Fetuin-A exerts a protective effect against experimentally induced intestinal ischemia/reperfusion by suppressing autophagic cell death
Autor: | Amira E Alsemeh, Nanees F. El-Malkey, Wesam M. R. Ashour, Nancy Husseiny Hassan, Husam M. Edrees |
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Rok vydání: | 2021 |
Předmět: |
Male
0301 basic medicine Programmed cell death Antioxidant alpha-2-HS-Glycoprotein Autophagic Cell Death medicine.medical_treatment Ischemia Inflammation Pharmacology Protective Agents General Biochemistry Genetics and Molecular Biology Jejunum 03 medical and health sciences 0302 clinical medicine medicine Animals Original Research business.industry Autophagy Jejunal Diseases medicine.disease Fetuin Enteritis Rats Intestines Disease Models Animal Oxidative Stress 030104 developmental biology medicine.anatomical_structure Reperfusion Injury 030220 oncology & carcinogenesis Beclin-1 Collagen medicine.symptom business Reperfusion injury |
Zdroj: | Exp Biol Med (Maywood) |
ISSN: | 1535-3699 1535-3702 |
Popis: | Intestinal tissue is highly susceptible to ischemia/reperfusion injury in many hazardous health conditions. The anti-inflammatory and antioxidant glycoprotein fetuin-A showed efficacy in cerebral ischemic injury; however, its protective role against intestinal ischemia/reperfusion remains elusive. Therefore, this study investigated the protective role of fetuin-A supplementation against intestinal structural changes and dysfunction in a rat model of intestinal ischemia/reperfusion. We equally divided 72 male rats into control, sham, ischemia/reperfusion, and fetuin-A-pretreated ischemia/reperfusion (100 mg/kg/day fetuin-A intraperitoneally for three days prior to surgery and a third dose 1 h prior to the experiment) groups. After 2 h of reperfusion, the jejunum was dissected and examined for spontaneous contractility. A jejunal homogenate was used to assess inflammatory and oxidative stress enzymes. Staining of histological sections was carried out with hematoxylin, eosin and Masson’s trichrome stain for evaluation. Immunohistochemistry was performed to detect autophagy proteins beclin-1, LC3, and p62. This study found that fetuin-A significantly improved ischemia/reperfusion-induced mucosal injury by reducing the percentage of areas of collagen deposition, increasing the amplitude of spontaneous contraction, decreasing inflammation and oxidative stress, and upregulating p62 expression, which was accompanied by beclin-1 and LC3 downregulation. Our findings suggest that fetuin-A treatment can prevent ischemia/reperfusion-induced jejunal structural and functional changes by increasing antioxidant activity and regulating autophagy disturbances observed in the ischemia/reperfusion rat model. Furthermore, fetuin-A may provide a protective influence against intestinal ischemia/reperfusion complications. |
Databáze: | OpenAIRE |
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