Effects of adrenalin on ovarian injury formed by ischemia reperfusion in rats

In this study, the impacts of adrenalin on ovarian injury caused by ischemia reperfusion were investigated in rats. In addition, it’s been investigated whether there is a correlation between adrenergic receptors and oxidant/anti-oxidant and COX1/COX-2 levels. It’s been observed that the COX-2 level that is responsible for MDA and inflammatory reaction (which are the indicators of oxidative stress in ovarian tissue to which ischemia reperfusion was applied) increased and the COX-1 levels that are responsible for GSH (an endogenic anti-oxidant with protective impact) were depressed. Adrenalin has prevented an increase in MDA and COX-2 activity in the ovarian tissue, to which I/R was applied, and prevented a reduction in GSH and COX-1 activity. However, adrenalin failed to prevent an MDA increase in ovarian tissue, to which alpha-2 adrenergic receptor blocker yohimbine was given (I/R formed), and also failed to prevent a GSH and COX-1 decrease. Adrenalin also failed to inhibit the COX-2 activity increase in ovarian tissue, to which beta blocker was applied. As a result, stimulation of the alpha-2 adrenergic receptors in an ovarian tissue causes an anti-oxidant and protective effect, while stimulation of beta-2 adrenergic receptors causes an anti-inflammatory effect. It’s been thought that adrenalin protects the ovarian tissue against ischemia reperfusion by stimulating the alpha-2 and beta-2 adrenergic receptors.Colegio de Farmacéuticos de la Provincia de Buenos Aire

The Impaired Balances of Oxidant/Antioxidant and COX-1/COX-2 in Ovarian Ischemia-Reperfusion Injury and Prevention by Nimesulide

WOS: 000321086300017The aims of this study were to investigate the association of ovarian I/R injury with oxidant/antioxidant and cyclooxygenase activity and to examine the effect of nimesulide in I/R injury. Rats were divided into four groups: sham group, ischemia-reperfusion group (IR), nimesulide 25 mg/kg group (NIM 25), and nimesulide 50 mg/kg group (NIM 50). The severe oxidative stress and inflammation that occurred in the ovarian tissue treated I/R were recovered by treatment of nimesulide. The histopathological findings, severe haemorrhage, oedema, vascular congestion accompanied with migration and adhesion of polimorphonuclear leukocytes in the endothelium were observed in the IR group that MDA, MPO and COX-2 levels were found high whereas GSH and COX-1 levels were found low. The severe histopathological findings in IR group were moderate in NIM-25 group whereas those were slight in NIM-50 group. This finding suggests that nimesulide prevents injury due to reperfusion following ischemia better when used with dosage 50 mg/kg

Exogenous ATP administration prevents ischemia/reperfusion-induced oxidative stress and tissue injury by modulation of hypoxanthine metabolic pathway in rat ovary

Gul, Mehmet Ali/0000-0002-5849-0116; Cetin, Nihal/0000-0003-3233-8009; Gul, Mehmet Ali/0000-0002-5849-0116; AKSOY, Ayse Nur/0000-0002-3793-9797WOS: 000339538600020In this study, xanthine oxidase (XO), malondialdehyde (MDA), myeloperoxidase (MPO) and glutathione (GSH) levels in the ovarian tissues of rats during the development of ischemia and postischemia-induced reperfusion were investigated, and the effect of ATP on ischemia-reperfusion (I/R) damage was biochemically and histopathologically examined. the results of the biochemical analyses demonstrated that ATP significantly reduced the level of XO and MDA and increased the amount of GSH in both ischemia and I/R-applied ovarian tissue at the doses administered. Furthermore, ATP significantly suppressed the increase in MPO activity that occurred following the application of post ischemia reperfusion in the ovarian tissue. the biochemical results obtained in the present study coincide with the histological findings. the severity of the pathological findings, such as dilatation, congestion, haemorrhage, oedema and polymorphonuclear nuclear leukocytes (PMNLs), increased in parallel with the increase observed in the products of XO metabolism. in conclusion, exogenously applied ATP prevented I/R damage by reducing the formation of XO in ischemic ovarian tissue

Exogenous ATP administration prevents ischemia/reperfusion-induced oxidative stress and tissue injury by modulation of hypoxanthine metabolic pathway in rat ovary

In this study, xanthine oxidase (XO), malondialdehyde (MDA), myeloperoxidase (MPO) and glutathione (GSH) levels in the ovarian tissues of rats during the development of ischemia and postischemia-induced reperfusion were investigated, and the effect of ATP on ischemia-reperfusion (I/R) damage was biochemically and histopathologically examined. The results of the biochemical analyses demonstrated that ATP significantly reduced the level of XO and MDA and increased the amount of GSH in both ischemia and I/R-applied ovarian tissue at the doses administered. Furthermore, ATP significantly suppressed the increase in MPO activity that occurred following the application of post ischemia reperfusion in the ovarian tissue. The biochemical results obtained in the present study coincide with the histological findings. The severity of the pathological findings, such as dilatation, congestion, haemorrhage, oedema and polymorphonuclear nuclear leukocytes (PMNLs), increased in parallel with the increase observed in the products of XO metabolism. In conclusion, exogenously applied ATP prevented I/R damage by reducing the formation of XO in ischemic ovarian tissue