Protective effects of Osthole on cerebral ischemia-reperfusion injury in rats and its mechanism
Qishen Lian
Abstract
Qishen Lian
Abstract
Aim To investigate the protective effects of Osthole(Ost)on cerebral ischemia-reperfusion injury in rats and its mechanism.Methods Focal cerebral ischemia-reperfusion model in rat was induced by transient occlusion of the middle cerebral artery for 2 hours and followed by 24 hours of reperfusion.5 and 10 mg·kg-1 Ost was injected respectively through sublingual vein 1 hour after the onset of ischemia.At 24 hours of reperfusion,the influence of Ost on neurological deficit score and brain edema were observed;the activities of iNOS and myeloperoxidasse(MPO)in the ischemic hemisphere cortex of the middle cerebral artery area were assayed by spectrophotometry;the content of nitric oxide(NO),interleukin-1beta(IL-1β)and interleukin-8(IL-8)was detected with spectrophotometry and radioimmunoassay respectively.Results Ost significantly reduced the neurological deficit score and the brain edema,inhibited the iNOS and MPO activity,and decreased the contents of NO,IL-1β and IL-8 in the brain tissue.Conclusion Ost had protective effects on cerebral ischemia-reperfusion injury in rats,and its mechanism might be partly due to the inhibition of inflammation induced by ischemia-reperfusion.
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Aim To investigate the protective effects of Osthole(Ost)on cerebral ischemia-reperfusion injury in rats and its mechanism.Methods Focal cerebral ischemia-reperfusion model in rat was induced by transient occlusion of the middle cerebral artery for 2 hours and followed by 24 hours of reperfusion.5 and 10 mg·kg-1 Ost was injected respectively through sublingual vein 1 hour after the onset of ischemia.At 24 hours of reperfusion,the influence of Ost on neurological deficit score and brain edema were observed;the activities of iNOS and myeloperoxidasse(MPO)in the ischemic hemisphere cortex of the middle cerebral artery area were assayed by spectrophotometry;the content of nitric oxide(NO),interleukin-1beta(IL-1β)and interleukin-8(IL-8)was detected with spectrophotometry and radioimmunoassay respectively.Results Ost significantly reduced the neurological deficit score and the brain edema,inhibited the iNOS and MPO activity,and decreased the contents of NO,IL-1β and IL-8 in the brain tissue.Conclusion Ost had protective effects on cerebral ischemia-reperfusion injury in rats,and its mechanism might be partly due to the inhibition of inflammation induced by ischemia-reperfusion.
Key concepts: Ischemia, Medicine, Anesthesia, Nitric oxide, Radioimmunoassay, Myeloperoxidase, Cerebral edema, Reperfusion injury