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Catalyst Award: Assessing the Role of Natural Compounds on Mechanisms of Apoptosis in RT4-D2P6T cells

Catalyst Award: Assessing the Role of Natural Compounds on Mechanisms of Apoptosis in RT4-D2P6T cells
催化剂奖:评估天然化合物对 RT4-D2P6T 细胞凋亡机制的作用
批准号:
1901040
负责人:
Rosalyn Reid
金额:
$14.99万
依托单位:
依托单位国家:
美国
项目类别:
Standard Grant
财政年份:
2019
资助国家:
美国
项目状态:
已结题
起止时间:
2019-07-15 至 2024-07-31

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中文摘要
翻译
Catalyst项目为历史上的黑人学院和大学提供支持,以建立教师的研究能力,加强科学、技术、工程和数学本科教育和研究。预计该奖项将进一步提高教师的研究能力,提高学院的研究和教学水平,并让本科生参与研究经验。Johnson C. Smith大学的这个项目将探索天然化合物通过神经元细胞凋亡永久抑制或阻止细胞死亡进程的能力。该项目将增加代表性不足的学生对衰老生物学实践探究性研究的接触和参与,并为STEM的研究生和专业前课程做好准备。这个项目的目标是寻找影响分子开关的天然化合物,这些化合物可能会永久地减缓或阻止神经元细胞凋亡的进程。核心假设是黄酮类化合物可能抑制、阻断或阻止HT22神经元细胞凋亡的进展。细胞凋亡导致的细胞死亡导致分子的激活,如半胱天冬酶,这些分子已被证明可以诱导细胞凋亡。虽然研究表明黄酮类化合物能够抑制人类正常星形胶质细胞的凋亡,但很少有研究关注这方面的黄酮类化合物的生物活性或在此作用中影响的分子靶点。本项目是一项体外研究,主要目的是评估黄酮类化合物对神经元细胞凋亡的影响,这是一个与系统生物学、神经生物学和营养科学领域密切相关的问题。本研究将利用神经细胞系HT22,评估槲皮素和大杉酮对分子靶点(caspases 3,8,9; iROS; iNOS)基因和蛋白表达的影响,并测量抗氧化化合物对体外细胞凋亡率的影响。这项研究的发现将增加通过神经元细胞凋亡抑制细胞死亡的知识。该奖项反映了美国国家科学基金会的法定使命,并通过使用基金会的知识价值和更广泛的影响审查标准进行评估,被认为值得支持。
英文摘要
Catalyst Projects provide support for Historically Black Colleges and Universities to work towards establishing research capacity of faculty to strengthen science, technology, engineering and mathematics undergraduate education and research. It is expected that the award will further the faculty member's research capability, improve research and teaching at the institution, and involve undergraduate students in research experiences. This project at Johnson C. Smith University will explore the ability of natural compounds to permanently inhibit or prevent the progression of cell death via apoptosis in neuronal cells. The project will increase the exposure and engagement of underrepresented students in hands-on, inquiry-based research in the biology of aging and prepare them for graduate and pre-professional programs in STEM.This project forwards the trajectory to find natural compounds that impact molecular switches that may permanently slow or stop the progression of apoptosis in neuronal cells. The central hypothesis is that flavonoids may inhibit, block or prevent the progression of apoptosis in HT22 neuronal cells. Cell death via apoptosis leads to the activation of molecules such as caspases which have been shown to induce apoptosis. Although studies show that flavonoids are able to inhibit apoptosis in human normal astrocytes, few studies have focused on this aspect of flavonoid bioactivity or the molecular targets impacted in this role. This project is an in-vitro study with the primary goal of assessing the effects of flavonoids on neuronal cell death via apoptosis, an issue that is critically associated to the fields of systems biology, neurobiology, and nutrition science. The neuronal cell line HT22, will be used in this study for the purpose of assessing the impact of quercetin and macluraxanthone on gene and protein expression of molecular targets (caspases 3, 8, 9; iROS; iNOS) and to measure the impact of antioxidant compounds on the rate of cell death via apoptosis in vitro. The findings from this study will increase knowledge of inhibition of cell death via apoptosis in neuronal cells.This award reflects NSF's statutory mission and has been deemed worthy of support through evaluation using the Foundation's intellectual merit and broader impacts review criteria.
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