging.205410. Epub 
      2024 Jan 8.