지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
초록· 키워드
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Objective: Production of ROS from glucose toxicity results in injury of pancreatic β-cells in diabetes models. This study was undertaken to examine the influence of Lespedeza Cuneata extract (LCE) on cytoprotective effects on glucose toxicity, insulin secretion and gene expression in RIN-m5F cells.
Methods: First, we measured LCE’s antioxidant activity by DPPH free radical-scavenging activity and SOD activity. After the various concentrations of LCE were added to the RIN-m5F cells, we measured cell viability with glucose stimulation by MTT assay and glucose-stimulated insulin secretion. We analyzed gene expression with Agilent whole mouse genome 44K oligo DNA microarray and searched for related pathways in KEGG (Kyoto Encyclopedia of Genes and Genomes). Lastly we measured INS-1, INS-2, INS-R, IRS-1, IRS-2, IRS-3, GLP-1R, and GLP-2R mRNA expression by real time RT-PCR.
Results: Free radical-scavenging activity, SOD activity and insulin secretion increased dependent on LCE concentration, but LCE did not show considerable cytoprotective effect on RIN-m5F cells. More than twice expressed gene was 6362 in Oligo DNA chip. In KEGG, the most related pathway was the metabolic pathway. In the insulin signaling pathway, up expressed genes were Irs1, Mapk8, Akt1, and Lipe and down expressed genes were Rhoq, Fbp2, Prkar2b, Gck, and Prkag1. In real time RT-PCR, IRS-2, and IRS-3 expression increased significantly compared to the control group on LCE 12㎍/㎖ concentration and GCK expression decreased significantly compared to the control group.
Conclusions: These results show that LCE encourages insulin secretion and insulin metabolism by complicated gene mechanisms. Further mechanism study and clinical study seem to be necessary about Lespedeza Cuneata.
Methods: First, we measured LCE’s antioxidant activity by DPPH free radical-scavenging activity and SOD activity. After the various concentrations of LCE were added to the RIN-m5F cells, we measured cell viability with glucose stimulation by MTT assay and glucose-stimulated insulin secretion. We analyzed gene expression with Agilent whole mouse genome 44K oligo DNA microarray and searched for related pathways in KEGG (Kyoto Encyclopedia of Genes and Genomes). Lastly we measured INS-1, INS-2, INS-R, IRS-1, IRS-2, IRS-3, GLP-1R, and GLP-2R mRNA expression by real time RT-PCR.
Results: Free radical-scavenging activity, SOD activity and insulin secretion increased dependent on LCE concentration, but LCE did not show considerable cytoprotective effect on RIN-m5F cells. More than twice expressed gene was 6362 in Oligo DNA chip. In KEGG, the most related pathway was the metabolic pathway. In the insulin signaling pathway, up expressed genes were Irs1, Mapk8, Akt1, and Lipe and down expressed genes were Rhoq, Fbp2, Prkar2b, Gck, and Prkag1. In real time RT-PCR, IRS-2, and IRS-3 expression increased significantly compared to the control group on LCE 12㎍/㎖ concentration and GCK expression decreased significantly compared to the control group.
Conclusions: These results show that LCE encourages insulin secretion and insulin metabolism by complicated gene mechanisms. Further mechanism study and clinical study seem to be necessary about Lespedeza Cuneata.
목차
서론
실험
결과
고찰
결론
참고문헌
참고문헌 (35)
참고문헌 신청
1. [학술지(정기간행물)] - Robertson RP / 2004 / Chronic oxidative stress as a central mechanism for glucose toxicity in pancreatic islet beta cells in diabetes / J Biol Chem 279 (41) : 42351 ~ 42354
2. [학술지(정기간행물)] - Robertson RP / 2003 / Glucose toxicity in beta-cells: type 2 diabetes, good radicals gone bad, and the glutathione connection / Diabetes 52 (3) : 581 ~ 587
3. [학술지(정기간행물)] - Robertson RP / 2004 / β-Cell glucose toxicity, lipotoxicity, and chronic oxidative stress in type 2 diabetes / Diabetes 53 (S1) : S119 ~ S124
4. [학술지(정기간행물)] - Yoon JS / 2006 / Glucose Oxidation and Production of Reactive Oxygen Species (ROS) in INS-1 Cells and Rat Islet Cells Exposed to High Glucose / Diabetes 30 : 246 ~ 253
5. [학술지(정기간행물)] - Wolff SP / 1987 / Glucose autoxidation and protein modification. The potential role of 'autoxidative glycosylation' in diabetes / J Bio chem 245 (1) : 243 ~ 250
2. [학술지(정기간행물)] - Robertson RP / 2003 / Glucose toxicity in beta-cells: type 2 diabetes, good radicals gone bad, and the glutathione connection / Diabetes 52 (3) : 581 ~ 587
3. [학술지(정기간행물)] - Robertson RP / 2004 / β-Cell glucose toxicity, lipotoxicity, and chronic oxidative stress in type 2 diabetes / Diabetes 53 (S1) : S119 ~ S124
4. [학술지(정기간행물)] - Yoon JS / 2006 / Glucose Oxidation and Production of Reactive Oxygen Species (ROS) in INS-1 Cells and Rat Islet Cells Exposed to High Glucose / Diabetes 30 : 246 ~ 253
5. [학술지(정기간행물)] - Wolff SP / 1987 / Glucose autoxidation and protein modification. The potential role of 'autoxidative glycosylation' in diabetes / J Bio chem 245 (1) : 243 ~ 250
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UCI(KEPA) : I410-ECN-0101-2014-519-000284009