2024 9th International Conference on Public Health and Medical Sciences

Aug. 10-12, 2024 Chengdu, China
Keynote Speakers

The information about the Keynote Speakers of ICPHMS2024 is as follows, which will be updated regularly.

Dr. Jing Du, Professor

Dr. Jing Du, Professor

Beijing Anding Hospital, Capital Medical University, Beijing, China

Biography:  Dr. Jing Du is a professor in Beijing Anding Hospital affiliated to Capital Medical University in Beijing, China. In Beijing Anding Hospital, she is engaged in the research of cellular and molecular pathophysiology and neuropsychopharmacology of mental diseases such as depression, anxiety, autism and schizophrenia. She was formerly a staff scientist at the National Institute of Mental Health of the National Institutes of Health(NIH) in USA. She has won many awards, including the NIH Performance Award in Recognition and Appreciation of Special Achievement issued by the National Institutes of Health. She is a Full member of the American College of Neuropsychopharmacology (ACNP). She has published 64 SCI articles in the field of neuropsychopharmacology. Her H index is 35. She is recognized nationally and internationally for her research contributions and achievements in psychopharmacology.

Topic: Nuclear Receptors Modulate Inflammasomes in the Pathophysiology and Treatment of Major Depressive Disorder

Abstract: Major depressive disorder is a common, chronic and recurrent disease. Existing drugs are ineffective to one third of patients, so it is urgent to develop novel and rapid antidepressants. Accumulative evidence has shown that immune inflammation, particularly inflammasome activity, plays an important role in the pathophysiology of MDD. We summarize the evidence on nuclear receptors (NRs), such as glucocorticoid receptor, vitamin D receptor, estrogen receptor, aryl-hydrocarbon receptor, and peroxisome proliferator-activated receptor(PPARs), in modulating the inflammasome activity and depression-associated behaviors. Chronic Social Defeat Stress (CSDS) depressed mice reduced the expression level in prefrontal cortex (PFC) of farnesoid X receptor(FXR), which is a nuclear receptor activated by CDCA. We found that CDCA treatment restored the level of FXR in the CSDS mice, decreased the activity of the NLRP3 inflammasome and caspase-1 and subsequently showed antidepressant effects in the tests of sucrose preference, tail suspension, and forced swimming in CSDS mouse model of depression. Moreover, we also found that ganoderic acid A (GAA) modulated CDCA receptor FXR, inhibited brain inflammatory activity, and showed antidepressant effects in the chronic social defeat stress depression model, tail suspension, forced swimming, and sucrose preference tests. GAA directly inhibited the activity of the NLRP3 inflammasome, and activated the synaptic AMPA by regulating FXR in the PFC of mice. If we knocked out FXR or injected the FXR-specific inhibitor z-gugglesterone (GS), the antidepressant effects induced by GAA were completely abolished. Proteomic analysis identified distinct proteins in CSDS (305), GAA-treated (949), and IMI-treated (289) groups. Enrichment in mitochondrial and synaptic proteins was evident from GO and PPI analyses. PRM analysis revealed significant expression changes in proteins crucial for mitochondrial and synaptic functions (namely, Naa30, Bnip1, Tubgcp4, Atxn3, Carmil1, Nup37, Apoh, Mrpl42, Tprkb, Acbd5, Dcx, Erbb4, Ppp1r2, Fam3c, Rnf112, and Cep41). Western blot validation in the prefrontal cortex showed increased levels of Mrpl42, Dcx, Fam3c, Ppp1r2, Rnf112, and Naa30 following GAA treatment. In another independent study, we found that oridonin significantly enhanced the expression of nuclear receptor PPAR-γ, GluA1 (Ser845) phosphorylation, GluA1 in the total protein extract of the prefrontal cortex (PFC), and showed antidepressant efficacy. Blocking nuclear receptor PPAR-γ was able to block antidepressant effects of oridonin. These studies demonstrate that nuclear receptor signaling regulates neuroimmune and antidepressant behaviors and is potential targets for the treatment of MDD.

Dr. Jinhui Wang, Associate Professor

Dr. Jinhui Wang, Associate Professor

Institute of Drug Discovery Technology, Ningbo University, Ningbo, China

Biography:  Dr. Jinhui Wang is now an associate professor at Ningbo University. In 2014, he was assigned to the University of Toulouse III, France, to pursue a doctorate in metal-organic chemistry and coordination chemistry, under the guidance of Professor Eric Benoist, dedicated to the application of metal-organic complexes in biological imaging research; In 2018, he was introduced to Ningbo University as an outstanding doctor and served as an assistant researcher. His research focuses on Cancer Imaging, Polymer Characterization, Polymerization Nano Drug Delivery and Nanotechnology for Drug Delivery.

Topic: Engineering of Phosphatidylserine-targeting ROS-responsive Polymeric Prodrug for the Repair of Ischemia-reperfusion-induced Acute Kidney Injury

Abstract: Ischemia-reperfusion-induced acute kidney injury (IR-AKI) commonly occurs in situations such as hemorrhagic shock, kidney transplantation, and cardiovascular surgery. In this study, we developed an ROS-responsive polymeric prodrugs (Zn-D/DTH) which could target the externalized PS of apoptotic cells, and then responsively released HDM (anti-inflammatory peptides) in the presence of intracellular ROS. Zn-D/DTH effectively ameliorated renal function and mitigated pathological alterations such as the loss of the brush border, tubular dilation, and accumulation of cellular debris within the tubular lumens. Furthermore, Zn-D/DTH greatly reduced the generation of pro-inflammatory factors like IL-6, COX-2, and iNOS in renal tissues, suggesting its protective role largely stems from suppression of the inflammatory response. Additional mechanism exploration revealed that Zn-D/DTH markedly decreased the expression levels of TLR4 and MyD88, as well as the phosphorylation of NF-κB in the damaged kidneys. This, in turn, reduced the number of apoptotic tubular cells and the activity of Caspase 9 and Caspase 3 caused by ischemia-reperfusion. Additionally, Zn-D/DTH treatment showed improvement in the long-term renal damage and fibrosis induced by ischemia-reperfusion. The experimental outcomes indicated that Zn-D/DTH attenuated renal ischemia-reperfusion injury and delayed the transition from acute kidney injury to chronic kidney disease by downregulating the TLR4/MyD88/NF-κB signaling pathway and reducing the expression of apoptotic caspases, thereby inhibiting inflammation and reducing cell apoptosis.

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