Abstract

Objective To explore the relations of propofol post-conditioning with expressions of P38 mitogen-activated protein kinase (P38MAPK), Bid, Bim and Puma when cortical neurons being exposed to oxygen-glucose deprivation/resuscitation (OGD). Methods Cortical neurons from SD rats within 24 h of birth were cultured in vitro and inoculated at 6- or 96- well plates; and then, they were divided into control (C) group, OGD (O) group, OGD+propofol post-conditioning (OP) group, OGD+propofol post-conditioning+SB202190 (OPS) group, SB202190 treatment (S) group and OGD+SB202190 (OS) group. In vitro cultured OGD cortical neurons for 90 min and resuscitaion for 24 h were established in the above groups excepted for C group; after OGD exposure, the cells in OP and OPS groups were treated with 50 μmol/L propofol for 2 h; the cells in OPS, S and OS groups were treated with SB202190 (50 μmol/L) to inhibit phosphorylation of P38MAPK. The neurons in the above groups then were collected. Neuronal apoptosis, viability and injury were assessed by Annexin V-FITC/PI asaay, MTT assay and lactate dehydrogenase (LDH) release assay, respectively. Mitochondrial membrane potential (MMP) was assessed by JC-1 fluorescece assay. ATP content was assessed by fluorescein-luciferase assay kit. The protein expressions of P38MAPK, Bid, Bim and Puma were assessed by Western blotting. Results As compared with those in the C group, significant increase of neuronal apoptosis, injury and expressions of Bid, Bim, Puma and phosphorylation of P38MAPK but decrease of viability, MMP and ATP content were noted in O group (P<0.05). As compared with those in the O group, significant decrease of neuronal apoptosis, injury and expressions of Bid, Bim, Puma, but increase of viability, MMP, ATP content and phosphorylation of P38MAPK were noted in the OP group (P<0.05). As compared with those in the OP group, significant increase of neuronal apoptosis, injury and expressions of Bid, Bim, Puma, but decrease of viability, MMP, and ATP content were noted in the OPS group (P<0.05). As compared with those in the O group, significant increase of neuronal apoptosis, injury and expressions of Bid, Bim, Puma, but decrease of viability, MMP, and ATP content were noted in the OS group (P<0.05). Conclusion The neuroprotection of propofol post-conditioning may be related with decrease of Bid, Bim and Puma suppressed by P38MAPK pathway. Key words: Propofol; Oxygen-glucose deprivation/resuscitation; P38 mitogen-activated protein kinase; Bid; Bim; Puma; Apoptosis

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