Key result
Thrombopoietin significantly reduced neurological deficit scores (1.76 vs 2.18) and brain edema after ischemia-reperfusion injury in rats compared to control.
Why the study?
Does thrombopoietin reduce cerebral ischemia-reperfusion injury in a rat model of stroke?
Does thrombopoietin reduce cerebral ischemia-reperfusion injury in a rat model of stroke?
Absolute Event Rate: 1.76% vs 2.18%
p-value: p=<0.05
Thrombopoietin protects against cerebral ischemia-reperfusion injury in rats by reducing brain edema and neurological deficits, potentially via suppression of NF-κB and MMP-9 expression.
Hypothesis-generating for thrombopoietin neuroprotection in cerebral ischemia; prospective trials needed before clinical adoption.
Objective: To determine the neuroprotective effects and underpinning mechanisms of thrombopoietin (TPO), Matrix Metalloproteinase-9(MMP-9) and Nuclear Factor-B (NF-B) after focal cerebral ischemia-reperfusion in rats. Methods: Male rats underwent 2 hours of right middle cerebral artery occlusion (MCAO) followed by 22 hours of reperfusion. PBS or TPO (0.1ug/kg) was administered from caudal vein before reperfusion. Neurologic deficits, brain edema, Evans blue (EB) extravasation, NF-B and MMP-9 expression were subsequently examined. Results: Ischemia-reperfusion injury produced a large area of edema. TPO significantly reduced edema and alleviated neurologic deficits after ischemia-reperfusion. Ischemia-induced increases of NF-B, MMP-9 and Evans blue extravasation were reduced by TPO intervention. Conclusion: TPO improved neurological function and ameliorated brain edema after stroke, partly by reducing the ischemia-induced increase of NF-B and MMP-9.
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Wu et al. (2018) studied Focal cerebral ischemia-reperfusion injury. Thrombopoietin (TPO) vs. PBS (Ischemia-reperfusion model group) was evaluated on Neurological deficit score (p=<0.05). Thrombopoietin significantly reduced neurological deficit scores (1.76 vs 2.18) and brain edema after ischemia-reperfusion injury in rats compared to control.
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