Glucagon-like peptide-1 (GLP-1) analogues might exert the cardioprotective effects via attenuating apoptosis. This study aimed to determine the protective effects and mechanism of exenatide, a GLP-1 analogue, on cardiomyocyte apoptosis using an in vitro model of hypoxia/reoxygenation (H/R). H9c2 cells were employed to establish an in vitro model of H/R. 200 nM exenatide pretreatment significantly reduced apoptosis measured by flow cytometry. To further study the antiapoptotic mechanism of exenatide, we used flow cytometry in combination with laser confocal microscopy to determine the interaction between exenatide and the process of mitochondria-mediated apoptosis. We found that exenatide pretreatment reduced the intracellular reactive oxygen species (ROS) levels and decreased the mitochondrial calcium overload caused by H/R. Furthermore, an increase of total superoxide dismutase (T-SOD) levels, a decrease of malondialdehyde (MDA) levels, a preservation of mitochondrial membrane potential (ΔΨm), a reduction of cytochrome-c release, a decline of cleaved caspase-3 expression, and caspase-3 activation were observed in exenatide-pretreated cultures. These results suggest that exenatide exerts a protective effect on preventing against H/R-induced apoptosis. Importantly, the protective effects of exenatide may be attributed to its role in improving mitochondrial function in H9c2 cells subjected to H/R.

Gastric carcinoma (GC) has high incidence and mortality rates in China. Surgery and chemotherapy are the main treatments. Photodynamic therapy (PDT) has become a new treatment modality, appearing in recent experimental studies and clinical trials in various tumors. This study explores the combined effect of gene transfection with PDT on GC cells using aloe emodin (AE)–encapsulated nanoliposomes, which acted as gene carrier as well as one photosensitizer (PS). AE‐encapsulated nanoliposomes (nano‐AE) were prepared by reverse evaporation method. Electron microscopy and nano‐ZS90 analyzer were used to detect its morphology, size, and wavelength. Western blot was used to detect the expression of the caspase‐3 after transfection. MTT assay and flow cytometry were employed to determine the cytotoxic and apoptotic rates, respectively. Hoechst 33342 staining was adopted to detect the morphological changes in death gastric cancer cells. Cellular reactive oxygen species (ROS) contents were measured by DCFH‐DA staining. Outcomes demonstrated that the nano‐AE has good properties as gene delivery carriers as well as a PS. The group in which the recombinant plasmid of r‐caspase‐3 was transfected had higher protein expression of the caspase‐3 than controls, meanwhile the proliferation rates of the transfected cells were inhibited by the nano‐AE‐mediated PDT in an energy‐dependent manner. In addition, in the transfected cells, the death rate increased to 77.3% as assessed 12 h after PDT (6.4 J/cm2). Hochest 33342 staining also revealed that the death rate increased significantly in the transfected group compared with other groups. Compared to control groups, the production of ROS in nano‐AE PDT group had quadrupled in SGC‐7901 cells as early as 1 h after PDT, while it is similar to the group of nano‐AE transfection and PDT. Nano‐AE‐mediated r‐caspase‐3 gene transfection coupled with PDT could inhibit the proliferation rate and increase the apoptotic rate remarkably in human gastric cancer cells.

Photodynamic therapy (PDT) is a promising treatment in cancer therapy, with a photosensitizer activated by visible light. Aloe‐emodin (AE) is a promising photosensitive agent. In this study, the photosensitizing effects and possible mechanisms of AE‐PDT in MG63 cells were evaluated. The efficiency of AE‐PDT was analyzed by MTT assay. The mode of cell death was investigated by Hoechst 33,342 staining and flow cytometer. The intracellular distribution of AE was detected with confocal microscopy. The formation of reactive oxygen species (ROS) was detected by DCFH‐DA. The mitochondrial membrane potential (MMP) was measured by Rhodamine 123. The expression of proteins including cytochrome c, caspase‐3, ‐9, and ‐12, CHOP and GRP78 was detected by western blot. Apoptosis is the primary mode of cell death in our study, which occurs in a manner of depending on AE concentration and irradiation dose. Confocal microscopy showed that AE was primarily localized on the mitochondria and endoplasmic reticulum (ER) of MG63 cells. AE‐PDT resulted in rapid increases of intracellular ROS production, which reached a peak at 2 h, followed by declining of mitochondrial membrane potential, releasing of cytochrome c from mitochondria into the cytoplasm, and up‐regulation of caspase‐3, ‐9, and ‐12, CHOP and GRP78. These results suggest that death of MG63 cells induced by AE‐PDT is triggered by ROS. Meanwhile, Mitochondria and ER serve as the subcellular targets, which are responsible for AE‐PDT‐induced death of MG63 cells.

The aim of the present study was to explore the effect of aloe-emodin (AE)-induced photodynamic activity in human gastric cancer cells. AE was used as a photosensitizer to explore the effect of photodynamic therapy (PDT) in human gastric cancer cells (SGC-7901). An MTT assay was used to detect the effect of AE-induced PDT in optimal concentrations and illumination energy densities in human gastric cancer cells. Following AE-induced PDT, morphological changes of the cells and the rate of cell death were evaluated by TUNEL assay and flow cytometry, respectively. The expression levels of caspase-9 and caspase-3 were determined by western blot analysis. The AE and AE-induced PDT demonstrated a significant inhibitive effect on the proliferation of human gastric cancer cells in dose-dependent and energy-dependent manners. For subsequent experiments, 10 µM AE and 12.8 J/cm2 illumination energy density were used. Typical morphological changes of apoptosis were observed in the cells using a TUNEL assay 12 h subsequent to AE-induced PDT. The percentage of apoptotic cells treated with AE-induced PDT significantly increased when compared with the control group, the 10 µM AE group and the illumination group (P<0.05). Upregulation of caspase-9 and caspase-3 protein levels was also observed following AE-induced PDT. The present study revealed that 10 µM AE-induced PDT had an inhibitory effect on human gastric cancer cells, and it may induce cell apoptosis by upregulating caspase-9 and caspase-3, which indicated that the mitochondrial pathway may be involved. AE-induced PDT has the potential to be a novel therapy for the treatment of human gastric cancer. However, further investigations are required.

A giant cell tumor in bone is the common primary bone tumor with aggressive features, occurring mainly in young adults. Photodynamic therapy is a new therapeutic technique for tumors. In this study, we investigated the effects of Pyropheophorbide-α methyl ester (MPPa)-mediated photodynamic therapy on the proliferation of giant cell tumor cells and its mechanism of action. Cell proliferation was evaluated using an MTT assay. Cellular apoptosis was detected by Hoechst nuclear staining, and flow cytometric assay. Mitochondrial membrane potential changes and cytochrome c, caspase-9, caspase-3, and Bcl-2 expression was assessed. Finally, we found that MPPa-mediated photodynamic therapy could effectively suppress the proliferation of human giant cell tumor cells and induce apoptosis. The mitochondrial pathway was involved in the MPPa-photodynamic therapy-induced apoptosis.