ArticleJournal of molecular neuroscience : MN2010
Presence of endogenous PACAP-38 ameliorated intestinal cold preservation tissue injury.
Article in Journal of molecular neuroscience : MN, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 20 citations in OpenAlex.
- The Effects of Rapamycin on the Intestinal Graft in a Rat Model of Cold Ischemia Perfusion and Preservation.Metabolites · 2022Article
- Protective Effects of PACAP in Peripheral Organs.Frontiers in endocrinology · 2020Review
- Targeting the PAC1 Receptor for Neurological and Metabolic Disorders.Current topics in medicinal chemistry · 2019Review
- PACAP and its role in primary headaches.The journal of headache and pain · 2018Review
- Comparative protein composition of the brains of PACAP-deficient mice using mass spectrometry-based proteomic analysis.Journal of molecular neuroscience : MN · 2014Article
- Molecular mechanisms underlying the Nephroprotective effects of PACAP in diabetes.Journal of molecular neuroscience : MN · 2014Article
- PACAP is an endogenous protective factor-insights from PACAP-deficient mice.Journal of molecular neuroscience : MN · 2012Article
- Effects of PACAP on oxidative stress-induced cell death in rat kidney and human hepatocyte cells.Journal of molecular neuroscience : MN · 2011Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cold preservation tissue injury remains an unsolved problem during small intestinal transplantation. Pituitary adenylate cyclase-activating polypeptide (PACAP) plays a central role in the intestinal physiology. The aim of our study was to compare the cold ischemic injury in wild-type and PACAP-38 deficient mice after small bowel cold storage. Cold ischemia was produced with small bowel preservation in a University of Wisconsin solution at 4°C in wild-type (n = 35) mice for 1 h (GI), for 3 h (GII), and for 6 h (GIII); and in PACAP-38 deficient (n = 35) mice for 1 h (GIV), for 3 h (GV), and for 6 h (GVI). Small bowel biopsies were collected after laparotomy (Control) and at the end of the ischemia periods. To determine oxidative stress parameters, malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD) were measured. Tissue damage was analyzed by qualitative and quantitative methods on hematoxylin/eosin-stained sections. In PACAP-38 deficient animals, tissue lipid peroxidation was elevated. These changes were significant after 6 h (153.04 ± 7.2) compared to sham-operated (110.44 ± 5.5) and compared to wild-type results (120.0 ± 1.1 µmol/g, p < 0.05). Meanwhile, the capacity and activity of the endogenous antioxidant system decreased significantly after 3 and 6 h preservation (GSH: 808.7 ± 5.2; 720.4 ± 8.7 vs. 910.4 ± µmol/g; SOD: 125.1 ± 1.4; 103.3 ± 1.9 vs. 212.11 ± 5.8 IU/g). Qualitative and quantitative histological results showed destruction of the mucous, submucous layers, and crypts in PACAP-38 deficient mice compared to wild-type tissues. These processes depended on the time of the cold preservation periods. Our present study showed that the presence of PACAP-38 in the small bowel tissue has a key role in the protection against intestinal cold preservation injury.
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