还原型烟酰胺腺嘌呤二核苷酸磷酸氧化酶与糖尿病肾病

糖尿病肾病（diabetic nephropathy,DN）是糖尿病常见的微血管并发症,其发病机制与代谢紊乱、肾小球血流动力学异常、细胞因子、环境和遗传等多方面因素有关,目前尚缺乏十分有效的防治措施。临床研究证实,还原型烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶及其产物反应性氧自由基（reactive oxygen species,ROS）所致的氧化应激与DN的发生发展密切相关,针对NADPH氧化酶的治疗和NADPH氧化酶抑制剂的研究对DN的防治具有重要意义,现综述如下。     

还原型烟酰胺腺嘌呤二核苷酸磷酸氧化酶与

糖尿病肾病(diabetic nephropathy,DN)是糖尿病常见的微血管并发症,其发病机制与代谢紊乱、肾小球血流动力学异常、细胞因子、环境和遗传等多方面因素有关,目前尚缺乏十分有效的防治措施.     

老年冠心病患者血清NOX2、NOX4 mRNA水平变化及其与预后的关系

目的 探究还原型烟酰胺腺嘌呤二核苷酸磷酸氧化酶(NOX)2、NOX4 mRNA在老年冠心病(CHD)患者血清中的水平变化及其与预后的关系.方法 选取该院收治的老年CHD患者146例为CHD组,另选取体检健康老年人146例为对照组.采用实时荧光定量PCR检测血清NOX2、NOX4 mRNA水平.比较CHD组与对照组、不同...     

NAD+对受照射L02肝细胞株bcl-2、bax、p53蛋白表达的影响

目的:探讨氧化型烟酰胺腺嘌呤二核苷酸对体外培养的人正常肝细胞株L02辐射损伤保护作用及可能的机制.方法:实验分3组,照射+NAD组、照射组和假照射组.采用MTT法检测NAD+对受照射L02细胞生长活性的影响;应用流式细胞仪检测各组细胞凋亡率以及凋亡相关蛋白bax、bcl-2、p53阳性表达率.结果:细胞受照射后加入NAD+能够对抗X射线照射对L02细胞的生长抑制作用,细胞生长活性较单照射组细胞活性显著提高、减少细胞凋亡(P＜0.05);照射后加NAD+组与照射组相比较,细胞p53、bax表达下调(P＜0.05)、bcl-2的表达上调(P＜0.05).结论:NAD+可以对抗L02细胞的X线辐射损伤,其作用机制很可能与P53信号传递途径有关.     

三磷酸胞苷对糖尿病周围神经病变患者神经传导速度的影响

背景：三磷酸胞苷(cytridini triphosphatis，CTP)主要用于脑血管意外及其后遗症，脑震荡，脑血管硬化，老年性痴呆等的治疗，而该药对糖尿病周围神经病变的作用又如何呢?目的：观察CTP改善糖尿病周围神经病变患者神经功能作用，并评价该药作用效果及神经电生理作用。设计：以患者为研究对象．前瞻性随机对照设计的验证性实验研究。单位：第四军医大学医院内分泌科病房。对象：1999—09／2000—02在第四军医大学西京医院内分泌科住院的糖尿病周围神经病变患者50例，符合纳入标准糖尿病周围神经病变患者50例，男28例．女22例。将50例患者随机分为治疗组和对照组各25例．均知情同意。方法：治疗组25例用CTP 60mg加入生理盐水100mL维生素D，1次／d。对照组25例用维生素B1 100mg和维生素B12 500μg，1次／d，东莨菪碱(654—2)20mg加人生理盐水100mL维生素D，1次／d，疗程均为14d。神经传导速度采用的是表面电极顺行性测定。主要观察指标：两组患者肢体神经传导速度。结果：治疗组患者经过CTP治疗14d后，双上肢及下肢正中神经、尺神经、腓总神经、胫神经传导速度明显高于对照组(P&;lt;0．05～0．01)。治疗组患者经过三磷酸胞苷14d治疗后．神经症状、神经体征评分(1．4&;#177;0．5，3．0&;#177;0．5)明显低于对照组(2．6&;#177;03，4．0&;#177;0．3)(t=3255，2．005，P&;lt;0．05)。结论：三磷酸胞苷能有效改善糖尿病周围神经病变患者的神经传导速度。     

三磷酸胞苷对糖尿病周围神经病变患者神经传导速度的影响

背景三磷酸胞苷(cytridini triphosphatis,CTP)主要用于脑血管意外及其后遗症,脑震荡,脑血管硬化,老年性痴呆等的治疗,而该药对糖尿病周围神经病变的作用又如何呢? 目的观察CTP改善糖尿病周围神经病变患者神经功能作用,并评价该药作用效果及神经电生理作用.设计以患者为研究对象,前瞻性随机对照设计的验证性实验研究.单位第四军医大学医院内分泌科病房.对象1999-09/2000-02在第四军医大学西京医院内分泌科住院的糖尿病周围神经病变患者50例,符合纳入标准糖尿病周围神经病变患者50例,男28例,女22例.将50例患者随机分为治疗组和对照组各25例,均知情同意.方法治疗组25例用CTP60mg加入生理盐水100mL维生素D,1次/d.对照组25例用维生素B1 100 mg和维生素B12 500 μg,1次/d,东莨菪碱(654-2)20 mg加入生理盐水100 mL维生素D,1次/d,疗程均为14 d.神经传导速度采用的是表面电极顺行性测定.主要观察指标两组患者肢体神经传导速度.结果治疗组患者经过CTP治疗14 d后,双上肢及下肢正中神经、尺神经、腓总神经、胫神经传导速度明显高于对照组(P<0.05～0.01).治疗组患者经过三磷酸胞苷14 d治疗后,神经症状、神经体征评分(1.4±0.5,3.0±0.5)明显低于对照组(2.6±0.3,4.0±0 3)(t=3.255,2.005,P<0 05).结论三磷酸胞苷能有效改善糖尿病周围神经病变患者的神经传导速度.     

氧化应激与糖尿病脑组织损伤关系的研究新进展

糖尿病是一种常见的内分泌代谢紊乱疾病,随着生活方式的改变和老龄化的进程,糖尿病的患病率急剧增加,而糖尿病脑组织损伤是糖尿病患者致死、致残的重要原因。研究表明,在糖尿病脑损伤的发生、发展过程中,氧化应激增多是糖尿病性脑组织损伤的重要因素[1]。而近年来研究发现烟酰胺腺嘌呤二核苷酸磷酸（NADPH）氧化酶是氧化应激的关键因素。本文就氧化应激、NADPH氧化酶、醛糖还原酶和糖尿病脑组织损伤的关系作系统的表述。     

尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4源性活性氧过量产生抑制胚胎干细胞向心肌细胞的分化

背景:作为信号传导通路中的第二信使,活性氧(主要指超氧离子和过氧化氢)对细胞的生长、分化起重要作用。过量的活性氧在心脏疾病中启动了心肌细胞的凋亡,尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4源性活性氧的过量产生诱导凋亡是否抑制了胚胎干细胞向心肌细胞的分化。目的:探讨尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4活性氧对心肌细胞分化的抑制作用。设计:随机对照实验观察。单位:卫生部北京医院老年医学研究所。材料:胚胎干细胞CGR8为本实验室自存,其他主要试剂除特别注明均购自Sigma公司。方法:实验于2003-10/2005-08在卫生部北京医院老年医学研究所进行。①将小鼠胚胎干细胞分化成胚小体。在分化4d后以不同浓度的过氧化氢(1,10,100,1000nmol/L)处理胚小体1h,在分化8d后观察心肌细胞的生成,分析活性氧对心肌细胞分化的影响。②将pcDNA3.1和pcDNA3.1-NOX4质粒分别转染CGR8细胞,同时以未进行转染的CGR8细胞为对照,以RT-PCR和WesternBlotting测定尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4mRNA和MLC2v蛋白水平,应用定量四唑氮蓝高水平表达尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4干细胞中活性氧水平。③采用活性氧清除剂N-乙酰半胱氨酸(5mmol/L)和过氧化氢酶(200U/mL)转染前处理2h作为对照,用Hoechst染色、TUNEL和DNAladder分析尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4过表达后CGR8细胞凋亡情况,同时检测转染尼克酰胺腺嘌呤二核苷酸磷酸氧化酶氧化酶4后CGR8细胞中p21、p53及Bcl-2的表达。主要观察指标:①活性氧对心肌细胞分化的影响。②胚胎干细胞中尼克酰胺腺嘌呤二核苷酸磷酸氧化酶的表达。③尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4过表达后活性氧产生量、心肌细胞的分化和胚胎干细胞凋亡的观察。④p53,p21和Bcl-2是否参与了尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4过表达诱导的细胞凋亡。结果:①不同水平的活性氧对心肌细胞分化具有不同的效应。在分化后4d用较低浓度(1～100nmol/L)的过氧化氢处理胚小体2h可明显促进心肌细胞分化(P<0.01),而较高浓度(>1μmol/L)的过氧化氢则显示出抑制作用(P<0.01)。②尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4在小鼠胚胎干细胞中的表达水平最高,尼克酰胺腺嘌呤二核苷酸磷酸氧化酶3虽然也在胚胎干细胞中表达,但表达水平低,而尼克酰胺腺嘌呤二核苷酸磷酸氧化酶1、2在胚胎干细胞中不表达。RT-PCR检测结果显示,与单纯转染pcDNA3.1细胞相比,转染pcDNA3.1-NOX4质粒的CGR8细胞中尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4过表达。③四唑氮蓝实验检测结果显示,高水平表达的尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4引起过量活性氧产生(P<0.05)。与未转染质粒的细胞相比,尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4过表达抑制了心肌细胞的分化(P<0.01)。WesternBlot结果显示高水平尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4导致胚小体内MLC2v蛋白水平降低。④p21和p53可能参与了NADPH氧化酶4诱导的凋亡过程。转染尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4的p53-/-ES细胞R72D27并未发生凋亡,高水平的Bcl-2可以抑制尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4过表达诱导的细胞凋亡。结论:尼克酰胺腺嘌呤二核苷酸磷酸氧化酶4在心肌细胞分化中起关键作用,p53和p21以及Bcl-2可能参与了凋亡信号通路的调控。     

依达拉奉对糖尿病周围神经病变大鼠坐骨神经的保护作用

目的:研究依达拉奉对糖尿病周围神经病变(DPN)大鼠坐骨神经的保护作用。方法:SD大鼠80只,采用链脲佐菌素(STZ)一次性腹腔注射诱导建立DPN模型,随机分为对照组和治疗组,治疗组每天给予3 mg/kg依达拉奉腹腔注射4周,观察摆尾温度阈值(TTT)、坐骨神经运动神经传导速度(MCV)、感觉神经传导速度(SCV)、神经形态和坐骨神经中一氧化氮(NO)含量、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性。结果:对照组大鼠TTT升高,MCV和SCV减慢(P<0.01),形态学明显异常,NO、MDA含量明显增多,SOD活性显著降低(P<0.01)。治疗组与对照组比较TTT明显降低,MCV和SCV明显加快,形态学明显改善,NO、MDA含量明显减少,SOD活性显著增高(P<0.01)。结论:依达拉奉可降低DPN大鼠坐骨神经损伤。     

超高频超声评价糖尿病大鼠坐骨神经的初步研究

目的 探讨超高频超声评价糖尿病大鼠坐骨神经病变的应用价值.方法 雄性SD大鼠50只,32只经高脂喂养1月后尾静脉注射链脲佐菌素诱导糖尿病大鼠模型并随机分为糖尿病3个月组(12只)和5个月组(20只),其余大鼠随机分为正常对照3个月组(8只)和正常对照5个月组(10只).采用超高频超声测量大鼠坐骨神经的截面积(CSA),行病理组织学检查并采用Image-Pro Plus图像分析软件统计神经纤维数量和神经纤维总面积.结果 糖尿病5个月组的CSA、神经纤维数和神经纤维总面积均较正常对照5个月组减小,差异有统计学意义(t =5.121,P＜0.05;t =7.113,P＜0.05;t=6.328,P＜0.05),糖尿病5个月组的CSA与神经纤维数和神经纤维总面积呈正相关(r =0.73,P＜0.05;r =0.71,P＜0.05).糖尿病3个月组的CSA与正常3个月组比较差异无统计学意义(P＞0.05),CSA与病理学指标无明显相关性(r =0.51,P=0.331;r=0.43,P=0.137).结论 超高频超声测量坐骨神经CSA能反映大鼠周围神经病变,为临床提供一种新的评价指标.     

电针联合依达拉奉对糖尿病周围神经病变大鼠坐骨神经的保护作用

目的 研究电针联合依达拉奉对糖尿病周围神经病变(DPN)大鼠坐骨神经的保护作用.方法 SD大鼠100只,10只作为正常组,其余90只采用链脲佐菌素(STZ)1次性腹腔注射诱导建立DPN模型,之后随机分为对照组、电针组和针药联合组,电针组取大鼠足三里、肾俞穴进行电针治疗,针药联合组同时给予依达拉奉(3 mg·kg-1·d-1)腹腔注射共4周.观察坐骨神经运动神经传导速度(MCV)、感觉神经传导速度(SCV)形态和坐骨神经中一氧化氮(NO)、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性.结果 与正常组比较,时照组大鼠MCV、SCV明显减慢(30.88±3.64)m/s,(28.65±9.44) m/s;(48.39±1.43)m/s,(47.44±8.68)m/s,形态学明显异常,NO、MDA含量明显增多(5.56±0.21)(μ)mol/L,(7.97±0.51)nmol/mg prot;(1.16±0.17)(μ)mol/L,(2.23±0.48)nmol/mg prot,SOD活性显著降低(10.62±1.53) U/mg prot,(20.48±1.55)U/mg prot(P＜0.01),电针组与对照组比较,大鼠MCV、SCV明显加快(36.43±2.28) m/s,(34.43±5.38)m/s(P＜0.01),形态学明显改善,但NO、MDA含量与SOD活性无显著变化(P＞0.05),针药联合组与电针组比较,大鼠MCV、SCV加快更明显(43.67±2.33) m/s,(41.47±5.32) m/s( P＜0.01),形态学有更明显改善,NO、MDA含量较对照组及电针组均明显减少(2.23±0.12)(μ)mol/L,(4.12±0.42)nmol/ mg prot,SOD活性则显著增高(16.69±1.76)U/mg prot(P＜0.01).结论 电针联合依达拉奉应用对DPN大鼠坐骨神经损伤有更明显的保护作用.     

针刺激对大鼠坐骨神经损伤后神经生长因子mRNA表达的影响

目的:探讨针刺对神经生长因子信使RNA(NGF mRNA)表达的影响,并且从这一角度分析评价电针频率的不同,及电针与手针对神经生长的影响。方法:78只雄性SD大鼠随机分为5组,治疗1组(n=18),疏波,电压2V,频率:F1:5Hz。治疗2组(n=18):疏波,电压2V,频率:F1:100Hz。治疗3组(n=18):手针。模型组(n=18):行坐骨神经损伤手术造模,不行治疗。对照组(n=6),正常成年大鼠。治疗组与模型组均行坐骨神经损伤手术造模,术后第2天开始给予电针及针刺治疗,电针正极接在近心端,负极接在远心端。分别夹在"环跳"、"足三里"处的针柄上,每次30min,每日2次。手针针刺相同穴位,每次30min,每日2次。术后1、2、6周取治疗组大鼠神经损伤部位远侧坐骨神经干0.6cm,应用原位杂交的方法和图像分析处理系统定量测定坐骨神经组织中NGF mRNA水平。结果:治疗组NGF mRNA表达明显增加,均高于模型组(均P<0.01);治疗1组NGF mRNA表达始终处于高水平,明显高于模型组(P<0.01)。结论:针刺激是促进周围神经损伤再生的重要手段,其中5Hz低频电针效果最佳。     

2型糖尿病周围神经病变患者上肢神经的超声研究

目的 应用高频超声探讨2型糖尿病周围神经病变（DPN）患者上肢神经多个位点的横截面积的变化及其临床意义。方法 对30例确诊为DPN的患者和30例健康对照者应用高频超声检查上肢正中神经、尺神经和桡神经的多个位点：包括正中神经腕管处、前臂中点、肘窝处及上臂中点的横截面积;尺神经平腕横纹处、前臂中点、肘管处及上臂中点的横截面积;桡神经桡神经沟处、肘窝处的横截面积,对比分析各位点的横截面积及神经的声像图特点并探讨其诊断价值。结果 DPN组正中神经在腕管处、前臂中点、肘窝处和上臂中点处的横截面积,尺神经在腕横纹处、肘管处和上臂中点处的横截面积,桡神经在桡神经沟的横截面积均大于对照组,差异有统计学意义（P<0.05）。结论 超声检查可以为DPN的早期发现和评价提供临床依据。     

Electrophysiological and functional effects of shock waves on the sciatic nerve of rats

Extracorporeal shockwave therapy (ESWT) has been applied in lithotripsy and treatments of musculoskeletal disorders over the past decade, but its effects on peripheral nerves remain unclear. This study investigated the short-term effects of shockwaves on the sciatic nerve of rats. The nerves were surgically exposed and then stimulated with shockwaves at three intensities. We evaluated the motor nerve conduction velocity (MNCV) of treated sciatic nerves before, immediately after (day 0) and at 1, 4, 7 and 14 d after shockwave treatment. Two functional tests-the sciatic functional index and the withdrawal reflex latency-were evaluated before and at 1, 4, 7 and 14 d after shockwave application. The rats were sacrificed on days 0, 1, 4, 7 and 14 for morphologic observation. The degassed treatment group received high-intensity shockwave treatment using degassed normal saline as the contact medium, and MNCV was measured before and on days 0, 1, 4, 7 and 14. The sham group received the same procedure as the treatment groups (i.e., the surgical operation to expose the sciatic nerve) but with no shockwave treatment. The control group received no surgical operation or shockwave treatment. The results showed moderate decrease in the MNCV after shockwave treatment and damage to the myelin sheath of large-diameter myelinated fibers. The effect was largest (reduction to 60.9% of baseline MNCV) and of longest duration (7 to 14 d) in the high-intensity group. There were no significant changes in functional tests. These results indicated that direct application of shockwaves can induce reversible segmental demyelination in large-diameter fibers, with the electrophysiological changes being positively correlated with the intensity of the shockwaves.     

Modulation of nicotinamide adenine dinucleotide phosphate oxidase expression and function by 3',4'-dihydroxyflavonol in phagocytic and vascular cells

Previously we have demonstrated that 3',4'-dihydroxyflavonol (DiOHF), a novel synthetic flavonol, protects against ischemia reperfusion injury in both heart and brain. In this study, we characterized the pharmacological effects of DiOHF on phagocytic and vascular NADPH oxidase. Superoxide release (lucigenin-enhanced chemiluminescence or cytochrome c reduction), NADPH oxidase activation (membrane translocation of p47phox), and subunit expression (real-time polymerase chain reaction and Western blot) were examined in differentiated HL-60 cells, human neutrophils, vascular endothelial and smooth muscle cells, and mouse aorta. DiOHF concentration dependently suppressed superoxide accumulation (EC(50) = 8.4 +/- 1.7 microM) in vascular smooth muscle cells, which appears to be attributable to its superoxide scavenging activity (EC(50) = 6.1 +/- 1.1 microM measured in a cell-free system). DiOHF had similar effects in HL-60 cells and isolated aortic rings. In HL-60 cells, but not endothelial or smooth muscle cells, DiOHF and quercetin (10 and 30 microM) significantly reduced the protein expression of p47phox, whereas p67phox was not altered. DiOHF did not affect phorbol ester-induced membrane translocation of either p47phox or protein kinase C in leukocytes. Our results suggest that suppression of NADPH oxidase-dependent superoxide accumulation may contribute to the cytoprotective actions of DiOHF during ischemia-reperfusion injury.     

In situ transverse elasticity and blood perfusion change of sciatic nerves in normal and diabetic rats

Background

Diabetic neuropathy is the most pervasive complication of diabetes mellitus and its etiopathology is not completely elucidated. The existing literature focuses on the histological and structural changes as well as the longitudinal mechanical properties of nerves. The main objective of this study is to investigate the in situ transverse biomechanical properties and changes of microcirculation of sciatic nerves in diabetic and normal control rats.

Methods

Quasi-static circular compression experiments were conducted on sciatic nerves of six normal and six diabetic Wistar rats. Local blood perfusion during the compression was also measured by laser Doppler flowmetry. The compressive stress and strain were estimated, in order to calculate the apparent Young’s modulus. The impact of diabetes on peripheral nerves was examined by analyzing the transverse elasticity and microcirculation changes.

Findings

The mean transverse apparent Young’s modulus of the sciatic nerves in diabetic rats was 210.7 kPa, which was nearly two times greater than that of normal controls (116.3 kPa). The pressure threshold that blood perfusion started to decrease in diabetic rats (24.1 mm Hg) was smaller than in the normal controls (47.1 mm Hg).

Interpretation

These results suggest that the sciatic nerve was stiffer in the diabetic rats. The structural changes in microvessels might lead to earlier decrease of blood perfusion in diabetic nerves under radial compression. These results provide information about the biomechanical and microcirculation changes of peripheral nerves inflicted by diabetes and may also serve as a reference for clinical nerve repair and regeneration for patients with diabetic neuropathy.     

Activities of xanthine oxidoreductase and antioxidant enzymes in different tissues of diabetic rats

Oxidative stress is an important pathogenic constituent in diabetic endothelial dysfunction. The aim of this study was to investigate whether an increase in oxidative stress related to xanthine oxidoreductase occurs in diabetes. Liver, brain, heart, and kidney xanthine oxidase (XO), xanthine dehydrogenase (XDH), antioxidant enzymes (glutathione peroxidase, superoxide dismutase, catalase), and nitrite levels were measured in control and early and late diabetic rat models. Although diabetes had no impact on liver XO and XDH activity, XDH activity in heart, kidney, and brain was significantly greater in late diabetic rats than in controls. Selenium glutathione peroxidase (GPx) activity was found to be lower in the liver, brain, kidney, and heart of late diabetic rats than in controls. The measured decrease in selenium GPx activity was also observed in early diabetic heart, kidney, and brain. No significant change was observed in liver, brain, and kidney copper/zinc superoxide dismutase (Cu/Zn SOD) activity in early and late diabetic rat models compared with that in controls, whereas heart Cu/Zn SOD activity was significantly decreased in both early and late diabetic rats. Liver and brain catalase activity remained similar among the different experimental groups, whereas increased heart and kidney catalase activity was observed in both early and late diabetic rats. Liver, kidney, and brain nitrite levels were found to be increased in early diabetic rat models compared with those in controls. These data suggest that the increased XDH and decreased selenium GPx activity observed in the later stages of diabetes leads to enhanced oxidative stress in the heart, kidney, and brain, resulting in secondary organ damage associated with the disease.     

The role of foot self-care behavior on developing foot ulcers in diabetic patients with peripheral neuropathy: A prospective study

BackgroundAlthough foot self-care behavior is viewed as beneficial for the prevention of diabetic foot ulceration, the effect of foot self-care behavior on the development of diabetic foot ulcer has received little empirical investigation.ObjectiveTo explore the relationship between foot self-care practice and the development of diabetic foot ulcers among diabetic neuropathy patients in northern Taiwan.MethodsA longitudinal study was conducted at one medical center and one teaching hospital in northern Taiwan.ParticipantsA total of 295 diabetic patients who lacked sensitivity to a monofilament were recruited. Five subjects did not provide follow-up data; thus, only the data of 290 subjects were analyzed. The mean age was 67.0 years, and 72.1% had six or fewer years of education.MethodsData were collected by a modified version of the physical assessment portion of the Michigan Neuropathy Screening Instrument and the Diabetes Foot Self-Care Behavior Scale. Cox regression was used to analyze the predictive power of foot self-care behaviors.ResultsA total of 29.3% (n = 85) of diabetic neuropathy patients developed a diabetic foot ulcer by the one-year follow-up. The total score on the Diabetes Foot Self-Care Behavior Scale was significantly associated with the risk of developing foot ulcers (HR = 1.04, 95% CI = 1.01–1.07, p = 0.004). After controlling for the demographic variables and the number of diabetic foot ulcer hospitalizations, however, the effect was non-significant (HR = 1.03, 95% CI = 1.00–1.06, p = 0.061). Among the foot self-care behaviors, lotion-applying behavior was the only variable that significantly predicted the occurrence of diabetic foot ulcer, even after controlling for demographic variables and diabetic foot ulcer predictors (neuropathy severity, number of diabetic foot ulcer hospitalizations, insulin treatment, and peripheral vascular disease; HR = 1.19, 95% CI = 1.04–1.36, p = 0.012).ConclusionsAmong patients with diabetic neuropathy, foot self-care practice may be insufficient to prevent the occurrence of diabetic foot ulcer. Instead, lotion-applying behavior predicted the occurrence of diabetic foot ulcers in diabetic patients with neuropathy. Further studies are needed to explore the mechanism of lotion-applying behavior as it relates to the occurrence of diabetic foot ulcer.