Bio: Dr. Jianbin Zhang has been engaged in the research on the mechanism and preventive strategy of special environmental injury. As the first author or corresponding author, he has published more than 17 papers in SCI journals. He is the associate editor of 1 monograph, participated in editing 5 textbooks. He is in charge of more than ten projects including NSFC and military logistics scientific research projects. and obtained 10 national software copyright and invention patents. He had the Shaanxi Outstanding Youth Fund, the first prize of Shaanxi Provincial Teaching Achievement, the first prize of the third Undergraduate College Teaching Method Innovation Competition in Shaanxi Province, the New Star of Science and Technology in Shaanxi Province, and the excellent doctoral thesis in Shaanxi Province. He is currently a committee member of Chinese Society of Toxicology.

Abstract: Lead pollution poses a tremendous threat to the organism's health, with the nervous system being the most severely harmed organ by lead. Lead neurotoxicity is attributed in key part to microglia activation. An understanding of the mechanism underlying microglia activation provides valuable insights into lead neurotoxicity and its prevention. It is of significance to investigate the molecular mechanism using NLRP3 to explain lead-induced microglia activation, as evidenced by our finding that NLRP3 inflammasome activation plays a vital role in the activation. The intestinal flora resides in the intestines, and their diverse changes can affect the nervous system of the host. Microglia morphology and function can be regulated by the intestinal flora, which also act as a regulator outside of the brain for microglia. Our preliminary results indicate that lead exposure can alter the structural diversity of the intestinal flora in mice, and we therefore hypothesize that the intestinal flora may be involved in lead neurotoxicity. Based on the role of microglia activation and NLRP3 inflammasome activation in lead neurotoxicity, this project aims to elucidate the mechanism behind disordered expression of intestinal flora and its metabolite SCFAs in microglia activation and NLRP3 inflammasome activation. A theoretical foundation is then provided for understanding the role and implications of the gut-brain axis in lead neurotoxicity and suggesting targets for the prevention and treatment of lead neurotoxicity.