2011Unpublished venueRequires access

Dexmedetomidine protects neurons against chemical hypoxia-induced injury

Feng Jian-qiang

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Abstract

Aim To explore whether alpha(α)-2-adrenoreceptor agonist dexmedetomidine protects PC12 cells against chemical hypoxia-induced injury.Meth-ods PC12 cells were treated with cobalt chloride(CoCl 2)to set up a chemical hypoxia-induced injury model.Cell viability was measured by cell counter kit(CCK-8).Morphological changes and number of apoptotic cells were detected by Hochest33258 staining,Intracellular level of reactive oxygen species(ROS)was tested by DCFH-DA staining and photofluorography.Mitochondrial membrane potential(MMP)was observed by rhodamine 123(Rh123)staining and photofluorography.Results At concentrations from 100 to 600μmol·L-1,dexmedetomidine dose-dependently inhibited CoCl2-induced cytotoxicity,increasing cell viability.Dexmedetomidine at 400μmol·L-1attenuated CoCl2-induced apoptotic effect,decreasing the number of apoptotic cells.Dexmedetomidine could also reduce overproduction of ROS and MMP loss induced by CoCl2.Conclusion Dexmedetomidine can protect PC12 cells against CoCl2-induced injury,which may be associated with its inhibitory effect on overproduction of ROS and preservation of MMP.

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Aim To explore whether alpha(α)-2-adrenoreceptor agonist dexmedetomidine protects PC12 cells against chemical hypoxia-induced injury.Meth-ods PC12 cells were treated with cobalt chloride(CoCl 2)to set up a chemical hypoxia-induced injury model.Cell viability was measured by cell counter kit(CCK-8).Morphological changes and number of apoptotic cells were detected by Hochest33258 staining,Intracellular level of reactive oxygen species(ROS)was tested by DCFH-DA staining and photofluorography.Mitochondrial membrane potential(MMP)was observed by rhodamine 123(Rh123)staining and photofluorography.Results At concentrations from 100 to 600μmol·L-1,dexmedetomidine dose-dependently inhibited CoCl2-induced cytotoxicity,increasing cell viability.Dexmedetomidine at 400μmol·L-1attenuated CoCl2-induced apoptotic effect,decreasing the number of apoptotic cells.Dexmedetomidine could also reduce overproduction of ROS and MMP loss induced by CoCl2.Conclusion Dexmedetomidine can protect PC12 cells against CoCl2-induced injury,which may be associated with its inhibitory effect on overproduction of ROS and preservation of MMP.

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Available abstract

Aim To explore whether alpha(α)-2-adrenoreceptor agonist dexmedetomidine protects PC12 cells against chemical hypoxia-induced injury.Meth-ods PC12 cells were treated with cobalt chloride(CoCl 2)to set up a chemical hypoxia-induced injury model.Cell viability was measured by cell counter kit(CCK-8).Morphological changes and number of apoptotic cells were detected by Hochest33258 staining,Intracellular level of reactive oxygen species(ROS)was tested by DCFH-DA staining and photofluorography.Mitochondrial membrane potential(MMP)was observed by rhodamine 123(Rh123)staining and photofluorography.Results At concentrations from 100 to 600μmol·L-1,dexmedetomidine dose-dependently inhibited CoCl2-induced cytotoxicity,increasing cell viability.Dexmedetomidine at 400μmol·L-1attenuated CoCl2-induced apoptotic effect,decreasing the number of apoptotic cells.Dexmedetomidine could also reduce overproduction of ROS and MMP loss induced by CoCl2.Conclusion Dexmedetomidine can protect PC12 cells against CoCl2-induced injury,which may be associated with its inhibitory effect on overproduction of ROS and preservation of MMP.

Key concepts: Dexmedetomidine, Viability assay, Chemistry, Reactive oxygen species, Apoptosis, Rhodamine 123, Pharmacology, Hypoxia (environmental)

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