| Summary: | 碩士 === 國立中興大學 === 獸醫學系暨研究所 === 100 === Normal islet beta-cell has insufficient antioxidative function; therefore raised intracellular reactive oxygen species (ROS) level will make beta-cell dysfunction and/or apoptosis in chronic hyperglycemia. In our previous study, we found cytopiloyne (CP), a polyacetylenic glucoside from Bidens pilosa (BP), has the ability to reduce high glucose-induced 30-33% ROS expression and 86-95% apoptosis in beta-cell lines. Moreover, CP can also slow down mice diabetic process, including decreased immunocytes infusion, beta cell death and increased insulin secretion in both NOD and db/db mice (type 1 and 2 diabetes animal model). We screened out a CP receptor (CPR) target gene and established CPR knockout mice (CPR-/- mice) to study CP anti-diabetic mechanism. Furthermore, we used streptozotocin (STZ) to study oxidative stress-induced diabetes on CPR-/- mice. The mechanisms of STZ includes DNA alkylation and generating of ROS on beta-cell. We have been observed STZ-treated CPR-/- mice have significantly lower plasma glucose, higher serum insulin, better shape islet area and weaker beta-cell ROS level compared with wide type mice (WT mice). The results indicated that CPR may be involved in ROS synthesis in beta-cell to attenuate STZ-induced diabetes. And we deliberated that CP may inhibit CPR activity and / or expression to slow down NOD and db/db mice diabetes. In the future, the technologies of translation medicine study could help us to establish diabetic laboratory animal model and develop novel structure / function of the anti-diabetic drugs.
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