Delayed treatment of stroke with recombinant tissue plasminogen activator (r-tPA) induces overexpression of matrix metalloproteinase 9 (MMP-9) which leads to breakdown of the blood-brain barrier (BBB) and causes more injuries to the brain parenchyma. In this study, the effect of ascorbic acid (AA), an antioxidant agent, on the delayed administration of r-tPA in a rat model of permanent middle cerebral artery occlusion (MCAO) was investigated. Forty male rats were randomly divided into four groups: untreated control rats (ischaemic animals), AA-treated (500 mg/kg; 5 hr after stroke) rats, r-tPA-treated (5 hr after stroke 1 mg/kg) rats and rats treated with the combination of AA and r-tPA. Middle cerebral artery occlusion was induced by occluding the right middle cerebral artery (MCA). Infarct size, BBB, brain oedema and the levels of MMP-9 were measured at the end of study. Neurological deficits were evaluated at 24 and 48 hr after stroke. Compared to the control or r-tPA-treated animals, AA alone (p < 0.001) or in combination with r-tPA (p < 0.05) significantly decreased infarct volume. Ascorbic acid alone or r-tPA + AA significantly reduced BBB permeability (p < 0.05), levels of MMP-9 (p < 0.05 versus control; p < 0.01 versus r-tPA) and brain oedema (p < 0.001) when compared to either the control or the r-tPA-treated animals. Latency to the removal of sticky labels from the forepaw was also significantly decreased after the administration of AA + r-tPA (p < 0.05) at 24 or 48 hr after stroke. Based on our data, acute treatment with AA may be considered as a useful candidate to reduce the side effects of delayed application of r-tPA in stroke therapy. Ischaemic brain injury (IBI) is one of the most common causes of mortality and morbidity in the world [1,2]. Ischaemic brain injury is accompanied by several side effects, including brain oedema, destruction of blood-brain barrier (BBB), inflammation and induction of oxidative stress [3]. Oxidative stress in turn leads to oedema and more destruction of BBB which causes additional brain damage [4]. Reperfusion with thrombolytic recombinant tissue plasminogen activator (r-tPA) remains the only treatment proved to be safe and effective when given within 3-4.5 hr after ischaemia onset [5]. It has been shown that delayed use of r-tPA leads to hyperperfusion which results in the accumulation of free radicals and the up-regulation of matrix metalloproteinases (MMPs) including 7] and these events lead to more injuries to the brain parenchyma. Under normal conditions, the endogenous and exogenous antioxidants scavenge free radicals and inhibit the harmful effects of oxidative stress [8]. Previous investigations revealed that after IBI, the concentrations of glutathione and ascorbic acid (AA) are decreased, while free radicals are increased [9,10], suggesting that increasing the concentration of AA, which may act as an antioxidant under these conditions, could be considered as new therapeutic strategy for treatment of IBI [11].One vitamer form of AA, vitamin C, is a...

To compare the serum concentrations of IgG to Helicobacter pylori and its virulence factor CagA in patients with ischaemic heart disease (IHD), we recruited 120 patients with IHD [acute myocardial infarction (AMI) (n = 60); unstable angina (UA) (n = 60)] and 60 sex-and age-matched healthy controls in this study. The seroprevalence of anti-H. pylori IgG was 86.7% in AMI, 91.7% in UA patients and 58.3% in the control group with mean titres of 33.2 U/ml [standard error (SE) 4.76], 57.96 U/ml (SE 7.54) and 25.72 U/ml (SE 4.01) respectively. The seroprevalence of anti-H. pylori in the patient groups was significantly higher than the control group. The mean levels of anti-H. pylori in the AMI and UA groups were also significantly higher than in the control group. The seroprevalence and mean titre of anti-CagA IgG did not differ significantly between patient and control groups.

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