2008Zhongguo yaolixue tongbaoRequires access

Protective effects of Osthole on cerebral ischemia-reperfusion injury in rats and its mechanism

Qishen Lian

Open publisher page 5 citations

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.

About this research paper

What this paper is about

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.

Why it matters

OpenAlex reports 5 citations for this work. Citation counts describe recorded attention and do not establish research quality.

Key contribution

A contribution statement is not available in the OpenAlex record.

Method / approach

Method details are not available in the OpenAlex metadata.

Main findings

Findings are not separately available in the OpenAlex metadata.

Limitations

Limitations are not available in the OpenAlex metadata.

Applications

Application details are not available in the OpenAlex metadata.

Available 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.

Key concepts: Ischemia, Medicine, Anesthesia, Nitric oxide, Radioimmunoassay, Myeloperoxidase, Cerebral edema, Reperfusion injury

Related papers

Back to paper searchBrowse research topicsOriginal source
Protective effects of Osthole on cerebral ischemia-reperfusion injury in rats and its mechanism — Research Paper | ScholarLens