Xuezhikang Attenuated the Functional and Morphological Impairment of Pancreatic Islets in Diabetic Mice Via the Inhibition of Oxidative Stress

被引:14
作者
Wang, Jun [1 ]
Jiang, WeiMin [2 ]
Zhong, Yong [1 ,3 ]
Lu, Bin [4 ]
Shao, JiaQing [4 ]
Jiang, ShiSen [1 ]
Gu, Ping [1 ,4 ]
机构
[1] Nanjing Univ, Dept Cardiol, Sch Med, Jinling Hosp,Nanjing Gen Hosp,Nanjing Mil Command, Nanjing 210002, Jiangsu, Peoples R China
[2] Jiangsu Prov Hosp Tradit Chinese Med, Dept Cardiol, Nanjing, Jiangsu, Peoples R China
[3] Nanjing Univ, Dept Hlth Care, Sch Med, Jinling Hosp,Nanjing Gen Hosp,Nanjing Mil Command, Nanjing 210002, Jiangsu, Peoples R China
[4] Nanjing Univ, Dept Endocrinol, Sch Med, Jinling Hosp,Nanjing Gen Hosp,Nanjing Mil Command, Nanjing 210002, Jiangsu, Peoples R China
关键词
oxidative stress; pancreatic islet; nicotinamide adenine dinucleotide phosphate oxidase; xuezhikang; diabetes; PREVIOUS MYOCARDIAL-INFARCTION; CORONARY SECONDARY PREVENTION; BETA-CELL MASS; NAD(P)H OXIDASE; CARDIOVASCULAR EVENTS; INSULIN-RESISTANCE; EXPRESSION; RATS; REGENERATION; DYSFUNCTION;
D O I
10.1097/FJC.0000000000000047
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Xuezhikang, purified from red yeast rice, is a traditional Chinese medicine with pleiotropic effects on the cardiovascular system. Oxidative stress plays a crucial role in the dysfunction of pancreas islet in diabetic condition and represents a promising therapeutical target for diabetes mellitus. Therefore, the purpose of this study was to explore the effects and possible mechanisms of xuezhikang on the microenvironment and insulin secretion by pancreatic islets in db/db diabetic mice. Our results showed that xuezhikang decreased the blood glucose level by improving glucose tolerance and insulin secretion in db/db mice. Xuezhikang protected islets from hyperglycemic injury as illustrated by the conserved beta-cell content and microenvironment. Furthermore, xuezhikang potently inhibited the expression of key factors in oxidative stress. In addition, administration of xuezhikang caused an upregulated expression of glucose-sensing apparatus. These observations provide evidence that the influence of xuezhikang on oxidative stress may at least partly account for its protective effects on the microenvironment and insulin secretion function of pancreatic islets in diabetes.
引用
收藏
页码:282 / 289
页数:8
相关论文
共 35 条
  • [1] [Anonymous], CHIN J CHIN MAT MED
  • [2] [Anonymous], PLOS ONE
  • [3] Pancreatic regeneration in type 1 diabetes: dreams on a deserted islet?
    Atkinson, MA
    Rhodes, CJ
    [J]. DIABETOLOGIA, 2005, 48 (11) : 2200 - 2202
  • [4] n-3 fatty acids and the metabolic syndrome
    Carpentier, Yvon A.
    Portois, Laurence
    Malaisse, Willy J.
    [J]. AMERICAN JOURNAL OF CLINICAL NUTRITION, 2006, 83 (06) : 1499S - 1504S
  • [5] Dai XH, 2000, CHIN J CARDIOL CHIN, V20, P692
  • [6] Are oxidative stress-activated signaling pathways mediators of insulin resistance and β-cell dysfunction?
    Evans, JL
    Goldfine, ID
    Maddux, BA
    Grodsky, GM
    [J]. DIABETES, 2003, 52 (01) : 1 - 8
  • [7] Hyperglycemia induces apoptosis of human pancreatic islet endothelial cells - Effects of pravastatin on the Akt survival pathway
    Favaro, Enrica
    Miceli, Ilaria
    Bussolati, Benedetta
    Schmitt-Ney, Michel
    Perin, Paolo Cavallo
    Camussi, Giovanni
    Zanone, Maria M.
    [J]. AMERICAN JOURNAL OF PATHOLOGY, 2008, 173 (02) : 442 - 450
  • [8] Freeman DJ, 2001, CIRCULATION, V103, P357
  • [9] Insulin secretory defects and impaired islet architecture in pancreatic β-cell-specific STAT3 knockout mice
    Gorogawa, S
    Fujitani, Y
    Kaneto, H
    Hazama, Y
    Watada, H
    Miyamoto, Y
    Takeda, K
    Akira, S
    Magnuson, MA
    Yamasaki, Y
    Kajimoto, Y
    Hori, M
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2004, 319 (04) : 1159 - 1170
  • [10] Hyperglycemia causes oxidative stress in pancreatic β-cells of GK rats, a model of type 2 diabetes
    Ihara, Y
    Toyokuni, S
    Uchida, K
    Odaka, H
    Tanaka, T
    Ikeda, H
    Hiai, H
    Seino, Y
    Yamada, Y
    [J]. DIABETES, 1999, 48 (04) : 927 - 932