Aloe-emodin Induces Apoptosis in Human Liver HL-7702 Cells through Fas Death Pathway and the Mitochondrial Pathway by Generating Reactive Oxygen Species

2017 ◽  
Vol 31 (6) ◽  
pp. 927-936 ◽  
Author(s):  
Xiaoxv Dong ◽  
Jing Fu ◽  
Xingbin Yin ◽  
Chunjing Yang ◽  
Jian Ni
Keyword(s):  
Reactive Oxygen Species ◽  
Human Liver ◽  
Reactive Oxygen ◽  
Mitochondrial Pathway ◽  
Oxygen Species ◽  
Aloe Emodin

scholarly journals Induction of Apoptosis in HepaRG Cell Line by Aloe-Emodin through Generation of Reactive Oxygen Species and the Mitochondrial Pathway

2017 ◽  
Vol 42 (2) ◽  
pp. 685-696 ◽  
Author(s):  
Xiaoxv Dong ◽  
Jing Fu ◽  
Xingbin Yin ◽  
Changhai Qu ◽  
Chunjing Yang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Viability ◽  
Reactive Oxygen ◽  
Mitochondrial Pathway ◽  
Phase Cell ◽  
Dependent Manner ◽  
Oxygen Species ◽  
Heparg Cell Line ◽  
Heparg Cells ◽  
Aloe Emodin

Background/Aims: Aloe-emodin (1,8-dihydroxy-3-hydroxymethyl-anthraquinone), an anthraquinone active compounds, is isolated from some traditional medicinal plants such as Rheum palmatum L. and Cassia occidentalis, which induce hepatotoxicity in rats. The aim of this study was to determine potential cytotoxic effects of aloe-emodin on HepaRG cells and to define the underlying mechanism. Methods: MTT was used to evaluate cell viability. Apoptotic cell death was analyzed via Annexin V-FITC/PI double staining. Intracellular reactive oxygen species (ROS) and mitochondrial membrane potential (MMP) were determined by flow cytometry, while the expression of apoptosis-related proteins was determined by Western blot analysis. Results: Treatment with aloe-emodin significantly reduced cell viability and induced apoptosis in HepaRG cells in a dose- and time-dependent manner. It provoked ROS generation and depolarization of MMP in HepaRG cells when compared with controls. Aloe-emodin dose-dependently increased release of mitochondrial cytochrome c, and levels of Fas, p53, p21, Bax/Bcl-2 ratio, as well as activation of caspase-3, caspase-8, caspase-9, and subsequent cleavage of poly(ADP-ribose)polymerase (PARP). It also induced S-phase cell cycle arrest by increasing the expression of p21 and cyclin E proteins while significantly decreasing the expression of cyclin A and CDK2. Conclusion: These results suggest that aloe-emodin inhibits cell proliferation and induces apoptosis in HepaRG cells, most probably through a mechanism involving both Fas death pathway and the mitochondrial pathway by generation of ROS. These findings underscore the need for risk assessment of human exposure to aloe-emodin.

Gossypol induced apoptosis of polymorphonuclear leukocytes and monocytes: Involvement of mitochondrial pathway and reactive oxygen species

2009 ◽  
Vol 31 (2) ◽  
pp. 320-330 ◽  
Author(s):  
Martha Barba-Barajas ◽  
Georgina Hernández-Flores ◽  
José M. Lerma-Díaz ◽  
Pablo C. Ortiz-Lazareno ◽  
Jorge R. Domínguez-Rodríguez ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Polymorphonuclear Leukocytes ◽  
Reactive Oxygen ◽  
Mitochondrial Pathway ◽  
Oxygen Species ◽  
Induced Apoptosis

scholarly journals Ivalin Induces Mitochondria-Mediated Apoptosis Associated with the NF-κB Activation in Human Hepatocellular Carcinoma SMMC-7721 Cells

Molecules ◽  
2019 ◽  
Vol 24 (20) ◽  
pp. 3809
Author(s):  
Zhuo Han ◽  
Fang-yuan Liu ◽  
Shi-qi Lin ◽  
Cai-yun Zhang ◽  
Jia-hui Ma ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Mitochondrial Pathway ◽  
Human Hepatocellular Carcinoma ◽  
Induction Effect ◽  
Oxygen Species ◽  
Microtubule Depolymerization ◽  
Apoptotic Effect

Ivalin, a natural compound isolated from Carpesium divaricatum, showed excellent microtubule depolymerization activities among human hepatocellular carcinoma in our previous work. Here, we investigated its functions on mitochondria-mediated apoptosis in hepatocellular carcinoma SMMC-7721 cells. DAPI (4′,6-diamidino-2-phenylindole) staining, annexin V-fluorexcein isothiocyanate (FITC) apoptosis detection, and western blotting were applied to explore the apoptotic effect of Ivalin. Next, the induction effect of Ivalin on the mitochondrial pathway was also confirmed via a series of phenomena including the damage of mitochondria membrane potential, mitochondria cytochrome c escape, cleaved caspase-3 induction, and the reactive oxygen species generation. In this connection, we understood that Ivalin induced apoptosis through the mitochondrial pathway and the overload of reactive oxygen species. Furthermore, we found that the activation of nuclear factor-κB (NF-κB) and subsequent p53 induction were associated with the apoptotic effect of Ivalin. These data confirmed that Ivalin might be a promising pro-apoptotic compound that can be utilized as a potential drug for clinical treatment.

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