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Cardioprotective effect of 5-lipoxygenase gene [ALOX5] silencing in ischemia-reperfusion

100%

Lisovyy O. O. , Dosenko V. E. , Nagibin V. S. , Tumanovska L. V. , Korol M. O. , Surova O. V. , Moibenko O. O.

Acta Biochimica Polonica

2009

tom 56

nr 4

687-694

It is well known that 5-lipoxygenase derivates of arachidonic acid play an important pathogenic role during myocardial infarction. Therefore, the gene encoding arachidonate 5-lipoxygenase (ALOX5) appears to be an attractive target for RNA interference (RNAi) application. In experiments on cultivated cardiomyocytes with anoxia-reoxygenation (AR) and in vivo using rat model of heart ischemia-reperfusion (IR) we determined influence of ALOX5 silencing on myocardial cell death. ALOX5 silencing was quantified using real-time PCR, semi-quantitative PCR, and evaluation of LTC4 concentration in cardiac tissue. A 4.7-fold decrease of ALOX5 expression (P < 0.05) was observed in isolated cardiomyocytes together with a reduced number of necrotic cardiomyocytes (P < 0.05), increased number live (P < 0.05) and unchanged number of apoptotic cells during AR of cardiomyocytes. Downregulation of ALOX5 expression in myocardial tissue by 19% (P < 0.05) resulted in a 3.8-fold reduction of infarct size in an open chest rat model of heart IR (P < 0.05). Thus, RNAi targeting of ALOX5 protects heart cells against IR injury both in culture and in vivo.

Hawthorn revisited: time- and dose-dependent cardioprotective action of WS-1442 special extract in the reperfusion-induced arrhythmia model in rats in vivo

80%

Zorniak M. , Porc M. P. , Krzeminski T. F.

nr 2

Carvedilol modifies antioxidant status of patients with stable angina

80%

Kowalski J. , Banach M. , Barylski M. , Irzmanski R. , Pawlicki L.

Cellular and Molecular Biology Letters

2008

tom 13

nr 2

230-239

The aim of this study was to evaluate the effect of carvedilol on the enzymatic antioxidative defence and plasma antioxidative activity in patients with stable angina. The study comprised 30 patients, aged 37–49 years with stable angina. Patients received carvedilol in escalating doses of 12.5 mg/24 h, 25 mg/24 h, and 50 mg/24 h for 4 weeks each. The control group was matched for age and gender, and consisted of 12 healthy volunteers, aged 39-49 years. Blood samples were collected from the cubital vein before and 4, 8 and 12 weeks after the therapy from the patients and once from the control group. For all the subjects, the superoxide dismutase (SOD-1), glutathione peroxidase (GSH-Px), catalase (CAT) activities in the erythrocytes and the antioxidant activity of the blood plasma were determined. The enzymatic antioxidative defence was significantly decreased in patients with stable angina in comparison to the healthy subjects. During the carvedilol therapy, an increase in the SOD-1, GSH-Px and CAT activities was observed. Moreover, 8 and 12 weeks after carvedilol therapy, the GSH-Px activity did not differ significantly from that observed in the group of healthy subjects. Carvedilol also increased the plasma antioxidative activity in patients with stable angina, but its level remained significantly lower than in the control group. In conclusion, carvedilol enhances antioxidant defense mechanisms in patients with chronic stable angina pectoris.