Chrysophanol Induced Glioma Cells Apoptosis via Activation of Mitochondrial Apoptosis Pathway

Abstract

Glioma is a common intracranial tumor originated from neuroglia cell. Chrysophanol is an anthraquinone derivative proved to exert anticancer effects in various cancers. This paper investigated the effect and mechanism of chrysophanol in glioma. Glioma cell lines U251 and SHG-44 were adopted in the experiments. The cells were treated with chrysophanol at different concentrations (0, 10, 20 50, 100 and 200 μM) for 48 h in the study, and then processed with MitoTempo. Mitochondria and cytosol were isolated to investigate the role of mitochondria during chrysophanol functioning on glioma cells. Cell viability was detected through 3-(4,5-Dimethyl-2-Thiazolyl)-2,5-Diphenyl Tetrazolium Bromide (MTT) assay, and cell apoptosis, cell cycle as well as relative reactive oxygen species (ROS) were assessed by flow cytometry. Expressions of Cytosol Cyt C, cleaved caspase-3, cleaved caspase-9, Cyclin D1 and Cyclin E were evaluated by western blot. In U251 and SHG-44 cells, with chrysophanol concentration rising, cell viability, expressions of Cyclin D1 and Cyclin E were decreased while cell apoptosis, levels of cleaved caspase-3, cleaved caspase-9 and Cytosol Cyt C as well as ROS accumulation were increased with cell cycle arrested in G1 phase. Besides, chrysophanol promoted ROS accumulation, cell apoptosis and transfer of Cyt C from mitochondria to cytosol in cells while MitoTempo partly reversed the effect of chrysophanol. Chrysophanol promoted cell apoptosis via activating mitochondrial apoptosis pathway in glioma.

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“…Western Blot Analysis. Western blot was operated according to the previous report [35]. The cells were lysed using the precooled radio immune-precipitation assay buffer (RIPA, Beyotime, Shanghai, China) including protease and phosphatase inhibitors (Sigma-Aldrich, USA).…”

NIR‐II Imaging‐Guided Mitochondrial‐Targeting Organic Nanoparticles for Multimodal Synergistic Tumor Therapy

“…As caspase‐9 and caspase‐3 are essential biomarkers in mitochondria‐mediated intrinsic apoptosis, immunohistochemical (IHC) analyses of the cleaved caspase‐3 and caspase‐9 were detected in vivo to prove that the ability of mitochondrial‐targeting could enhance cellapoptosis. [ 37 ] The critical disappearance of the cell nuclei and the evident increase of cleaved caspase‐9 and cleaved caspase‐3 further proved the severe apoptosis in the mitochondrial‐targeting FE‐T NPs‐treated tumors ( Figure ). The mitochondrial location of FE‐T NPs, generated ROS and hyperthermia, resulting in mitochondrial dysfunction and photoinduced apoptosis via the mitochondria initiated apoptotic pathway.…”

“…Determining caspase‐3 activity could prove mitochondrial‐targeting enhanced apoptosis, because caspase‐3 is a critical biomarker in mitochondria‐mediated intrinsic apoptosis. [ 37 ] The cleaved caspase‐3 in different treatments was investigated with immunofluorescence (IF) staining (Figure 3E; Figure S17C, Supporting Information). Without 808 nm laser irradiation, the fluorescence intensities of FE NPs and FE‐T NPs groups were comparable with the PBS‐treated groups, revealing weak expression of cleaved caspase‐3.…”

“…According to the data, these two nanoparticles were inclined to accumulate in the livers and spleens due to their large sizes. [37,38] Interestingly, more accumulation of fluorescence signals in the liver and spleens after the injection of FE NPs, resulting in less signals in tumor sites. In contrast, FE-T NPs were inclined to accumulate in the tumor sites with less uptake by livers and spleens compared with FE NPs.…”