Correlation between activation of MSK1/CREB signaling axis and inhibition of neuronal apoptosis by dl-3-n-butylphthalide after intracerebral hemorrhage in rats
Objective:To investigate the inhibitory mechanism of dl-3-n-butylphthalide(NBP)on neuronal apoptosis after intracerebral hemorrhage(ICH)through the mitogen and stress activated protein kinase1-cAMP-response element binding protein(MSK1-CREB)signaling axis.Methods:A rat model of ICH was established using collagenase type Ⅶ injection into the caudate nucleus.Groups were set up as follows:control,sham operation(Sham),ICH + NBP and ICH + normal saline(NS).Neurological function was assessed using the modified neurological severity score(Mnss).Brain water content was measured by the wet-dry weight method.Expression levels of Caspase-3,B-cell lymphoma-2(Bcl-2),Camp-response element binding protein(CREB),and mitogen and stress activated protein kinase1 (MSK1)in the perihematoma tissue were detected by Western blotting and immunofluorescence analysis.Results:NBP treatment significantly improved neurological deficits after ICH in rats,alleviated brain edema,and inhibited the expression of Caspase-3 while increasing the expression of Bcl-2,CREB,and MSK1.Conclusion:NBP inhibits neuronal apoptosis after ICH in rats through the MSK1-CREB signaling axis,a theoretical basis for the application of NBP in the treatment of ICH.
intracerebral hemorrhage(ICH)neuronapoptosisdl-3-n-butylphthalidemitogen and stress activated protein kinase1(MSK1)
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