AIM： To clarify the mechanism underlying the antidiabetic activities of cortex cinnamomi extract （CCE）. METHODS： To induce in vivo diabetes, mice were injected with streptozotocin （STZ） via a tail vein （100 mg ...AIM： To clarify the mechanism underlying the antidiabetic activities of cortex cinnamomi extract （CCE）. METHODS： To induce in vivo diabetes, mice were injected with streptozotocin （STZ） via a tail vein （100 mg STZ/kg body weight）. To determine the effects of CCE, mice were administered CCE twice daily for 7 d by oral gavage starting 1 wk before the STZ injection. Blood glucose and plasma insulin concentration were measured as an index of diabetes. Also, to induce cytotoxicity of RINm5F cells, we treated with cytokines （IL-1β （2.0 ng/mL） and IFN-γ （100 U/mL））. Cell viability and nitric oxide production were measured colorimetrically. Inducible nitric oxide synthase （iNOS） mRNA and protein expression were determined by RT-PCR and Western blotting, respectively. The activation of NF-κβ was assayed by using gel mobility shift assays of nuclear extracts. RESULTS： Treatment of mice with STZ resulted in hyperglycemia and hypoinsulinemia, which was further evidenced by immunohistochemical staining of islets. However, the diabetogenic effects of STZ were completely prevented when mice were pretreated with CCE. The inhibitory effect of CCE on STZ-induced hyperglycemia was mediated through the suppression of iNOS expression. In rat insulinoma RINm5F cells,CCE completely protected against interleukin-1β and interferon-y-mediated cytotoxicity. Moreover, RINm5F cells incubated with CCE showed significant reductions in interleukin-1β and interferon-y-induced nitric oxide production and in iNOS mRNA and protein expression, and these findings correlated well with in vivo observations. CONCLUSION： The molecular mechanism by which CCE inhibits iNOS gene expression appears to involve the inhibition of NF-κβ activation, These results reveal the possible therapeutic value of CCE for the prevention of diabetes mellitus progression,展开更多
Objective： To examinie the synergistic effects of Banxia Xiexin Decoction （半夏泻心汤, Known as Banhasasim-tang in Korean） extract （BXDE） on cisplatin-induced cytotoxicity in the A549 human lung cancer ceil lines...Objective： To examinie the synergistic effects of Banxia Xiexin Decoction （半夏泻心汤, Known as Banhasasim-tang in Korean） extract （BXDE） on cisplatin-induced cytotoxicity in the A549 human lung cancer ceil lines. Methods： A549 cells were treated with varying concentrations （50-200μg/mL） of cisplatin and BXDE alone or in combination for 96 h. We used 1-（4,5-dimethylthiazol-2-yl）-3,5-diphenylformazan assay and flow cytometry to analyze cell viability and apoptosis, respectively. Results： The exposure of cells to cispiatin and BXDE alone or in combination decreased ceil viability dose- and time-dependently （P〈0.05）, which was found to be mediated by the apoptotic pathway as confirmed by the increase in the annexin V^＋/propidium iodide stained cell population and a ladder pattern of discontinuous DNA fragments. Furthermore, the apoptosis was inhibited by the pan-caspase inhibitor, benzyloxycarbonyI-Val-Ala-Asp （OMe） fluoromethylketone （z-VAD-FMK）. Conclusions： BXDE significantly potentiated apoptotic effects of cisplatin in A549 cells. Moreover, apoptosis induced by BXDE might be the pivotal mechanism mediating its chemopreventative action against cancer.展开更多
基金Supported by the Regional Research Center Program of the Korean Ministry of Education & Human Resources Development through the Center for Healthcare Technology Development
文摘AIM： To clarify the mechanism underlying the antidiabetic activities of cortex cinnamomi extract （CCE）. METHODS： To induce in vivo diabetes, mice were injected with streptozotocin （STZ） via a tail vein （100 mg STZ/kg body weight）. To determine the effects of CCE, mice were administered CCE twice daily for 7 d by oral gavage starting 1 wk before the STZ injection. Blood glucose and plasma insulin concentration were measured as an index of diabetes. Also, to induce cytotoxicity of RINm5F cells, we treated with cytokines （IL-1β （2.0 ng/mL） and IFN-γ （100 U/mL））. Cell viability and nitric oxide production were measured colorimetrically. Inducible nitric oxide synthase （iNOS） mRNA and protein expression were determined by RT-PCR and Western blotting, respectively. The activation of NF-κβ was assayed by using gel mobility shift assays of nuclear extracts. RESULTS： Treatment of mice with STZ resulted in hyperglycemia and hypoinsulinemia, which was further evidenced by immunohistochemical staining of islets. However, the diabetogenic effects of STZ were completely prevented when mice were pretreated with CCE. The inhibitory effect of CCE on STZ-induced hyperglycemia was mediated through the suppression of iNOS expression. In rat insulinoma RINm5F cells,CCE completely protected against interleukin-1β and interferon-y-mediated cytotoxicity. Moreover, RINm5F cells incubated with CCE showed significant reductions in interleukin-1β and interferon-y-induced nitric oxide production and in iNOS mRNA and protein expression, and these findings correlated well with in vivo observations. CONCLUSION： The molecular mechanism by which CCE inhibits iNOS gene expression appears to involve the inhibition of NF-κβ activation, These results reveal the possible therapeutic value of CCE for the prevention of diabetes mellitus progression,
基金Supported by a Grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute(KHIDI)funded by the Ministry of Health&Welfare,Republic of Korea(No.HI14C0750)
文摘Objective： To examinie the synergistic effects of Banxia Xiexin Decoction （半夏泻心汤, Known as Banhasasim-tang in Korean） extract （BXDE） on cisplatin-induced cytotoxicity in the A549 human lung cancer ceil lines. Methods： A549 cells were treated with varying concentrations （50-200μg/mL） of cisplatin and BXDE alone or in combination for 96 h. We used 1-（4,5-dimethylthiazol-2-yl）-3,5-diphenylformazan assay and flow cytometry to analyze cell viability and apoptosis, respectively. Results： The exposure of cells to cispiatin and BXDE alone or in combination decreased ceil viability dose- and time-dependently （P〈0.05）, which was found to be mediated by the apoptotic pathway as confirmed by the increase in the annexin V^＋/propidium iodide stained cell population and a ladder pattern of discontinuous DNA fragments. Furthermore, the apoptosis was inhibited by the pan-caspase inhibitor, benzyloxycarbonyI-Val-Ala-Asp （OMe） fluoromethylketone （z-VAD-FMK）. Conclusions： BXDE significantly potentiated apoptotic effects of cisplatin in A549 cells. Moreover, apoptosis induced by BXDE might be the pivotal mechanism mediating its chemopreventative action against cancer.
