The biochemical and histopathological effects of salusin alpha and salusin beta on cold restricted stress induced gastric injury

Salusin-α and salusin-β are recently discovered bioactive endogenous peptides with both haemodynamic and mitogenic activity. Salusin-α and salusin-β immunoreactivity has been detected in the stomach and intestine. Our study is designed to examine the oxidative stress, cytokines and histological effects of administration of salusin-α and salusin-β on cold-restricted stress (CRS)-induced gastric ulcers. A total of 32 Sprague Dawley, male rats were divided into four groups randomly. Group1: Control; Group2: CRS (Rats were placed individually in the restriction chamber and were subjected to the cold restricted stress at 4°C for 4 h); Group3: CRS+5nmol/kg Salusin-α; Group4: CRS+5nmol/kg Salusin-β. We determined malondialdehyde (MDA), myeloperoxidase (MPO), superoxide dismutase (SOD), salusin-α and salusin-β levels from stomach tissue, tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β)) levels from serum. Multiple comparison tests of Kruskal-Wallis and Dunn have been used for the analysis of the data. All the results were presented as mean±SD. When compared to the control group; while salusin-α level significantly increases in the group to which CRS has been applied, Salusin-β has shown a slight increase. While MDA, MPO, TNF-α, IL1-1β, and SOD activity in group subjected to the CRS changed, in the groups administered salusin-α and salusin-β, MDA, MPO and TNF-α levels decreased, and SOD activity and IL-1β levels increased. The mucosal injury and caspase-3 expression increasing with the application of CRS in the histological examinations decreased with the application of salusins. The suppression of salusin-α and salusin-β on caspase-3 expression by means of their effects on oxidative injury and TNF-α levels shows that these two hormones could be an anti-ulcerative agent

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Medicine Science-Cover
  • ISSN: 2147-0634
  • Yayın Aralığı: Yılda 4 Sayı
  • Başlangıç: 2012
  • Yayıncı: Effect Publishing Agency ( EPA )
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