ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Steroid Receptor Coactivator-Interacting Protein (SIP) Suppresses Myocardial Injury Caused by Acute Pancreatitis.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Review
- Cardiac complications in acute pancreatitis: an under-diagnosed clinical concern.World journal of emergency medicine · 2025Article
- HSP70 Ameliorates Septic Lung Injury via Inhibition of Apoptosis by Interacting with KANK2.Biomolecules · 2022Article
- Article
- The Neuroprotective Effect of Steroid Receptor Coactivator-Interacting Protein (SIP) in Astrocyte Model of 1-Methyl-4-Phenylpyridinium (MPP⁺)-Induced Parkinson's Disease.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
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