Type 1 diabetes mellitus(T1DM)is associated with an increased risk of diabetic cardiomyopathy(DCM).Nuclear factor kappa B(NF-kB)and Wnt/β-catenin/GSK3p have been demonstrated to play pathogenic roles in diabetes.In t...Type 1 diabetes mellitus(T1DM)is associated with an increased risk of diabetic cardiomyopathy(DCM).Nuclear factor kappa B(NF-kB)and Wnt/β-catenin/GSK3p have been demonstrated to play pathogenic roles in diabetes.In this study,we evaluated the roles of these two pathways in T1 DM-induced cardiomyopathy in rats.Streptozotocin(STZ)-induced type 1 diabetic rats were treated with pyrrolidine dithiocarbamate(PDTC)or meisoindigo(Me)to inhibit NF-kB and Wnt/β-catenin/GSK3P respectively for 4 or 8 weeks.As compared with untreated diabetic rats,treatment with either PDTC or Me partly attenuated the myocardial hypertrophy and interstitial fibrosis,improved cardiac function,and exhibited reduction in inflammatory reaction.In addition,we found that inhibiting NF-κB and Wnt/β-catenin/GSK3β pathways could regulate glucose and lipid metabolism.The effects were associated with the decrease of NF-κB activity and the downregulation of some proinflammatory cytokines,including tumor necrosis factor-alpha(TNF-α)and interleukin(IL)-2.Our data suggested that the activities of NF-κB and Wnt/β-catenin/GSK3β pathways were both increased and inhibiting NF-κB and Wnt/β-catenin/GSK3β signaling pathways might improve myocardial injury in T1DM rats.展开更多
Objective： To investigate the protective effects of icaritin （ICT）, one of the active ingredients in Epimedii Folium, on mouse model of cerebral ischemia-reperfusion （I/R） in vivo. Methods： ICR mice were subject...Objective： To investigate the protective effects of icaritin （ICT）, one of the active ingredients in Epimedii Folium, on mouse model of cerebral ischemia-reperfusion （I/R） in vivo. Methods： ICR mice were subjected to an I h transient middle cerebral artery occlusion （MCAO） and fol- lowed by 24 h of reperfusion. Neurological deficits, infarct volume, brain edema and survive rate were measured, respectively. The levels of brain IL-1β, TNF-a, ROS and DNA-binding activity of NF-KB p65 were measured by ELISA kits. The levels of malondialdehyde （MDA） and activities of superoxide dismu- tase （SOD） were detected by spectrophotometry, and the release of nitric oxide （NO） were detected by Griess kit. Results： ICT markedly reduced the neurological deficit scores, brain edema, infarct volume and increased the survival rate of the cerebral I/R mice. The expression of IL-Iβ, TNF-α, NO, MDA and DNA-binding activity of NF-KB p65 were significantly inhibited by ICT, while the activity of SOD were up-regulated at the same time. Conclusion： ICT possessed significant neuroprotective effects in cerebral I/R mice, which might be related to prevent neuroinflammatory and oxidative damage.展开更多
基金the Research Award Fund for Outstanding Young Scientists Plan in Shandong Province of China(No.BS2013SW008)the Innovation Project of Shandong Academy of Medical Sciences.
文摘Type 1 diabetes mellitus(T1DM)is associated with an increased risk of diabetic cardiomyopathy(DCM).Nuclear factor kappa B(NF-kB)and Wnt/β-catenin/GSK3p have been demonstrated to play pathogenic roles in diabetes.In this study,we evaluated the roles of these two pathways in T1 DM-induced cardiomyopathy in rats.Streptozotocin(STZ)-induced type 1 diabetic rats were treated with pyrrolidine dithiocarbamate(PDTC)or meisoindigo(Me)to inhibit NF-kB and Wnt/β-catenin/GSK3P respectively for 4 or 8 weeks.As compared with untreated diabetic rats,treatment with either PDTC or Me partly attenuated the myocardial hypertrophy and interstitial fibrosis,improved cardiac function,and exhibited reduction in inflammatory reaction.In addition,we found that inhibiting NF-κB and Wnt/β-catenin/GSK3β pathways could regulate glucose and lipid metabolism.The effects were associated with the decrease of NF-κB activity and the downregulation of some proinflammatory cytokines,including tumor necrosis factor-alpha(TNF-α)and interleukin(IL)-2.Our data suggested that the activities of NF-κB and Wnt/β-catenin/GSK3β pathways were both increased and inhibiting NF-κB and Wnt/β-catenin/GSK3β signaling pathways might improve myocardial injury in T1DM rats.
基金financially supported by the Natural Foundation of Shandong Province (ZR2015QL002)
文摘Objective： To investigate the protective effects of icaritin （ICT）, one of the active ingredients in Epimedii Folium, on mouse model of cerebral ischemia-reperfusion （I/R） in vivo. Methods： ICR mice were subjected to an I h transient middle cerebral artery occlusion （MCAO） and fol- lowed by 24 h of reperfusion. Neurological deficits, infarct volume, brain edema and survive rate were measured, respectively. The levels of brain IL-1β, TNF-a, ROS and DNA-binding activity of NF-KB p65 were measured by ELISA kits. The levels of malondialdehyde （MDA） and activities of superoxide dismu- tase （SOD） were detected by spectrophotometry, and the release of nitric oxide （NO） were detected by Griess kit. Results： ICT markedly reduced the neurological deficit scores, brain edema, infarct volume and increased the survival rate of the cerebral I/R mice. The expression of IL-Iβ, TNF-α, NO, MDA and DNA-binding activity of NF-KB p65 were significantly inhibited by ICT, while the activity of SOD were up-regulated at the same time. Conclusion： ICT possessed significant neuroprotective effects in cerebral I/R mice, which might be related to prevent neuroinflammatory and oxidative damage.
