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�й�ҩѧ��־ 2015, Vol. 50 Issue (3) :232-238    DOI: 10.11669/cpj.2015.03.011
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1.���ϴ�ѧҩѧԺҩ��ѧ������, ���� 510632;
2.��俨����˹��ҽѧԺ,��� ˹�¸��Ħ 17177;
3.���ϴ�ѧ��ҩ����Ȼҩ���о���, ���� 510632
WANG Jing-ru1,2,YE Kai-he1,LÜ Yan-qing1,WEI Song-cheng1,ZHANG Xiao-qi3,YE Wen-cai3,YE Chun-ling1*
1.Department of Pharmacology, Pharmacy College of Jinan University, Guangzhou 510632, China;
2. The Karolinska Institute in Sweden, Stockholm 17177, Sweden;
3.Research Institute of Traditional Chinese Medicine and Natural Medicine of Jinan University, Guangzhou 510632, China

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ժҪ Ŀ�� ���췬ʯ����(guavenoic acid,GA)��INS-1�ȵ���ϸ���������˵����á����� ����INS-1�ȵ���ϸ��,���跬ʯ���� 0.3��1��3��10��30 nmol��L-1,����հ׶����顢��ý�����鼰����ҩ��,ҩ������ʱ���Ϊ48 h��650 ��mol��L-1 H2O2��Ԥϸ��2 h������������ģ��,���ļ׻�ż�����������ҩ���INS-1��ϸ���������˵ı�������,�ú�Ⱦɫ���۲�ϸ���˱仯,����ʽϸ�������ҩ���ϸ�����������ɵ�����,��˫Ⱦ-��ʽϸ�������ҩ���ϸ�������ı������á���� ����������ģ����Ƚ�,�ͼ����ķ�ʯ����(0.3��1 nmol��L-1)����������INS-1��ϸ������(P<0.05��P<0.01);��Ⱦɫ�����ʾ,����������ģ�������,��Ũ�ȷ�ʯ����(0.3 nmol��L-1)������,ϸ��ӫ��ǿ�Ƚ�����0.3��1��3 nmol��L-1��ʯ�������ʮ�������ؽ��Ͷ���ӫ���(DCF)ӫ��ǿ��(P<0.01),������ϸ���ڻ������IJ�����0.3 nmol��L-1��ʯ�����������ֿ�ϸ�������ķ���(P<0.05)������ ��ʯ�����ܶԿ�INS-1ϸ����������,������������ϸ���ڻ������IJ������Կ�ϸ�������йء�
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Abstract�� OBJECTIVE To investigate the effects of guavenoic acid(GA) on protection against oxidative damage in INS-1 cells. METHODS INS-1�� cells were cultured in vitro. Control group, medium group, model group, drug groups and positive group were set. INS-1 cells were treated with GA in 0.3, 1, 3, 10, 30 nmol��L-1 for 48 h. Using 650 ��mol��L-1H2O2 challenges the INS-1 cells for 2 h to establish the oxidative damage model(OD), the cell viability was tested by MTT assay, the nuclear was stained by Hoechst 33258, the ROS in OD-INS-1 was tested by ROS-kit and the apoptosis was tested via double staining-fcm. RESULTS Compared with model group, at low concentration GA(0.3, 1 nmol��L-1) could protect INS-1 cells exposed to H2O2 significantly(P<0.05 or P<0.01). Nuclear staining results showed that compared with the oxidative damage model group, cells treated with 0.3 nmol��L-1 GA, and emitting weaker cell fluorescence. 0.3, 1, 3 nmol��L-1 GA could reduce the DCF fluorescence intensity very significantly(P<0.01). At 0.3 nmol��L-1, GA can significantly resist the occurrence of apoptosis(P<0.05). CONCLUSION GA could protect INS-1 cells from oxidative damage, maybe achieved by inhibiting intracellular ROS generation and against apoptosis.
Keywords�� guavenoic acid,   INS-1�� cells,   oxidative damage     
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WANG Jing-Ru-, , YE Kai-He- etc .Effects of Guavenoic Acid on Protection against Oxidative Damage in INS-1 Cells and Its Mechanisms[J]  Chinese Pharmaceutical Journal, 2015,V50(3): 232-238
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[1] GARDNER D G, SHOBACK D M. Greenspan��s Basic & Clinical Endocrinology. 9th ed. New York:McGraw-Hill Medical, 2011.[2] GEMBAL M, GILON P, HENQUIN J C. Evidence that glucose can control insulin release independently from its action on ATP-sensitive K+ channels in mouse B cells. J Clin Investigat, 1992, 89(4):1288-1295.[3] PI J, BAI Y, ZHANG Q, et al. Reactive oxygen species as a signal in glucose-stimulated insulin secretion. Diabetes, 2007, 56(7):1783-1791.[4] SINGH U, DEVARAG S, JIALAL I. Vitamin E, oxidative stress, and inflammation. Annu Rev Nut, 2005, 25:151-174.[5] PEREIRA E C, FERDERBAR S, BERTOLAMI M C, et al. Biomarkers of oxidative stress and endothelial dysfunction in glucose intolerance and diabetes mellitus.Clin Biochem, 2008, 41(18):1454-1460.[6] YOKOZAWA T, KIM Y, KIM H Y, et al. Protective effect of persimmon peel polyphenol against high glucose-induced oxidative stress in LLC-PK(1)cells. Food Chem Toxicol, 2007, 45(10):1979-1987.[7] LEE S H, HAN J S, HEO S J, et al. Protective effects of dieckol isolated from Ecklonia cava against high glucose-induced oxidative stress in human umbilical vein endothelial cells. Toxicol in Vitro, 2010, 24(2):375-381.[8] GUTIERREZ R M, MITCHELL S, SOLIS R V. Psidium guajava:A review of its traditional uses, phytochemistry and pharmacology. J Ethnopharmacol, 2008, 117(1):1-27.[9] MARTIN M A, FERNANDEZ-MILLAN E, RAMOS S, et al. Cocoa flavonoid epicatechin protects pancreatic beta cell viability and function against oxidative stress. Mol Nutr Food Res, 2014, 58(3):447-456. BRASNYO P, MOLNAR G A, MOHAS M, et al. Resveratrol improves insulin sensitivity, reduces oxidative stress and activates the Akt pathway in type 2 diabetic patients. Br J Nutr, 2011, 106(3):383-389. ROBERTSON R P, HARMON J, TRAN P O, et al. Glucose toxicity in ��-cells:Type 2 diabetes, good radicals gone bad, and the glutathione connection. Diabetes, 2003, 52(3):581-587. ROBERTSON R P, HARMON J S. Diabetes, glucose toxicity, and oxidative stress:A case of double jeopardy for the pancreatic islet �� cell. Free Rad Biol Med, 2006, 41(2):177-184. CUMAOGLU A, RACKOVA L, STEFEK M, et al. Effects of olive leaf polyphenols against H2O2 toxicity in insulin secreting ��-cells. Acta Biochim Pol, 2011,58(1):45-50. CHENG Q, DONG W, QIAN L, et al. Visfatin inhibits apoptosis of pancreatic ��-cell line, MIN6, via the mitogen-activated protein kinase/phosphoinositide 3-kinase pathway. J Mol Endocrinol, 2011, 47(1):13-21. LACRAZ G, FIGEAC F, MOVASSAT J, et al. Diabetic GK/Par rat ��-cells are spontaneously protected against H2O2-triggered apoptosis. A cAMP-dependent adaptive response. Am J Physiol-Endocrinol Metab, 2010, 298(1):17-27. RAALTE D H, KWA K A A, GENUGTEN R E, et al. Islet-cell dysfunction induced by glucocorticoid treatment:Potential role for altered sympathovagal balance. Metabolism, 2013, 62(4):568-577. WANG Y, LI Y, YIN J, et al. Autophagy regulates inflammation following oxidative injury in diabetes. Autophagy, 2013, 9(3):272-277. TAKAHASHI H, TRAN P O T, LEROY E, et al. D-Glyceraldehyde causes production of intracellular peroxide in pancreatic islets, oxidative stress, and defective beta cell function via non-mitochondrial pathways. J Biol Chem, 2004, 279(36):37316-37323. BONEKAMP N A, VOLKL A, FAHIMI H D, et al. Reactive oxygen species and peroxisomes:Struggling for balance. Biofactors, 2009, 35(4):346-355. SCHRADER M, FAHIMI H D. Peroxisomes and oxidative stress. Biochim Biophys Acta(BBA)-Mol Cell Res, 2006, 1763(12):1755-1766. DEL GUEEEA S, LUPI R, MARSELLI L, et al. Functional and molecular defects of pancreatic islets in human type 2 diabetes. Diabetes, 2005, 54(3):727-735. LEE S H. Bioactive compounds extracted from ecklonia cava by using enzymatic hydrolysis protects high glucose-induced damage in INS-1 pancreatic beta-cells. Appl Biochem Biotechnol, 2012, 167(7):1973-1985.
[1] ���������*�������࣬����.�ڹ���轻�ɫ�ն��������ܶ�֬��������Ѫ����Ƥϸ���ı�������[J]. �й�ҩѧ��־, 2013,48(8): 606-611
[2] ��־�㣬���أ����� �����������㣬�ξ���.�������պ�ҩѪ�忹�����������ļ�ϸ���������о�[J]. �й�ҩѧ��־, 2012,47(19): 1547-1551
[3] ������;����;������;�콭ƽ.�ח�����ȡ���D-���������Ǽ���˥��С���������˵ı�������[J]. �й�ҩѧ��־, 2008,43(08): 591-593
[4] ������;����;��ܰ��;��ԭ.�ʲ����臨�����С���Ը�������Ӱ���ʵ���о�[J]. �й�ҩѧ��־, 2007,42(12): 899-902
[5] ����;������;������.����Ҷ��ȡ���H2O2�յ��ľ���ϸ����������������[J]. �й�ҩѧ��־, 2006,41(10): 750-753
[6] ����ϼ;������;����Ӿ.��ܺ�����������ϸ���������˵ı�������[J]. �й�ҩѧ��־, 2006,41(06): 420-423
[7] ¬�»�;����˳;�ξ�ɽ;̷��;��Ԫ��;�ƻ�;����.������ܻ�ͪ�������ɻ������˺�ϸ��Ĥ���˵ı�������[J]. �й�ҩѧ��־, 2004,40(08): 587-589
[8] ������;��ï;������;.�쵤Ҷ����ص����⿹��������[J]. �й�ҩѧ��־, 2001,36(12): 810-814
[9] ������;����;���;������;.��轶���-1�������ɻ�����С������������˵�����[J]. �й�ҩѧ��־, 2001,36(10): 669-672
[10] ����÷;���緼;�����;��ⴺ.��������ù�Դ�����ȱѪ�������˵ı������ü������о�[J]. �й�ҩѧ��־, 2001,36(04): 248-251
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