PowerPoint Presentation

[Audio] Multiple sclerosis is an autoimmune disorder that affects the central nervous system, characterized by inflammation and destruction of the fatty substance that insulates neurons. It can cause a wide range of symptoms depending on the area of the brain and spinal cord affected. Its pathological characteristics include infiltration of T cells and macrophages into the white matter, leading to localized demyelinating lesions. This is an unpredictable and debilitating disease that can cause physical, psychological, and cognitive disabilities..

[Audio] The incidence of multiple sclerosis is on the rise in the Asia Pacific region. According to Li et al. in 2022, 2.9 million people are affected worldwide, with China showing an incidence rate of 0.055 in children and 0.288 in adults per 100000. This alarming increase in MS cases is not only concerning, but it also poses an immense economic burden. The health, mobility, medical and unemployment costs associated with MS are reducing the quality of life of many affected individuals..

[Audio] MS (Multiple Sclerosis) is an autoimmune disease that impacts the central nervous system. The body's immune system mistakenly attacks the myelin sheath, the protective layer surrounding nerve cells, causing inflammation and destruction of the myelin sheath. This leads to disruption of nerve cells' ability to transmit electrical signals to the body, resulting in physical and cognitive difficulties. A key element contributing to MS is the CD4+ T lymphocyte, a type of T cell, which enters the central nervous system from the periphery and promotes myelin destruction as it triggers various levels of inflammation. These inflammatory reactions obstruct the transmission of nerve signals, potentially impacting cognitive function..

[Audio] MS, an autoimmune disease of the central nervous system, is characterized by localized inflammation and demyelination of white matter. Treatment typically focuses on either neuroprotection or the suppression of inflammation. The FDA has approved several drugs to treat MS, including Natalizumab, Fentanyl fingolimod, and IFN-β; however, these options can be costly and have potential side effects and toxicity. It is important to collaborate with medical professionals to develop an appropriate treatment plan for each patient..

[Audio] Multiple sclerosis is a serious autoimmune disease of the central nervous system which manifests in inflammation and demyelination of the white matter. This affects the movement and communication of information between the brain and other parts of the body. Traditional Chinese medicines have been considered for their role in managing the disease due to their abundant resources, low side effects and economical cost. Tripterygium glycosides, matrine and sinomenine as well as other active ingredients of traditional Chinese medicines have been researched for their effectiveness in treating MS..

[Audio] Geniposide, an iridoid glycoside extracted from Gardenia jasminoides fruit, has promising potential in the field of therapeutics. It has been found to not only inhibit the production of inflammation-related enzymes and inflammatory factors, but also exert neuroprotective effects in brain disease models and affect the proliferation and differentiation of CD4+ T cells. Our group has discovered that geniposide can reduce the risk of Alzheimer's disease by blocking the interaction between amyloid beta and the receptor for advanced glycation end products. This has been demonstrated to activate microglia and stimulate an inflammatory response in mice with AD disease model, ultimately improving cognitive function in mice..

[Audio] We will now discuss Multiple Sclerosis as an autoimmune disease of the central nervous system. RAGE expression plays a key role in this disease, and is related to a mixture of different ligands, small molecule inhibitors and genes. Interaction of these molecules and genes can cause inflammation, angiogenesis and oxidative stress, all of which contribute to the disease. Investigating these components further is essential for gaining a deeper understanding of the development and progression of Multiple Sclerosis..

[Audio] Multiple sclerosis is an autoimmune disorder affecting the central nervous system. It is caused by inflammation and destruction of the myelin sheath of nerve fibers. Studies have demonstrated that several ligands, such as RAGE, Aβ, HMGB1, and S100, are linked to various immune-associated conditions, including hypertension, diabetes, renal disease, atherosclerosis, tumor proliferation, cognitive dysfunction, and Alzheimer’s disease..

[Audio] RAGE, the receptor for Advanced Glycation End Products, has an important role in immune diseases such as Multiple Sclerosis, as it affects the proliferation, differentiation, and migration of naive CD4+T cells. It is known that RAGE ligands, like S100b and HMGB1, interact with AGEs to evoke an inflammatory response in the central nervous system. This contributes to comprehending further the part of RAGE in MS and how it is linked with the pathology of the illness..

[Audio] Multiple sclerosis is an autoimmune disease that impacts the central nervous system. Characterized by localized inflammation and demyelination of white matter, much research has been conducted to understand the molecular pathways involved. Two of these pathways are the S100B protein and RAGE, the receptor for advanced glycation end products. Both have been connected to multiple sclerosis and are thought to play a significant role in the cognitive changes linked to the condition. The objective is to uncover compounds to promote neuroprotection, with the hope of diminishing inflammation and cognitive issues associated with the illness..

[Audio] Though our knowledge of the RAGE pathway's role in the development of multiple sclerosis is still incomplete, studies suggest that the levels of S100b in the serum of MS patients is higher. Additionally, the effects of S100b on the naive CD4+ T cells related to multiple sclerosis have yet to be investigated. Despite our current understanding being limited on the role S100b could have in treating multiple sclerosis, further exploration of the matter is worthwhile..

[Audio] Our objective for this particular slide is to examine the impact of Geniposide on an EAE mouse model and its molecular mechanism of effect in EAE. We aim to explore the role of S100b-RAGE pathway on the proliferation, migration and differentiation of CD4+ T cells. This research aims to investigate the potential of Geniposide as a therapeutic agent for multiple sclerosis..

[Audio] The recent discovery of geniposide as a potential treatment for Multiple Sclerosis is a significant milestone, providing a theoretical foundation for the further development of drugs that can treat this inflammatory and demyelinating disease. Additionally, this research is innovating our understanding of the RAGE mechanism in MS, potentially leading to the development of new treatment strategies..

[Audio] Our research focuses on the potential treatment of multiple sclerosis through the S100B-RAGE pathway utilizing geniposide intervention. Multiple sclerosis is an autoimmune disease of the central nervous system, characterized by localized inflammation and demyelination of white matter. To this end, we have built an EAE mouse model using CD4+ T cells from various sources injected into C57BL/6 mice that are CD4Cre RAGE-/-. Through this model, we have observed and rated the clinical symptoms that occur as well as examined the pathological scoring features. We have also explored geniposide's mechanism on the S100B-RAGE pathway mediated responses to monitor the neuroinflammation and understand the effect of geniposide on the EAE mouse model..

[Audio] Multiple sclerosis is an autoimmune disease that has a debilitating impact on the central nervous system. It is identified by inflammation and destruction of myelin, the insulation that covers nerve cells. In this presentation, we will examine a mouse model of multiple sclerosis that was induced by a polypeptide and the protective effect of geniposide, a compound. Figure 1 displays a comparison between mice that were inflicted with the disorder, and mice that were not. The graph also shows the contrast in the body weights of the mice, along with neurological function scores. Remarkably, the mice that were given the geniposide showed greater protection. This study could be an advancement in finding treatments for multiple sclerosis..

[Audio] An experiment examining the effects of the autoimmune disease Multiple Sclerosis was conducted on mice. The graph displayed illustrates the results of the experiment, demonstrating that mice with injections of Geniposide experienced a considerable decrease in the occurrence of Multiple Sclerosis compared to the uninduced and EAE+DD water groups. The data provide a strong indication of the success of Geniposide as a potential remedy for Multiple Sclerosis..

[Audio] Spleen samples from mice with multiple sclerosis displayed interesting changes in the ratios of certain cell subpopulations, as observed in Figure 4. Examining the CD4+ T cell population, the samples showed significant changes in the proportions of CD44+ IFN-γ+ T cells, CD44+ IL-17+ T cells, CD44+ GM-CSF+ T cells and CD25+ Foxp3+ T cells compared to the non-induced and EAE+DD water groups. These changes offer a better understanding of the immune mechanisms of multiple sclerosis..

[Audio] Multiple sclerosis is an autoimmune disease caused by localized inflammation and demyelination of white matter in the central nervous system. This slide focuses on the protein S100b and how it promotes differentiation of naive CD4+ T cells into Th17 cell subsets. Results from testing concentrations ranging from 0 to 1000 nM show a statistically significant increase in the number of CD4+IL-17+ T cells, suggesting that S100b plays an important role in the differentiation of white matter and inflammatory response related to multiple sclerosis..

[Audio] Multiple Sclerosis is an autoimmune disease of the central nervous system which is characterized by localized inflammation and demyelination of white matter. Our team has set an experimental schedule to analyze the possible effects of geniposide on the disease's progression. We will be undertaking both in vivo and in vitro experiments over the next two years to explore the effects of geniposide on the S100b-RAGE pathway. Specifically, we will be studying the drug's ability to modify CD4+ T cell differentiation pathways and its potential to inhibit inflammation and microglial activation. Our research will allow us to evaluate the immunomodulatory properties of geniposide and its consequences on Multiple Sclerosis with the hope of eventually publishing our results..

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