Changes of c-fos, malondialdehyde and lactate in brain tissue after global cerebral ischemia under different brain temperatures

Abstract

Under global cerebral ischemia, the effect of different brain temperature on cerebral ischemic injury was studied. Male Sprague-Dawley rats were divided into normothermic (37-38°C) ischemia, mild hypothermic (31-32°C) ischemia, hyperthermic (41-42°C) ischemia and sham-operated groups. Global cerebral ischemia was established using the Pulsinelli four-vessel occlusion model and brain temperature was maintained at defined level for 60 min after 20-min ischemia. The expression of c-fos protein and the levels of malondialdehyde (MDA) and lactate in brain regions were detected by immunochemistry and spectrophotometrical methods, respectively. C-fos positive neurons were found in the hippocampus and cerebral cortex after cerebral ischemia reperfusion. Mild hypothermia increased the expression of c-fos protein in both areas, whereas hyperthermia decreased the expression of c-fos protein in the hippocampus at 24 h reperfusion, and the cerebral cortex at 48 h reperfusion when compared to normothermic conditions. In normothermic, mild hypothermic and hyperthermic ischemia groups, the levels of MDA and lactate in brain tissue were increased at 24, 48 and 72 h reperfusion following 20-min ischemia as compared with the sham-operated group (P<0.01). The levels of MDA and lactate in mild hypothermic group were significantly lower than those in normothermic group (P<0.01). It is suggested that brain temperature influences the translation of the immunoreactive protein product of c-fos after global cerebral ischemia, and MDA and lactate are also affected by hypothermia and hyperthermia.

Psychological distress, social support and medication adherence in patients with ischemic stroke in the mainland of China

“…It was led to conclude that ischemic stroke patients one year after hemiplegia have psychological distress, low level of social support and poor medication adherence in the mainland of China. Therefore, it is necessary to mobilize the government, medical institutions and various social support groups to offer psychological interventions to relieve the stress of patients with ischemic stroke, and improve their medication adherence.Stroke is the second-leading cause of death worldwide and the first cause of morbidity [1] . Up to 16% of patients die within the first month after their stroke [2] , and within 1 year after the stroke event nearly 55% die or experience severe consequences [3] .…”

“…Stroke is the second-leading cause of death worldwide and the first cause of morbidity [1] . Up to 16% of patients die within the first month after their stroke [2] , and within 1 year after the stroke event nearly 55% die or experience severe consequences [3] .…”

Serum C-reactive protein, fibrinogen and D-dimer in patients with progressive cerebral infarction

“…Following brain infarction, the reduction of cerebral blood after ischemia initially causes oxygen and glucose deprivation and acute cell death, eventually leading to increasing edema and enlargement of the infarct lesion [32-35]. Haemostatic activation may be an important cause or contributor to progressing ischemic stroke [36].…”

Effects and Comparison of Curcumin on Morphology Changes of Chronic Cerebral Hypoperfusion in Young and Aged Rats

“…Curcumin has a variety of pharmacological effects, such as antitumoric, anti-inflammatory, as well as antioxidative effects [2,8]. Studies showed that curcumin could increase the expression of MDA and proto oncogene in hypoxic-ischemic brain tissue of rats, decrease the apoptosis of nerve cells and exert neuroprotective effects [9,10]. Chen reports that in 3 hours after ischemia and 24h after intraperitoneal injection of curcumin can alleviate the damage of hippocampus CA1 area via the protection of antioxidant enzymes and glutathione [11].…”