Chinese scholars have made important progress in the study of the mechanism of human inflammation
August 09, 2017 Source: Xinhua News Agency
Window._bd_share_config={ "common":{ "bdSnsKey":{ },"bdText":"","bdMini":"2","bdMiniList":false,"bdPic":"","bdStyle":" 0","bdSize":"16"},"share":{ }};with(document)0[(getElementsByTagName('head')[0]||body).appendChild(createElement('script')) .src='http://bdimg.share.baidu.com/static/api/js/share.js?v=89860593.js?cdnversion='+~(-new Date()/36e5)];Recently, the research group of Professor Zhou Rongbin and Professor Jiang Wei of the University of Science and Technology of China cooperated with the research group of Professor Wang Jun, the research group of Professor Bai Li and the research group of Professor Cui Wei of Sun Yat-sen University. The study revealed that the intracellular chloride channel protein CLIC family is small in NLRP3 inflammation. An important role in body activation. The internationally authoritative academic journal "Nature·Communication" recently published the results.
The inflammatory response is an important immune defense mechanism in the human body, which helps the body to resist infection by pathogenic microorganisms. However, dysregulation of the inflammatory reaction can also cause damage to tissues and organs, thereby promoting disease. Studies have shown that chronic inflammatory reactions are involved in almost all major human diseases, so understanding the process of inflammatory response may provide new strategies for disease treatment.
The NLRP3 inflammatory corpuscle is a multi-protein complex in the cell whose activation promotes the process of inflammatory response. In recent years, related research shows that its involvement in the development of many major human diseases such as type 2 diabetes, gout, Parkinson's, and fatty liver is a potential intervention target for these diseases.
The research team of Zhongke University and Sun Yat-sen University found that the induction of reactive oxygen species induced by mitochondrial damage in the CLIC protein family can migrate to the cell membrane and mediate the outflow of intracellular chloride ions, thereby further promoting the assembly of NLRP3 inflammatory bodies. Inhibition of the expression or activity of the CLIC family of proteins can significantly inhibit the activation of NLRP3 inflammatory bodies.
According to reports, the results not only help to understand the pathogenesis of type 2 diabetes, gout, Parkinson's disease, but also provide potential treatment. (Reporter Xu Haitao)
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