JNK/MAPK信号通路介导活化素B对皮肤创伤愈合的调控的开题报告【摘要】活性氧化素B（ROS-B）作为氧化应激信号分子参与皮肤创伤愈合过程，在愈合过程中扮演重要作用。本研究旨在探讨JNK/MAPK信号通路是否介导ROS-B对皮肤创伤愈合的调控。实验中采用大鼠实验模型，利用足底毛细血管裂伤模型建立皮肤创伤愈合模型。通过HE染色、Masson染色以及免疫组织化学染色法检测皮肤创伤愈合程度以及JNK/MAPK信号通路的表达变化。结果显示，在皮肤创伤愈合过程中，ROS-B的水平升高，并且JNK/MAPK信号通路被激活；通过应用ROS-B抑制剂和JNK/MAPK抑制剂，发现这两种药物可以抑制ROS-B及其下游JNK/MAPK的活化，同时减缓大鼠创伤愈合的速度。综上，JNK/MAPK信号通路介导ROS-B对皮肤创伤愈合的调控，为研究ROS-B参与皮肤创伤愈合机制提供了新的思路。【关键词】活性氧化素B；JNK/MAPK信号通路；皮肤创伤愈合；大鼠实验模型【Abstract】ReactiveoxygenspeciesB(ROS-B)playsanimportantroleintheprocessofskinwoundhealingbyactingasanoxidativestresssignalingmolecule.ThisstudyaimstoinvestigatewhethertheJNK/MAPKsignalingpathwaymediatestheregulationofROS-Bonskinwoundhealing.Intheexperiment,aratmodelwasused,andafootmicrovascularrupturemodelwasestablishedtoestablishaskinwoundhealingmodel.ThedegreeofskinwoundhealingandthechangesinJNK/MAPKsignalingpathwayexpressionweredetectedbyHEstaining,Massonstainingandimmunohistochemicalstaining.TheresultsshowedthatthelevelofROS-Bincreasedduringskinwoundhealing,andtheJNK/MAPKsignalingpathwaywasactivated.ByapplyingROS-BinhibitorsandJNK/MAPKinhibitors,itwasfoundthatbothdrugscouldinhibittheactivationofROS-BanditsdownstreamJNK/MAPK,andatthesametime,slowdowntherateofratwoundhealing.Therefore,theJNK/MAPKsignalingpathwaymediatestheregulationofROS-Bonskinwoundhealing,providingnewideasforstudyingthemechanismofROS-Binskinwoundhealing.【Keywords】ReactiveoxygenspeciesB;JNK/MAPKsignalingpathway;Skinwoundhealing;Ratmodel