PMID- 26949603
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20160307
LR  - 20200929
IS  - 2222-3959 (Print)
IS  - 2227-4898 (Electronic)
IS  - 2222-3959 (Linking)
VI  - 9
IP  - 1
DP  - 2016
TI  - Inhibition of zymosan-induced cytokine and chemokine expression in human corneal 
      fibroblasts by triptolide.
PG  - 9-14
LID - 10.18240/ijo.2016.01.02 [doi]
AB  - AIM: To investigate the effects of triptolide on proinflammatory cytokine and 
      chemokine expression induced by the fungal component zymosan in cultured human 
      corneal fibroblasts (HCFs). METHODS: HCFs were cultured in the absence or 
      presence of zymosan or triptolide. The release of interleukin (IL)-6, IL-8, and 
      monocyte chemoattractant protein-1 (MCP-1) into culture supernatants was measured 
      with enzyme-linked immunosorbent assays. The cellular abundance of the mRNAs for 
      these proteins was determined by reverse transcription and real-time polymerase 
      chain reaction analysis. The phosphorylation of mitogen-activated protein kinases 
      (MAPKs) and the endogenous nuclear factor-kappaB (NF-kappaB) inhibitor IkappaB-alpha was examined 
      by immunoblot analysis. The release of lactate dehydrogenase (LDH) activity from 
      HCFs was measured with a colorimetric assay. RESULTS: Triptolide inhibited the 
      zymosan-induced release of IL-6, IL-8, and MCP-1 from HCFs in a concentration- 
      and time-dependent manner. It also inhibited the zymosan-induced up-regulation of 
      IL-6, IL-8, and MCP-1 mRNA abundance in these cells. Furthermore, triptolide 
      attenuated zymosan-induced phosphorylation of the MAPKs extracellular 
      signal-regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK), and p38 as well 
      as the phosphorylation and degradation of IkappaB-alpha. Triptolide did not exhibit 
      cytotoxicity for HCFs. CONCLUSION: Triptolide inhibited proinflammatory cytokine 
      and chemokine production by HCFs exposed to zymosan, with this action likely 
      being mediated by suppression of MAPK and NF-kappaB signaling pathways. This compound 
      might thus be expected to limit the infiltration of inflammatory cells into the 
      cornea associated with fungal infection.
FAU - Liu, Yang
AU  - Liu Y
AD  - Department of Ophthalmology, First Hospital of Jilin University, Changchun 
      130021, Jilin Province, China.
FAU - Li, Jing
AU  - Li J
AD  - Department of Ophthalmology, First Hospital of Jilin University, Changchun 
      130021, Jilin Province, China.
FAU - Liu, Ye
AU  - Liu Y
AD  - Department of Pathology, First Hospital of Jilin University, Changchun 130021, 
      Jilin Province, China.
FAU - Wang, Ping
AU  - Wang P
AD  - Department of Otolaryngology-Head and Neck Surgery, First Hospital of Jilin 
      University, Changchun 130021, Jilin Province, China.
FAU - Jia, Hui
AU  - Jia H
AD  - Department of Ophthalmology, First Hospital of Jilin University, Changchun 
      130021, Jilin Province, China.
LA  - eng
PT  - Journal Article
DEP - 20160118
PL  - China
TA  - Int J Ophthalmol
JT  - International journal of ophthalmology
JID - 101553860
PMC - PMC4768509
OTO - NOTNLM
OT  - corneal fibroblast
OT  - fungal keratitis
OT  - inflammation
OT  - triptolide
OT  - zymosan
EDAT- 2016/03/08 06:00
MHDA- 2016/03/08 06:01
PMCR- 2016/01/18
CRDT- 2016/03/08 06:00
PHST- 2015/01/26 00:00 [received]
PHST- 2015/04/27 00:00 [accepted]
PHST- 2016/03/08 06:00 [entrez]
PHST- 2016/03/08 06:00 [pubmed]
PHST- 2016/03/08 06:01 [medline]
PHST- 2016/01/18 00:00 [pmc-release]
AID - ijo-09-01-009 [pii]
AID - 10.18240/ijo.2016.01.02 [doi]
PST - epublish
SO  - Int J Ophthalmol. 2016 Jan 18;9(1):9-14. doi: 10.18240/ijo.2016.01.02. 
      eCollection 2016.