中南大学学报(医学版)
中南大學學報(醫學版)
중남대학학보(의학판)
JOURNAL OF CENTRAL SOUTH UNIVERSITY (MEDICAL SCIENCES)
2006年
6期
814-818
,共5页
糖尿病%肥胖%炎症%心肌病%心肌细胞死亡%金属硫蛋白
糖尿病%肥胖%炎癥%心肌病%心肌細胞死亡%金屬硫蛋白
당뇨병%비반%염증%심기병%심기세포사망%금속류단백
diabetes%obesity%inflammation%cardiomyopathy%cardiac cell death%metallothionein
糖尿病心肌病(DCM)是糖尿病引发的一种慢性心肌病理改变.在这一慢性病理过程中,急性心肌反应如心肌细胞死亡起关键性的启动作用.除了高血糖,炎症反应也是引起糖尿病性心肌病心肌细胞死亡的一个重要因素.研究证实,糖尿病或肥胖经常可导致全身包括心脏中的肿瘤坏死因子-α(TGF-α),白介素-1 8和血小板激活抑制因子-1(PAI-1)的升高.这些细胞因子引起心肌细胞死亡的机制主要是与氧化和/或氮化损伤相关.金属硫蛋白做为一个有效的抗氧化剂,可以保护心肌免受氧化应激损伤以及细胞因子引发的心肌细胞死亡,从而有效地防止DCM的发生.应用特异性的超氧化抑制剂可以完全阻断细胞因子导致的心肌细胞死亡,所以抑制氧化应激可以有效防止心肌死亡.因此,糖尿病诱发的炎症因子通过氧化应激反应所诱发的心肌细胞死亡是糖尿病心肌病(DCM)发生发展中的重要始动因子.
糖尿病心肌病(DCM)是糖尿病引髮的一種慢性心肌病理改變.在這一慢性病理過程中,急性心肌反應如心肌細胞死亡起關鍵性的啟動作用.除瞭高血糖,炎癥反應也是引起糖尿病性心肌病心肌細胞死亡的一箇重要因素.研究證實,糖尿病或肥胖經常可導緻全身包括心髒中的腫瘤壞死因子-α(TGF-α),白介素-1 8和血小闆激活抑製因子-1(PAI-1)的升高.這些細胞因子引起心肌細胞死亡的機製主要是與氧化和/或氮化損傷相關.金屬硫蛋白做為一箇有效的抗氧化劑,可以保護心肌免受氧化應激損傷以及細胞因子引髮的心肌細胞死亡,從而有效地防止DCM的髮生.應用特異性的超氧化抑製劑可以完全阻斷細胞因子導緻的心肌細胞死亡,所以抑製氧化應激可以有效防止心肌死亡.因此,糖尿病誘髮的炎癥因子通過氧化應激反應所誘髮的心肌細胞死亡是糖尿病心肌病(DCM)髮生髮展中的重要始動因子.
당뇨병심기병(DCM)시당뇨병인발적일충만성심기병리개변.재저일만성병리과정중,급성심기반응여심기세포사망기관건성적계동작용.제료고혈당,염증반응야시인기당뇨병성심기병심기세포사망적일개중요인소.연구증실,당뇨병혹비반경상가도치전신포괄심장중적종류배사인자-α(TGF-α),백개소-1 8화혈소판격활억제인자-1(PAI-1)적승고.저사세포인자인기심기세포사망적궤제주요시여양화화/혹담화손상상관.금속류단백주위일개유효적항양화제,가이보호심기면수양화응격손상이급세포인자인발적심기세포사망,종이유효지방지DCM적발생.응용특이성적초양화억제제가이완전조단세포인자도치적심기세포사망,소이억제양화응격가이유효방지심기사망.인차,당뇨병유발적염증인자통과양화응격반응소유발적심기세포사망시당뇨병심기병(DCM)발생발전중적중요시동인자.
Pathogenesis of diabetic cardiomyopathy (DCM) is a complicate and chronic process that is secondaryto acute cardiac responses to diabetes. One of the acute responses is cardiac cell death that plays a critical role in the initiation and development of DCM. Besides hyperglycemia, inflammatory response in the diabetic heart is also a majorcause for cardiac cell death. Diabetes or obesity often causes systemic and cardiac increases in tumor necrosis factor-alpha, interleukin-18 and plasminogen activator inhibitor-1. However, how these cytokines cause cardiac cell death remains unclear. It has been considered to relate to oxidative and/or nitrosative stress. We have demonstrated that metallothionein as a potent antioxidant or stress protein significantly protected the heart from oxidative damage and cell death caused by these cytokines, leading to effective prevention of DCM. The direct link of the inhibition of oxidative stress and damage to the prevention of cardiac cell death was defined by addition of superoxide or peroxynitrite specific inhibitor to completely prevent cytokine-induced cardiac cell death. Cardiac cell death is induced by the inflammatory cytokines that is increased in response to diabetes. Inflammatory cytokineinducedcardiac cell death is mediated by oxidative stress and is also the major initiator for DCM development.