Effect of TRPV1 combined with lidocaine on cell state and apoptosis of U87-MG glioma cell lines

来源 :Asian Pacific Journal of Tropical Medicine | 被引量 : 0次 | 上传用户:aini143
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Objective:To study the effects of Transient receptor potential cation channel,subfamily V,member 1(TRPV1) combined with lidocaine on status and apoptosis of U87-MG glioma cell line,and explore whether local anesthetic produces neurotoxicity by TRPVI.Methods:U87-MG cells were divided into control group,gene silencing group,empty vector group and TRPV gene up-rcgulation group.For cells in each group,flow cytometry was employed to detect the intracellular calcium ion concentration and mitochondrial membrane potential at different lime point from cellular perspective.Cell apoptosis of U87-MG was assayed by flow cytometry and MTT from a holistic perspective.Results:Calcium ion concentration increased along with time.The concentration in TRPV1 gene up-regulation group was significantly higher than those in other groups at each time point(P<0.05).After adding lidocaine.mitochondrial membrane potential in U87-MG significantly increased(P<0.05).This increasing trend in TRPV1 gene up-regulation group was more significant than other groups(P<0.05).while in TRPV1 gene silencing group,the trend significantly decreased(P<0.05).Flow cytometry result and MTT result both showed that cell apoptosis in each group significantly increased after lidocaine was added(P<0.05).This increasing trend in TRPV1 gene up-regulation group was more significant than other groups(P<0.05),while in TRPV1 gene silencing group,the trend significandy decreased(P<0.05).Moreover,apoptosis was more severe along with the increasing concentration of lidocaine(P<0.05).Conclusions:In this study,it was proved that lidocaine could dose-dependently induce the increase of intracellular calcium ion concentration,mitochondrial membrane potential and apoptosis in U87-MG glioma cell line.The up-regulation of TRPV1 enhanced cytotoxicity of lidocaine,which revealed the correlations between mem.Lidocaine might have increased intracellular calcium ion concentration by activating TRPVI gene and induced apoptosis of U87-GM glioma cell line by up-regulating mitochondrial membrane potential. Objective: To study the effects of Transient receptor potential cation channel, subfamily V, member 1 (TRPV1) combined with lidocaine on status and apoptosis of U87-MG glioma cell line, and explore whether local anesthetic due neurotoxicity by TRPVI. Methods: U87- MG cells were divided into control group, gene silencing group, empty vector group and TRPV gene up-rcgulation group. For cells in each group, flow cytometry was employed to detect the intracellular calcium ion concentration and mitochondrial membrane potential at different lime point from cellular Perspective. Cell apoptosis of U87-MG was assayed by flow cytometry and MTT from a holistic perspective. Results: Calcium ion concentration increased along with time. The concentration in TRPV1 gene up-regulation group was significantly higher than those in other groups at each time After addition of lidocaine, mitochondrial membrane potential in U87-MG significantly increased (P <0.05). This increasing trend in TRPV1 gene up-regulation While in TRPV1 gene silencing group, the trend significantly decreased (P <0.05). Flow cytometry result and MTT result both showed that cell apoptosis in each group significantly increased after lidocaine was added (P <0.05) .This increasing trend in TRPV1 gene up-regulation group was more significant than other groups (P <0.05), while in TRPV1 gene silencing group, the trend significantly and decreased (P <0.05) .Moreover, apoptosis was more severe along with the increasing concentration of lidocaine (P <0.05) .Conclusions: In this study, it was proved that lidocaine could dose-dependently induce the increase of intracellular calcium ion concentration, mitochondrial membrane potential and apoptosis in U87-MG glioma cell line . The up-regulation of TRPV1 enhanced cytotoxicity of lidocaine, which revealed the correlations between mem. Lidocaine might have increased intracellular calcium ion concentration by activating TRPVI gene and induced apoptosis of U87-GM glioma cell line by up-regulating mitochondrial membrane potential.
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