PMID- 23765438
OWN - NLM
STAT- MEDLINE
DCOM- 20140923
LR  - 20220317
IS  - 1720-8386 (Electronic)
IS  - 0391-4097 (Linking)
VI  - 36
IP  - 11
DP  - 2013 Dec
TI  - The adipocytokine resistin stimulates the production of proinflammatory cytokines 
      TNF-alpha and IL-6 in pancreatic acinar cells via NF-kappaB activation.
PG  - 986-92
LID - 10.3275/9002 [doi]
AB  - BACKGROUND: Resistin, an adipocytokine secreted by fat tissues, has been 
      associated with the inflammatory response, though its role in inflammation during 
      acute pancreatitis (AP) remains unclear. OBJECTIVE: The proinflammatory response 
      following acinar cell injury impacts pancreatitis severity, necessitating better 
      understanding of functional consequences associated with pancreatic acinar cell 
      resistin exposure and resultant effects on proinflammatory signaling. METHODS: 
      Amylase-secreting rat pancreatic acinar AR42J cells were subjected to 1, 10, or 
      100 ng/ml recombinant rat resistin treatments. Cytotoxicity was evaluated by 
      amylase secretion and lactate dehydrogenase (LDH) release. Tumor necrosis 
      factor-alpha (TNF-alpha) and interleukin 6 (IL-6) mRNA and protein expressions were 
      determined by real-time real time-PCR and enzyme-linked immunosorbent assay, 
      respectively. Nuclear NF-kappaB p65 subunit protein level was measured by western 
      blotting. RESULTS: Significantly increased amylase secretion and LDH release was 
      observed in the 100 ng/ml resistin treatment (p<0.01). Both TNF-alpha and IL-6 
      protein expression levels increased in a concentration-dependent manner when 
      treated with resistin. Pretreatment of resistin- treated AR42J cells with the 
      NF-kappaB inhibitor PDTC, which decreases the NF-kappaB p65 subunit protein expression 
      levels in the nuclei, produced significantly lower mRNA expression levels for 
      both TNF-alpha and IL-6 compared with those produced by resistin-treated cells 
      (p<0.01). CONCLUSIONS: Resistin exhibits some cytotoxic activity in rat 
      pancreatic acinar AR42J cells and stimulates proinflammatory cytokine TNF-alpha and 
      IL-6 production via NF-kappaB activation. Thus, overproduction of obesity-related 
      circulating resistin and associated lowgrade inflammation may result in mild 
      injury to pancreatic acini, increasing AP severity and risk.
FAU - Jiang, C Y
AU  - Jiang CY
AD  - Department of General Surgery, Huadong Hospital Affiliated To Fudan University, 
      Shanghai 200040, China.
FAU - Wang, W
AU  - Wang W
FAU - Tang, J X
AU  - Tang JX
FAU - Yuan, Z R
AU  - Yuan ZR
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130610
PL  - Italy
TA  - J Endocrinol Invest
JT  - Journal of endocrinological investigation
JID - 7806594
RN  - 0 (Interleukin-6)
RN  - 0 (NF-kappa B)
RN  - 0 (Resistin)
RN  - 0 (Retn protein, rat)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 3.2.1.- (Amylases)
SB  - IM
MH  - Acinar Cells/drug effects/*metabolism
MH  - Amylases/metabolism
MH  - Animals
MH  - Interleukin-6/*biosynthesis
MH  - NF-kappa B/*physiology
MH  - Pancreatitis/physiopathology
MH  - Rats
MH  - Resistin/pharmacology/*physiology
MH  - Tumor Necrosis Factor-alpha/*biosynthesis
EDAT- 2013/06/15 06:00
MHDA- 2014/09/24 06:00
CRDT- 2013/06/15 06:00
PHST- 2013/06/15 06:00 [entrez]
PHST- 2013/06/15 06:00 [pubmed]
PHST- 2014/09/24 06:00 [medline]
AID - 9002 [pii]
AID - 10.3275/9002 [doi]
PST - ppublish
SO  - J Endocrinol Invest. 2013 Dec;36(11):986-92. doi: 10.3275/9002. Epub 2013 Jun 10.