Cortex cinnamomi extract prevents streptozotocin- and cytokine-induced β-cell damage by inhibiting NF-κB  

作　　者：Kang-Beom Kwon Eun-Kyung Kim Eun-Sil Jeong Young-Hoon Lee Young-Rae Lee Jin-Woo Park Do-Gon Ryu Byung-Hyun Park 

机构地区：[1]Department of Physiology,School of Oriental Medicine,Wonkwang University,Iksan 570-749,South Korea [2]Department of Oral Anatomy,School of Dentistry,Chonbuk National University,Jeonju 561-756,Jeonbuk,South Korea [3]Department of Biochemistry,Medical School,Institute for Healthcare Technology Development,Medical Research Center,Chonbuk National University,Jeonju 561-756,Jeonbuk,South Korea

出　　处：《World Journal of Gastroenterology》2006年第27期4331-4337,共7页世界胃肠病学杂志（英文版）

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

摘　　要：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,AIM: To clarify the mechanism underlying the anti-diabetic 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) mRIMA and protein expression were determined by RT-PCR and Western blotting, respectively. The activation of NF-κB 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-1βand interferon-γ-mediated cytotoxicity. Moreover, RINm5F cells incubated with CCE showed significant reductions in interleukin-lp and interferon-γ-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-κB activation. These results reveal the possible therapeutic value of CCE for the prevention of diabetes mellitus progression.

关 键 词：Cortex cinnamomi Diabetes STREPTOZOTOCIN CYTOKINE NF-ΚΒ 

分 类 号：R285.5[医药卫生—中药学]