2002Di-san junyi daxue xuebaoRequires access

Relationship between activity of protein kinase C and apoptosis of cultured neurons after hypoxia

He Huang

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Abstract

Objective To explore the effect and possible mechanism of protein kinase C (PKC) on the apoptosis of cultured neurons after hypoxia Methods Model of cultured rat neurons under hypoxia condition was established. Calphostin C, an inhibitor for the catalytic subunit of PKC, at 4 different concentrations were separately cocultured for 2 h with the neurons having been cultivated under hypoxic condition for different times The activity of membrane PKC (mPKC), the expression of Bcl 2 and the situation of neuron apoptosis were studied Results With the prolonging of hypoxic time the activity of mPKC was increased significantly And the expression of Bcl 2 was decreased obviously and positive rate of TUNEL were significantly increased in a calphostin C concentration dependent manner Conclusion ① The activation of mPKC and Bcl 2 are involved in the apoptosis of neurons after hypoxia ② Hypoxia and calphostin C can aggravate the hypoxic neuronal apoptosis through the signal transduction of Bcl 2 ③ The activation of PKC can protect neuron against hypoxia

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Objective To explore the effect and possible mechanism of protein kinase C (PKC) on the apoptosis of cultured neurons after hypoxia Methods Model of cultured rat neurons under hypoxia condition was established. Calphostin C, an inhibitor for the catalytic subunit of PKC, at 4 different concentrations were separately cocultured for 2 h with the neurons having been cultivated under hypoxic condition for different times The activity of membrane PKC (mPKC), the expression of Bcl 2 and the situation of neuron apoptosis were studied Results With the prolonging of hypoxic time the activity of mPKC was increased significantly And the expression of Bcl 2 was decreased obviously and positive rate of TUNEL were significantly increased in a calphostin C concentration dependent manner Conclusion ① The activation of mPKC and Bcl 2 are involved in the apoptosis of neurons after hypoxia ② Hypoxia and calphostin C can aggravate the hypoxic neuronal apoptosis through the signal transduction of Bcl 2 ③ The activation of PKC can protect neuron against hypoxia

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Available abstract

Objective To explore the effect and possible mechanism of protein kinase C (PKC) on the apoptosis of cultured neurons after hypoxia Methods Model of cultured rat neurons under hypoxia condition was established. Calphostin C, an inhibitor for the catalytic subunit of PKC, at 4 different concentrations were separately cocultured for 2 h with the neurons having been cultivated under hypoxic condition for different times The activity of membrane PKC (mPKC), the expression of Bcl 2 and the situation of neuron apoptosis were studied Results With the prolonging of hypoxic time the activity of mPKC was increased significantly And the expression of Bcl 2 was decreased obviously and positive rate of TUNEL were significantly increased in a calphostin C concentration dependent manner Conclusion ① The activation of mPKC and Bcl 2 are involved in the apoptosis of neurons after hypoxia ② Hypoxia and calphostin C can aggravate the hypoxic neuronal apoptosis through the signal transduction of Bcl 2 ③ The activation of PKC can protect neuron against hypoxia

Key concepts: Calphostin C, Hypoxia (environmental), Protein kinase C, Apoptosis, Calphostin, Cell biology, Neuron, TUNEL assay

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