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Mechanism underlying methyl eugenol attenuation of intestinal ischemia/reperfusion injury
- Saleh, Hanan, El-Shorbagy, Haidan M.
- Applied physiology, nutrition and metabolism 2017 v.42 no.10 pp. 1097-1105
- DNA, antioxidant biomarkers, apoptosis, blood serum, caspase-3, enzyme-linked immunosorbent assay, gene expression, gene expression regulation, immunohistochemistry, interleukin-6, ischemia, lactate dehydrogenase, malondialdehyde, messenger RNA, methyl eugenol, mortality, nitric oxide, oxidative stress, protective effect, protein content, rats, reactive oxygen species, reperfusion injury, small intestine, tumor necrosis factor-alpha
- Intestinal ischemia/reperfusion (I/R) injury is associated with a high risk of mortality in the clinical situation. Many factors are involved in I/R, including reactive oxygen species, cytokine release, and apoptosis. We aimed to determine whether a pure methyl eugenol (ME) given before intestinal ischemia, protects against intestinal I/R injury and the possible mechanism involved in this protection. Rat received ME (100 mg/kg) for 30 days then underwent intestinal I/R with 30 min ischemia and 60 min reperfusion. Serum lactate dehydrogenase (LDH) level, tissue malondialdehyde (MDA), as well as some antioxidant biomarkers were assessed, while the serum level of tumor necrosis factor alpha (TNF-α) was determined by ELISA. The change in TNF-α and interleukin 6 (IL-6) gene expressions were evaluated and confirmed by assessing protein level of TNF-α in the intestinal tissue by immunohistochemistry. Apoptosis was evaluated using DNA-laddering assay and by detecting caspase-3 immunohistochemically. Administration of ME prior to I/R injury resulted in a modulation of the production of MDA, LDH, and nitric oxide and restoration of the tested oxidative stress biomarkers. Pretreatment with ME downregulated messenger RNA of TNF-α and IL-6 inflammatory cytokines and their protein expressions in I/R rats. Marked inhibition of the apoptotic DNA and improvement of the architectures of small intestine were observed after pretreatment with ME. ME exhibits a protective effect against intestinal I/R via amelioration of the oxidative stress and inflammatory cytokines gene expression. Therefore, the supplementation of ME prior to intestinal I/R might be helpful in the attenuation of I/R complications.