PMID- 21783711
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20121002
LR  - 20110725
IS  - 1382-6689 (Print)
IS  - 1382-6689 (Linking)
VI  - 22
IP  - 2
DP  - 2006 Sep
TI  - Effects and mechanisms of Clematis mandshurica Maxim. as a dual inhibitor of 
      proinflammatory cytokines on adjuvant arthritis in rats.
PG  - 205-12
LID - 10.1016/j.etap.2006.03.010 [doi]
AB  - Effect and mechanism of Clematis mandshurica Maxim. water extract (CMA), a dual 
      inhibitor of interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF-alpha), on rat 
      adjuvant arthritis (AA) were investigated. Complete Freund's adjuvant (CFA) was 
      used to induce AA in rats. The extents of inflammation and treatment response 
      were evaluated with regard to lymphocyte proliferation. Serial evaluation was 
      carried out on days 1, 7, 14, 21 and 28 after creation of inflammation. The 
      lymphocyte proliferation study revealed cellular immunosuppression during the 
      early phase of the disease. Administration of CMA on the same day or 5 days prior 
      to inflammatory insult into the joint significantly reduced the inflammation as 
      compared to the untreated animals in a dose dependent manner. The administration 
      of CMA (2, 5 and 10mg/kg, subcutaneously (s.c.)) inhibited the inflammatory 
      response and restored the weight of body and immune organs of AA rats. 
      Synoviocytes proliferation of AA rats significantly increased, and the levels of 
      TNF-alpha and IL-1 in supernatants of synoviocytes in AA rats were also elevated 
      compared with the nonimmunized rats group. The administration of CMA (2, 5 and 
      10mg/kg, s.c.) reduced the above changes significantly. In contrast to TNF-alpha and 
      IL-1, IL-10 production and the level of its mRNA of synoviocytes in AA rats were 
      apparently decreased. CMA (2, 5 and 10mg/kg, s.c.) markedly increased IL-10 in 
      synoviocytes at protein and transcription level. The results indicated that CMA 
      had a beneficial effect on rats AA due to modulating inflammatory cytokines 
      production of synoviocytes, which played a crucial role in pathogenesis of this 
      disease.
FAU - Suh, Suk-Jong
AU  - Suh SJ
AD  - Department of Biological Science, Sungkyunkwan University, Chunchun-Dong 300, 
      Jangan-Gu, Suwon City, Kyunggi-Do 440-746, Republic of Korea.
FAU - Kim, Kap-Sung
AU  - Kim KS
FAU - Lee, Seung-Deuk
AU  - Lee SD
FAU - Lee, Chang Hwan
AU  - Lee CH
FAU - Choi, Hoon Seok
AU  - Choi HS
FAU - Jin, Un-Ho
AU  - Jin UH
FAU - Chang, Young-Chae
AU  - Chang YC
FAU - Kim, Cheorl-Ho
AU  - Kim CH
LA  - eng
PT  - Journal Article
DEP - 20060612
PL  - Netherlands
TA  - Environ Toxicol Pharmacol
JT  - Environmental toxicology and pharmacology
JID - 9612020
EDAT- 2006/09/01 00:00
MHDA- 2006/09/01 00:01
CRDT- 2011/07/26 06:00
PHST- 2005/10/03 00:00 [received]
PHST- 2006/03/24 00:00 [accepted]
PHST- 2011/07/26 06:00 [entrez]
PHST- 2006/09/01 00:00 [pubmed]
PHST- 2006/09/01 00:01 [medline]
AID - S1382-6689(06)00057-3 [pii]
AID - 10.1016/j.etap.2006.03.010 [doi]
PST - ppublish
SO  - Environ Toxicol Pharmacol. 2006 Sep;22(2):205-12. doi: 
      10.1016/j.etap.2006.03.010. Epub 2006 Jun 12.