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
Deep vein thrombosis (DVT) remains a significant clinical challenge, with complex underlying pathophysiological mechanisms. Among the myriad factors contributing to DVT, the transcription factors NF-κβ and HIF-1α h...Deep vein thrombosis (DVT) remains a significant clinical challenge, with complex underlying pathophysiological mechanisms. Among the myriad factors contributing to DVT, the transcription factors NF-κβ and HIF-1α have been increasingly recognized for their roles. This study aims to deepen the understanding of NF-κβ and HIF-1α in the pathogenesis of DVT and explore potential therapeutic implications. This research investigates the expression of NF-κβ and HIF-1α in patients with DVT compared to a healthy control group, utilizing ELISA techniques for quantification. The results of the study showed that the expression of NF-κβ and HIF-1α in the blood samples of patients with DVT was significantly higher than that of normal subjects, and the difference was statistically significant (P κβ and HIF-1α in the peripheral blood of DVT patients, suggesting their critical roles in inflammation and hypoxia regulation, with potential for future research into their mechanisms and therapeutic applications.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,
文摘Deep vein thrombosis (DVT) remains a significant clinical challenge, with complex underlying pathophysiological mechanisms. Among the myriad factors contributing to DVT, the transcription factors NF-κβ and HIF-1α have been increasingly recognized for their roles. This study aims to deepen the understanding of NF-κβ and HIF-1α in the pathogenesis of DVT and explore potential therapeutic implications. This research investigates the expression of NF-κβ and HIF-1α in patients with DVT compared to a healthy control group, utilizing ELISA techniques for quantification. The results of the study showed that the expression of NF-κβ and HIF-1α in the blood samples of patients with DVT was significantly higher than that of normal subjects, and the difference was statistically significant (P κβ and HIF-1α in the peripheral blood of DVT patients, suggesting their critical roles in inflammation and hypoxia regulation, with potential for future research into their mechanisms and therapeutic applications.
