ABSTRACT
Desmoglein,which is a kind of Ca2+ dependent desmosomal cadherins protein,is a major part of the desmosomes.The desmoglein that distributes in the epithelium,myocardium and other tissues plays a very important role in the cell junction.In recent years,the detection of the abnormal expression and function of the desmoglein was proved in many diseases,such as skin,mucous membrane and tumor related diseases.Drugs may have an important effect in the treatment of diseases by interfering with the expression and function of desmoglein.In this paper,the distribution of several subtypes of the family of desmosomes and their functions in the related diseases are reviewed,which may also provide some new clues for the new drug research on the target of desmogleins.
ABSTRACT
Objective To investigate the protective effects of Kudiezi (KDZ) Injection on cerebral ischemia reperfusion injury in rats and to explore its protective mechanism.Methods The rat model of middle cerebral artery occlusion (MCAO) was established by modified suture method,and cerebral blood flow was monitored using laser Doppler flowmetry (LDF).Male SD rats were randomly divided into control group,model group,Kudiezi Injection high and low dose groups.After ischemia-reperfusion for 24 h,the neurological scores were evaluated.After anesthesia,the blood samples and brain tissues were collected,and the expression of inflammatory was detected by Elisa.Western blotting was used to detect the expression of TLR-4 and NF-κB protein.Results Behavioral scores showed that neural function defect was serious in model group compared with control group (P ＜ 0.01).In model group,cerebral index and cerebral infarction area were significantly higher than those of the control group;After KDZ intervention,the symptoms of neurological deficit was alleviated (P ＜ 0.01),the cerebral index and cerebral infarction area of mode were decreased,and the neuronal necrosis was reduced.Kudiezi Injection could significantly reduce the cerebral homogenate and serum levels of TNF-α (P ＜ 0.05) and increase IL-10 level (P ＜ 0.05).Westem blotting showed that Kudiezi Injection could reduce the expression of TLR-4 and NF-κB protein (P＜0.05).Conclusion Kudiezi Injection has protective effect on cerebral ischemia reperfusion rats.After ischemia-reperfusion,Kudiezi Injection could reduce the levels of TNF-α and raise IL-10.Its mechanism may be associated to the down-regulation of TLR-4/NF-κB signaling pathway.
ABSTRACT
Objective To investigate the protective effects of Kudiezi (KDZ) Injection on cerebral ischemia reperfusion injury in rats and to explore its protective mechanism.Methods The rat model of middle cerebral artery occlusion (MCAO) was established by modified suture method,and cerebral blood flow was monitored using laser Doppler flowmetry (LDF).Male SD rats were randomly divided into control group,model group,Kudiezi Injection high and low dose groups.After ischemia-reperfusion for 24 h,the neurological scores were evaluated.After anesthesia,the blood samples and brain tissues were collected,and the expression of inflammatory was detected by Elisa.Western blotting was used to detect the expression of TLR-4 and NF-κB protein.Results Behavioral scores showed that neural function defect was serious in model group compared with control group (P ＜ 0.01).In model group,cerebral index and cerebral infarction area were significantly higher than those of the control group;After KDZ intervention,the symptoms of neurological deficit was alleviated (P ＜ 0.01),the cerebral index and cerebral infarction area of mode were decreased,and the neuronal necrosis was reduced.Kudiezi Injection could significantly reduce the cerebral homogenate and serum levels of TNF-α (P ＜ 0.05) and increase IL-10 level (P ＜ 0.05).Westem blotting showed that Kudiezi Injection could reduce the expression of TLR-4 and NF-κB protein (P＜0.05).Conclusion Kudiezi Injection has protective effect on cerebral ischemia reperfusion rats.After ischemia-reperfusion,Kudiezi Injection could reduce the levels of TNF-α and raise IL-10.Its mechanism may be associated to the down-regulation of TLR-4/NF-κB signaling pathway.