2013Zhongguo xin yao zazhiRequires access

Study on the mechanism of triptolide for inducing apoptosis of human liver cells

Ling He

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Abstract

Objective: To investigat the apoptosis effects of triptolide on L-02 cells and the possible mitochondrial respiratory chain-induced apoptosis mechanism.Methods: The apoptosis effects of triptolide on L-02 cells were evaluated using flow cytometry.JC-1 fluorescent staining was used to observe the mitochondrial membrane potential change of triptolide-treated cells.The effects of mitochondrial respiratory chain complex inhibitors on the release of ROS and cell apoptosis were analyzed.Results: Flow cytometry assay showed that the inhibition of triptolide on cell proliferation was positively correlated with the incubation concentration and time.JC-1 staining revealed the typical decrease of mitochondrial membrane potential.Compared with triptolide group,the ROS release level of triptolide+rotenone group significantly decreased(P0.05),while cell apoptosis was also significantly inhibited(P0.05)in the presence of mitochondrial respiratory chain complex inhibitors.Conclusion: Triptolide probably inhibits the proliferation and induces the apoptosis of L-02 cells by up-regulating of ROS release from mitochondrial respiratory chain complex Ⅰ and Ⅲ.

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Objective: To investigat the apoptosis effects of triptolide on L-02 cells and the possible mitochondrial respiratory chain-induced apoptosis mechanism.Methods: The apoptosis effects of triptolide on L-02 cells were evaluated using flow cytometry.JC-1 fluorescent staining was used to observe the mitochondrial membrane potential change of triptolide-treated cells.The effects of mitochondrial respiratory chain complex inhibitors on the release of ROS and cell apoptosis were analyzed.Results: Flow cytometry assay showed that the inhibition of triptolide on cell proliferation was positively correlated with the incubation concentration and time.JC-1 staining revealed the typical decrease of mitochondrial membrane potential.Compared with triptolide group,the ROS release level of triptolide+rotenone group significantly decreased(P0.05),while cell apoptosis was also significantly inhibited(P0.05)in the presence of mitochondrial respiratory chain complex inhibitors.Conclusion: Triptolide probably inhibits the proliferation and induces the apoptosis of L-02 cells by up-regulating of ROS release from mitochondrial respiratory chain complex Ⅰ and Ⅲ.

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Available abstract

Objective: To investigat the apoptosis effects of triptolide on L-02 cells and the possible mitochondrial respiratory chain-induced apoptosis mechanism.Methods: The apoptosis effects of triptolide on L-02 cells were evaluated using flow cytometry.JC-1 fluorescent staining was used to observe the mitochondrial membrane potential change of triptolide-treated cells.The effects of mitochondrial respiratory chain complex inhibitors on the release of ROS and cell apoptosis were analyzed.Results: Flow cytometry assay showed that the inhibition of triptolide on cell proliferation was positively correlated with the incubation concentration and time.JC-1 staining revealed the typical decrease of mitochondrial membrane potential.Compared with triptolide group,the ROS release level of triptolide+rotenone group significantly decreased(P0.05),while cell apoptosis was also significantly inhibited(P0.05)in the presence of mitochondrial respiratory chain complex inhibitors.Conclusion: Triptolide probably inhibits the proliferation and induces the apoptosis of L-02 cells by up-regulating of ROS release from mitochondrial respiratory chain complex Ⅰ and Ⅲ.

Key concepts: Triptolide, Apoptosis, Flow cytometry, Mitochondrion, Mitochondrial respiratory chain, Pi, Cell, Cell biology

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