The aim of the present study was to investigate the effect of resveratrol on apoptosis in SGC-7901 gastric cancer cells and its molecular mechanisms of action. Following resveratrol treatment, the inhibition rate of SGC-7901 cells was determined using an MTT assay. The morphological changes in apoptosis were observed by fluorescence microscopy based on acridine orange/ethidium bromide double staining. Furthermore, cell cycle and apoptosis were detected using flow cytometry, and the expression levels of nuclear factor κB (NF-κB) as well as apoptosis-associated proteins [B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax), cleaved caspase-3 and cleaved caspase-8] were analyzed by western blotting. The results of the present study indicated that resveratrol was able to significantly inhibit the viability of SGC-7901 cells in a dose- and time-dependent manner. When treated with 200 µM resveratrol, the inhibition rate of SGC-7901 cells reached ~50%. In the presence of resveratrol, the proportion of apoptotic cells was also increased in a dose-dependent manner. Flow cytometry revealed that resveratrol induced S-phase arrest of SGC-7901 cells. When treated with 50, 200 and 400 µM resveratrol, the proportions of SGC-7901 cells in the S-phase were respectively increased to 33.8±2.42, 60.01±2.43 and 56.05±2.67%, compared with 25.62±3.29% for the control group cells in S-phase. Additionally, the levels of the pro-apoptotic proteins Bax, cleaved caspase-3 and cleaved caspase-8 were upregulated in a dose-dependent manner, whereas the level of the anti-apoptotic protein Bcl-2 was downregulated dose-dependently. Importantly, the activation of NF-κB (p65) was evidently decreased following treatment with resveratrol compared with in the control group. In conclusion, the results of the present study revealed that resveratrol was able to inhibit viability and induce apoptosis in SGC-7901 cells by suppressing NF-κB activation. Therefore, resveratrol may be considered as a potential drug candidate for the treatment of gastric cancer.
Curcumin is an anticancer compound that exerts anti-proliferative and apoptotic effects via multiple molecular targets. The purpose of the present study was to investigate the anticancer effects of curcumin in combination with 5-fluorouracil plus cisplatin (FP) on the MGC-803 human gastric cancer cell line. Following treatment with curcumin and/or FP for 24, 48 and 72 h, cell viability, cell cycle progression and the apoptosis rate were evaluated using an MTT assay, flow cytometry and dual acridine orange/ethidium bromide staining, respectively. In addition, colony formation, Transwell migration and caspase-3/caspase-8 activity assays were performed. The expression of the apoptosis regulator B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax) were detected by western blotting analysis. Following treatment with curcumin and/or FP, cell viability, colony formation and cell migration were significantly reduced compared with the untreated control group. The rate of apoptosis, caspase-3/caspase-8 activity and the expression of Bax were significantly increased, whereas Bcl-2 expression was significantly reduced following treatment with curcumin and/or FP, compared with the untreated control group. The efficacy of curcumin combined with low-dose FP was significantly increased, compared with that of curcumin combined with high-dose FP (P<0.05). Therefore, curcumin may enhance the anticancer effects of FP chemotherapy in MGC-803 cells through the promotion of apoptosis via the caspase-3/caspase-8, Bcl-2 and Bax signaling pathways. These results suggest that curcumin may serve as a synergistic drug with chemotherapy regimen FP for the treatment of gastric cancer.
Anemone flaccida Fr. Schmidt, a Traditional chinese Medicine, has been used in the treatment of rheumatoid arthritis (RA) for numerous years. However, the specific mechanisms remain to be elucidated. Thus, the present study aimed to investigate the main chemical constituents and potential mechanisms of Anemone flaccida Fr. Schmidt. The ethanol extract obtained from Anemone flaccida Fr. Schmidt (eaF) was analyzed using mass spectrometry to determine the main components and the therapeutic effects of eaF on RA were verified using a collagen-induced arthritis (CIA) rat model. results of the present study demonstrated that synovial hyperplasia and pannus of the model rats were significantly improved following eaF treatment. Moreover, the protein expression levels of VeGF and cd31-labeled neovascularization were significantly reduced in the synovium of CIA rats following treatment with eaF, compared with those of the untreated model group. Subsequently, in vitro experiments were carried out to verify the impact of eaF on synovial proliferation and angiogenesis. results of the western blot analysis revealed that eaF inhibited the Pi3K signaling pathway in endothelial cells, which is associated with anti-angiogenesis. in conclusion, results of the present study demonstrated the therapeutic effects of Anemone flaccida Fr. Schmidt on ra and preliminarily revealed the mechanisms of this drug in the treatment of ra.
Lead (Pb) is an environmental element that has been implicated in the development of dementia and Alzheimer’s disease (AD). Additionally, innate immune activation contributes to AD pathophysiology. However, the mechanisms involved remain poorly understood. The choroid plexus (CP) is not only the site of cerebrospinal fluid (CSF) production, but also an important location for communication between the circulation and the CSF. In this study, we investigated the involvement of the CP during Pb exposure by evaluating the expression of the monocyte chemoattractant protein-1 (MCP-1). MCP-1 is highly expressed in the CP compared to other CNS tissues. MCP-1 regulates macrophage infiltration and is upregulated in AD brains. Our study revealed that Pb exposure stimulated MCP-1 expression, along with a significantly increased macrophage infiltration into the CP. By using cultured Z310 rat CP cells, Pb exposure stimulated MCP-1 expression in a dose-related fashion and markedly activated both NF-κB and p38 MAP kinase. Interestingly, both SB 203580, a p38 inhibitor, and BAY 11-7082, an NF-κB p65 inhibitor, significantly blocked Pb-induced MCP-1 expression. However, SB203580 did not directly inhibit NF-κB p65 phosphorylation. In conclusion, Pb exposure stimulates MCP-1 expression via the p38 and NF-κB p65 pathways along with macrophage infiltration into the CP.
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