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16 May 2018 : Laboratory Research  

Steroid Receptor Coactivator-Interacting Protein (SIP) Suppresses Myocardial Injury Caused by Acute Pancreatitis

Xin Chen1BEF, Bin Zhu2ACDG*

DOI: 10.12659/MSM.906968

Med Sci Monit 2018; 24: LBR3204-3211

Abstract

BACKGROUND: Steroid receptor coactivator-interacting protein (SIP) inhibits the activation of nuclear factor-kappa B (NF-κB) by interacting with p65. The occurrence of acute pancreatitis (AP) is closely associated with pro-inflammatory response. The present study aimed to investigate the role of SIP on myocardial injury caused by AP.

MATERIAL AND METHODS: Rat pancreatic acinar tumor cell line AR42J cells were treated with caerulein to establish AP cell models. The levels of TNF-α, IL-6, cTnI, CK-MB, and LDH1 were detected by ELISA assay. The mRNA and protein expression levels of SIP, p-p65, and p65 were detected by qRT-PCR and western blot analysis, respectively. Next, the AP cell models were non-transfected or transfected with SIP plasmids or SIP siRNA. ELISA assay was also performed to test the levels of TNF-α, IL-6, cTnI, CK-MB, and LDH1. Moreover, qRT-PCR and western blot analysis were performed to measure the mRNA and protein expression levels of SIP, p-p65, and p65, respectively.

RESULTS: Caerulein upregulated the levels of TNF-α, IL-6, cTnI, CK-MB, and LDH1. These upregulations were reduced by SIP plasmids and promoted by SIP siRNA, respectively. Caerulein also increased the mRNA and protein expression levels of p-p65. However, the increases were attenuated by SIP plasmids and enhanced by SIP siRNA, respectively.

CONCLUSIONS: In conclusion, the results suggested that SIP may inhibit the inflammatory response by deactivating p65, thus reducing the myocardial damage caused by AP.

Keywords: Nuclear Receptor Coactivator 2, Pancreatitis, Acute Necrotizing, Receptor Activator of Nuclear Factor-kappa B

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Medical Science Monitor eISSN: 1643-3750
Medical Science Monitor eISSN: 1643-3750