BACKGROUND

Vasogenic brain edema is the most important complication of ischemic stroke that aggravates primary brain injury. Ischemia-Reperfusion (IR)-induced Blood-Brain Barrier (BBB) impairment limits the use of recombinant tissue plasminogen activator (r-tPA) by increasing the possibility of hemorrhagic transformation and contributing to vasogenic edema and neuroinflammation. This study examined the effects of post-ischemic treatment with calcitriol on cerebral infarction, vasogenic edema formation and BBB disruption in a rat model of ischemic stroke.

METHODS

Male Sprague-Dawley rats were divided into three main groups, including the sham, IR + vehicle and IR + calcitriol groups. Transient focal cerebral ischemia was induced by a 60-min-long occlusion of the left middle cerebral artery. The infarct volume, brain edema, BBB permeability and antioxidant enzyme activities were evaluated 24 h after ischemia. Immunohistochemical analysis was conducted to investigate cell apoptosis and Brain-Derived Neurotrophic Factor (BDNF) protein expression five days after ischemia.

RESULTS

Compared to the IR + vehicle group, the IR + calcitriol group showed a reduced brain infarction volume, attenuated brain edema formation and improved BBB function. These protective effects were followed by the upregulation of antioxidant enzyme activities in the brain tissue. Additionally, a diminished cell apoptosis and an increased BDNF immunoreactivity were obtained in the IR + calcitriol group.

CONCLUSION

Calcitriol may reduce brain injury and attenuate vasogenic edema by upregulating antioxidant enzymes activities, reducing cell apoptosis and increasing BDNF protein in the brain tissue in a rat model of ischemic stroke.