Abstract
Previous studies have indicated that bone morphogenetic protein-7 (BMP-7) is neuroprotective against cerebral ischemia/reperfusion (IR) injury. The present study was undertaken to determine the molecular mechanisms involved in this effect. Adult male Wistar rats were subjected to 2 h of transient middle cerebral artery occlusion (MCAO), followed by 24 h of reperfusion. BMP-7 (10−4 g/kg) or vehicle was infused into rats at the onset of reperfusion via the tail vein. Neurological deficits, infarct volume, histopathological changes, oxidative stress-related biochemical parameters, neuronal apoptosis, and apoptosis-related proteins were assessed. BMP-7 significantly improved neurological and histological deficits, reduced the infarct volume, and decreased apoptotic cells after cerebral ischemia. BMP-7 also markedly enhanced the activities of antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX), and reduced the level of malondialdehyde (MDA) in IR rats. In addition, Western blot analysis indicated that BMP-7 prevented cytochrome c release, inhibited activation of caspase-3, caspase-9 and caspase-8. Our data suggested that BMP-7 has protective effects against cerebral IR injury in rats, and the neuroprotective effects may be attributed to attenuating oxidative stress and inhibiting neuronal apoptosis.
Highlights
Stroke is a leading cause of death and adult disability worldwide [1,2]
bone morphogenetic protein-7 (BMP-7) treatment significantly improved the neurological score compared with the vehicle group (p < 0.05) (Figure 1)
In this study we demonstrated that BMP-7 protected against cerebral IR injury by reducing infarct volume, improving neurological and histological deficits, and these beneficial effects were associated with inhibition of oxidative stress or neuronal apoptosis-related pathways, such as reduction of the MDA content, elevation of superoxide dismutase (SOD) and GSH-PX activities, inhibition of cytochrome c release, and suppression of caspase-3, caspase-9 and caspase-8 activation
Summary
Stroke is a leading cause of death and adult disability worldwide [1,2]. Ischemic stroke accounts for approximately 80% of all strokes, and occurs when a major cerebral artery is blocked by a thrombus or embolism [3]. This blockage leads to brain injury through a complex series of pathophysiological events leading to neuronal cell death and subsequent neurological dysfunction. There is a compelling need to develop novel therapeutic options for patients with ischemic stroke
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