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  • Title: Neuroprotection by plumbagin involves BDNF-TrkB-PI3K/Akt and ERK1/2/JNK pathways in isoflurane-induced neonatal rats.
    Author: Yuan JH, Pan F, Chen J, Chen CE, Xie DP, Jiang XZ, Guo SJ, Zhou J.
    Journal: J Pharm Pharmacol; 2017 Jul; 69(7):896-906. PubMed ID: 28464236.
    Abstract:
    OBJECTIVES: This study was designed to assess the effects of plumbagin on isoflurane-induced neurotoxicity. METHODS: Neonatal Sprague Dawley rat pups were treated with plumbagin (50, 100 or 150 mg/kg body weight, orally) from postnatal day 2. The pups on postnatal day 7 were subjected to isoflurane (0.75%) exposure for 6 h. Neuronal apoptosis in the hippocampal tissues was detected by TUNEL assay and FluroJade B staining following isoflurane exposure. Protein expressions were analysed by immunoblotting. RT-PCR was performed to assess mRNA levels of brain-derived neurotrophic factor (BDNF) and TrkB. KEY FINDINGS: We observed reduced apoptosis in hippocampal CA1, CA3 and dentate gyrus regions along with severely reduced pro-apoptotic factors (Bad, Bax and cleaved caspase-3) expression and raised levels of Bcl-2, Bcl-xL, survivin, xIAP and cIAPs (cell survival proteins) in plumbagin supplemented rats. Decrease in the levels of JNK, phospho-JNK, c-Jun and phospho-c-Jun with enhanced ERK1/2 levels was observed on plumbagin pretreatment. Down-regulated PI3K/Akt signalling following isoflurane was activated by plumbagin as evidenced by raised PI3K/Akt pathway proteins - mTORc1, Akt, phospho-Akt, GSK-3β, phospho-GSK-3β, PTEN and NF-κBp65 in the hippocampal tissues as detected by Western blotting. The mRNA levels were enhanced on plumbagin supplementation. CONCLUSIONS: Plumbagin exerted its neuroprotective effects by effectively suppressing isoflurane-induced neuronal apoptosis via regulating BDNF-TrkB-PI3/Akt and ERK/JNK signalling.
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