The extract of Citrus reticulata has been studied for its biological activities, due to its citrus flavonoid content. The extract and its flavonoid compounds exhibit growth inhibition property in several cancer cell lines and in vivo models. Conversely, the extract can also induce cell proliferation and angiogenesis, and shows estrogenic effects by in vitro and in vivo. Because of the contrasting effects that depend on the concentration or dosage, the precise action of the extract and its flavonoids need to be elucidated in various cell types. The objective of this study is to evaluate the effect of Citrus reticulata peel extract (Citrus extract) and hesperidin, a citrus flavonoid, on the modulation of cell proliferation in the RAW 264.7 macrophage cell line. Cell viability under Citrus extract or hesperidin treatment was assessed by using the MTT assay. The expression of interleukin-10 (IL-10), an antiinflammatory cytokine, modulated by Citrus extract was also examined by immunostaining. Low concentrations of Citrus extract at 1 and 100μg/mL were able to induce cell proliferation, although in significant, as shown by cell viability of 138 and 114%, respectively. At higher concentrations of 500, 750, and 1000μg/mL, Citrus extract decreased cell viability significantly by up to 64, 46, and 36%, respectively. Accordingly, hesperidin at low (3.1μg/mL −61.1μg/mL) concentration increased cell viability significantly by up to 116-136% where as high (152.6203μg/mL-305.3203μg/mL) concentration reduced cell viability significantly by up to 10-61%. The value of the 50% inhibitory concentration (IC50) of Citrus extract was more than three times higher (756μg/mL) than that of hesperidin (203μg/mL = 332μM). Additionally, 250μg/mL of Citrus extract was able to induce IL-10 expression compared to control. These results demonstrated that Citrus extract and hesperidin exerted a biphasic effect on macrophage cells. The future development of Citrus extract as a co-chemotherapeutic, anticancer, or immunomodulatory agent should include careful consideration of its biphasic effect on each cell type.
Development of a chemotherapeutic agent and boron carrying pharmaceutical based on triple-negative breast cancer is important due to its metastatic progression. Metastases are often more dangerous than the primary tumor and they are responsible for 90% of all cancer deaths. The purpose of this study was to explore the anti-metastatic activities of the PGB-0 complex with fructose (PGB-0-F) against 4T1 breast cancer cells. A scratch wound healing assay was carried out to determine the migration inhibition ability of PGB-0-F, while MMP-9 expression was analysed using gelatin zymography. The testing of anti-migration activity showed that PGB-0-F inhibited in 4T1 cells, whereas the gelatin zymography assay revealed a suppression of MMP-9 expression. PGB-0-F inhibited closure on 4T1 metastatic breast cancer cells line compared with the control. PGB-0-F decreased the MMP-9 expression level compared with the control. Based on these results, PGB-0-F has the potential to be developed as a chemotherapeutic agent, and especially as an anti-metastatic agent.
BACKGROUND: Zingiber officinale Rosc. is estrogenic and thus can be developed as an anti-osteoporosis. Difructose anhydride III (DFA III), possesses anti-osteoporosis potencies. This study aimed to investigate the anti-osteoporosis activity of ginger rhizome water extract (GE) and DFA III from dahlia tubers in ovariectomized (OVX) rat models and to determine their anti-osteoclastogenic effect in vitro.METHODS: This study was conducted using 25 female rats. Blood sampling was carried out at the beginning and end of treatments. Femur bones were isolated after daily 14-day treatments, measured for density, and processed for histological staining. RAW 264.7 cells were induced by osteoclast differentiation factor. A cell viability assay was employed to determine the cytotoxicity of DFA III and GE. The inhibition of osteoclastogenesis was investigated by tartrate-resistant acid phosphatase staining.RESULTS: All groups showed no difference in body weight elevation and serum lipid profiles. The GE and DFA III caused no effect on bone density. However, the GE or DFA III groups showed higher osteoblast numbers compared with the control groups. A significantly less osteoclast was found in the GE+DFA III group. The GE and DFA III showed no toxicity on RAW 264.7 cells. GE showed strong inhibitory effects on the post stimulation osteoclastogenesis model. The combination of GE and DFA III was synergistic in reducing the osteoclastogenesis confluency in RAW 264.7 cells.CONCLUSION: The data support our hypothesis that GE and DFA III can decrease the risk of osteoporosis by osteoclastogenesis inhibition.KEYWORDS: Dahlia spp., estrogenic, ginger, osteoclast, osteoporosis, ovariectomy, RAW 264.7 cell
The incidence of Breast Cancer Metastasis (MBC) can be categorized in stage IV as well as being the leading cause of death in cases of breast cancer. MBC prognosis is known to be weak, frequent recurrent, and MBC patients have only a survival rate of about 5 years. One of the proteins that causes breast cancer metastasis is Human Epidermal Growth Factor 2 (HER2). Pentagamaboron-0 (PGB-0), a newly curcumin analogue performed cytotoxic effect on HER2-positive breast cancer cells but it is practically water-insoluble. The aims of this study are to determine anti-metastatic activity of a more soluble form of PGB-0 namely PGB-0 fructose complex (PGB-0-F) toward HER2 positive cancer (MCF-7/HER2) cells. PGB-0-F was obtained from Cancer Chemoprevention Research Centre Faculty of Pharmacy Universitas Gadjah Mada. Based on scratch wound healing assay result, PGB-0-F inhibited cell migration especially in combination with doxorubicin at the concentration 15 μM. Under gelatin zymography assay, PGB-0-F in combination with doxorubicin decreased Matrix Metalloproteinases 9 (MMP-9) expression compare to the doxorubicin. Hence, PGB-0-F has a potency to be developed as anti-metastatic agent on HER2 overexpression breast cancer.Keywords : HER2, MCF-7/HER2, PGB-0-F, Metastasis
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