Plasma Oxidants and Antioxidants in Acute Ischaemic Stroke

Aygül, Recep; Kotan, Dilcan; Demirbas, F; Ulvi, Hızır; Denız, Orhan

doi:10.1177/147323000603400411

Cited by 42 publications

(24 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The result is consistent with the previous report that plasma SOD and glutathione peroxidase activities were significantly decreased and malondialdehyde levels were significantly increased in patients with acute ischaemic stroke. The reduced SOD activity may be related to the exhaustion of this antioxidant by the challenge of free radical stress [20]. However, SOD activity was increased in a dose‐dependent way after the pre‐treatment of rats with protopine.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Protopine on the Focal Cerebral Ischaemic Injury in Rats

Xiao

Liu

et al. 2007

Basic Clin Pharma Tox

View full text Add to dashboard Cite

Protopine, an isoquinoline alkaloidis, is known to produce many effects such as vasodilation, down-regulation of glutamate levels in brain and decrease of intracellular calcium. However, so far there is no report on the effect of protopine in cerebral ischaemia. In this study, the effect of protopine on the focal cerebral ischaemia was investigated in rats. Male Sprague-Dawley rats were divided into five groups: sham-operated group, vehicle-treated group and three doses of protopine-treated groups (0.98, 1.96 and 3.92 mg/kg). Protopine was intraperitoneally administered to rats once daily for 3 days prior to the ischaemia and 0.9% normal saline to rats in the vehicle-treated group in the same pattern. Rats in the sham-operated group were given 0.9% normal saline without the ischaemia. The focal cerebral ischaemia was induced by the middle cerebral artery occlusion for 24 hr via the intraluminal filament technique. The results showed that pretreatment with protopine reduced the cerebral infarction ratio and serum lactate dehydrogenase activity, and improved the ischaemia-induced neurological deficit score and histological changes of brain in a dose-dependent manner. The further studies demonstrated that protopine increased superoxide dismutase activity in serum, and decreased total calcium and terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling (TUNEL)-positive cells in the ischaemic brain tissue in the middle cerebral artery occlusion rats. The results indicate that protopine is able to produce an effective protection on the injury caused by the focal cerebral ischaemia in rats possibly through the multiple effects of calcium antagonism, antioxidation and depression of cell apoptosis.Cerebral ischaemia or stroke is one of the leading causes of death and the single most common cause of severe disability in many countries. Human cerebral ischaemia often results from a transient or permanent occlusion of the middle cerebral artery. Brain tissue has a relatively high consumption of oxygen and glucose, and almost exclusively depends on oxidative phosphorylation for energy production. Following focal cerebral ischaemia, energy failure from critical blood perfusion deficit leads to disruption of ion homeostasis, generation of free radicals, initiation of apoptosis, inflammation and release of excitatory amino acids, most notably glutamate [1,2]. These result in a progressive accumulation of intracellular sodium and calcium ions, which can precipitate in necrosis and/or apoptosis of vulnerable neurones [1,3,4].Protopine is an isoquinoline alkaloid with multiple pharmacological actions. Protopine reduces intracellular calcium [5], inhibits arachidonic acid and platelet-activating factorinduced platelet aggregation by decreasing the cytosolic calcium in the rabbit [6] and suppresses thromboxane A 2 synthesis and inflammatory process via the cyclooxygenase pathway [7]. Protopine also down-regulates glutamate level in rat brain through activation of glutamate dehydrogenase [8]. In addition, it h...

show abstract

Section: Discussionmentioning

confidence: 99%

Protective Effect of Protopine on the Focal Cerebral Ischaemic Injury in Rats

Xiao

Liu

et al. 2007

Basic Clin Pharma Tox

View full text Add to dashboard Cite

show abstract

“…Demirkaya et al (2001) found that red blood cell GPx activity decreased in the first 24 hours after the onset of stroke symptoms as compared with the control group. Aygul et al (33) also observed that GPx activity in plasma and red blood cells decreased in IS patients.…”

Section: Discussionmentioning

confidence: 91%

Oxidative Stress and Antioxidant Markers in Serum and Red Blood Cell of Patients with Ischemic and Hemorrhagic Stroke: A Case-Control Study

et al. 2016

View full text Add to dashboard Cite

Background and Aim: Oxidative stress is a major mechanism involved in stroke pathogenesis. The present study evaluated and compared oxidative stress parameters in patients with ischemic and hemorrhagic stroke (IS and HS) at the time of hospitalization and 1 week after hospitalization. Methods: This was a case-control study with 87 stroke patients (58 IS and 29 HS) as the case and 58 normal individuals as the control group. Sampling was done at the time of hospitalization and after 1 week. The serum total antioxidant capacity (TAC), thiol group, and F2-isoprostan levels were measured using Ferric Reducing Antioxidant Power (FRAP), Elman, and Enzyme Linked Immunosorbent Assay ELISA methods, respectively. Results: At the time of hospitalization, there was no significant difference in TAC and F2-isoprostan levels between the case and

show abstract