Effects of N–acetyl cysteine on serum podocalyxin and pentraxin levels in an experimental lower extremity ischemia–reperfusion injury model
Abstract
Ischemia–reperfusion injury causes oxidative stress and inflammation, leading to skeletal muscle damage. This study investigates the role of N–acetylcysteine in modulating oxidative stress and inflammatory biomarkers specifically Podocalyxin and Pentraxin 3 in a rat model of lower extremity Ischemia–reperfusion injury. An experimental, controlled animal study conducted at the Experimental Research Center of Firat University. Twenty–four female Sprague–Dawley rats were allocated into four groups: control, sham, Ischemia–reperfusion, and Ischemia–reperfusion treated with N–acetylcysteine. Ischemia was induced by clamping the infrarenal abdominal aorta for 120 min, followed by 120 min of reperfusion. A single dose of N–acetylcysteine (150 mg·kg-1, i.p.) was administered at the onset of reperfusion in the treatment group. Levels of serum Total Oxidative Status and Total Antioxidant Status, as well as the expression of Podocalyxin and Pentraxin 3 in tissue, were evaluated. A significant increase in Oxidative Status levels and a significant decrease in Antioxidant Status levels were observed in the Ischemia–reperfusion group compared to the control group. After administering N–acetylcysteine, there was a significant decrease in Oxidative Status levels and a significant increase in Antioxidant Status levels when compared to the Ischemia–reperfusion group. Histological evaluation showed that N–acetylcysteine reduced edema, hemorrhage, and overall tissue injury scores. Immunohistochemical analyses revealed increased Podocalyxin and Pentraxin 3 expression in Ischemia– reperfusion group tissues, which was notably diminished in the N–acetylcysteine – treated group. N–acetylcysteine demonstrated protective effects against Ischemia–reperfusion–induced oxidative and inflammatory damage in skeletal muscle by reducing serum and tissue levels of Podocalyxin and Pentraxin 3. These findings suggest its therapeutic potential in mitigating Ischemia– reperfusion injury and highlight Podocalyxin and Pentraxin 3 as promising biomarkers for tissue damage and treatment monitoring.
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