Detection and significance of blood rheology and coagulation function index in elderly patients with type 2 diabetes mellitus complicated with cerebral infarction

Objective: To investigate the level of blood rheology and coagulation function in elderly patients with type 2 diabetes mellitus (T2DM) and cerebral infarction and its significance. Methods: A total of 81 elderly patients with T2DM and cerebral infarction were selected as the observation group, 80 cases of T2DM patients without cerebral infarction were selected as T2DM group, and 80 healthy elderly people as control group. According to the Adama classification, the patients in the observation group were divided into three groups: lacunar infarction group (n=28), small infarction group (n=39) and large infarction group (n=14). The blood rheology and coagulation function indexes levels among the groups were compared. Results: The single factor variance analysis showed that the differences of the high shear whole blood viscosity, plasma viscosity, low shear whole blood viscosity, APTT, PT, FIB and D-D levels among the control group were significant, T2DM group and observation group were statistically significant. Compared with the control group, the high shear whole blood viscosity, plasma viscosity, low shear whole blood viscosity, FIB and D-D levels in the T2DM group and observation group were significantly increased, PT and APTT were decreased sharply, and in the observation group high shear whole blood viscosity, plasma viscosity, low shear whole blood viscosity, FIB and D-D levels were significantly higher than that of T2DM group APTT, and PT were significantly lower than those of T2DM group. Lacunar infarction group, small infarction group and large infarction group with increased infarct size, with high shear whole blood viscosity, plasma viscosity, low shear whole blood viscosity, FIB and D-D levels were significantly increased, while APTT and PT were significantly decreased. Conclusion: T2DM and cerebral infarction patients with abnormal blood rheology and coagulation function, the index examination has important clinical value for cerebral infarction area evaluation.

Magnetic resonance imaging combined with serum endolipin and galactagoglobin-3 to diagnose cerebral infarction in the elderly with diabetes mellitus

BACKGROUND Magnetic resonance imaging(MRI)combined with serum endothelin and galactagoglobin-3(Gal-3)can improve the clinical diagnosis of diabetes mellitus complicated with cerebral infarction.AIM To analyze the clinical value of MRI combined with serum endolipin and Gal-3 for the diagnosis of cerebral infarction in the elderly with diabetes mellitus.METHODS One hundred and fifty patients with acute cerebral infarction hospitalized between January 2021 and December 2023 were divided into two groups according to comorbid diabetes mellitus,including 62 and 88 cases in the diabetic and nondiabetic cerebral infarction groups.Serum samples were collected to detect the expression of serum endolipoxins,and Gal-3,and cranial MRI was performed at admission.Differences between the two groups were compared to analyze the diagnostic value of these parameters.RESULTS Serum endolipin and Gal-3 expression were higher in the diabetic cerebral infarction group(P<0.05).The arterial wall area,vessel area,normalized wall index,and lumen stenosis rate were higher in the diabetic cerebral infarction group,while the rate of arterial lumen moderate and severe stenosis was 48.39% higher(36.36%,P<0.05).The percentage of large(29.03%)and multiple infarcts(33.87%)in the diabetic cerebral infarction group was higher(13.64% and 20.45%),and the incidence rate of lacunar infarcts was lower(37.10%vs 65.91%)(P<0.05).The total incidence of arterial plaque in patients in the diabetic cerebral infarction group was 96.77% higher(69.32%),while the incidence of necrotic lipid core plaque was 58.06%higher(26.14%)(P<0.05).Receiver operating characteristic curve analysis was performed to assess the diagnosis utility of these techniques.MRI in combination with serum endoglin and Gal-3 had the highest area under the curve,the Yoden index,sensitivity and specificity(P<0.05).CONCLUSION The expression of serum endolipin and Gal-3 in elderly patients with diabetes mellitus with cerebral infarction showed an elevated trend,and the degree of luminal stenosis was severe.MRI predominantly revealed large and multiple infarct foci.This combined index examination can improve the clinical diagnosis of diabetes mellitus combined with cerebral infarction.

Effect of Acupuncture on Plasmic Levels of Insulin,Glucagon and Hypercoagulability in NIDDM Complicated by Acute Cerebral Infarction

Twenty-one cases of acute cerebral infarction secondary to NIDDM were treated with acupuncture and conventional therapy, and compared with 16 cases treated with conventional therapy alone. The results showed that acupuncture was more effective in reducing insulin and glucagon levels (P

Bilateral cerebral infarction in diabetic ketoacidosis and bilateral internal carotid artery occlusion:A case report and review of literature

BACKGROUND Diabetic ketoacidosis(DKA)is a serious complication of type 1 diabetes mellitus(T1DM).Very rarely does DKA lead to cerebral edema,and it is even rarer for it to result in cerebral infarction.Bilateral internal carotid artery occlusion(BICAO)is also rare and can cause fatal stroke.Moreover,case reports about acute cerebral infarction throughout both internal carotid arteries with simultaneous BICAO are very scarce.In this study,we present a patient with BICAO,T1DM,hypertension,and hyperlipidemia,who had a catastrophic bilateral cerebral infarction after a DKA episode.We briefly introduce BICAO and the mechanisms by which DKA results in cerebral infarction.CASE SUMMARY A 41-year-old woman presented with ischemic stroke that took place 3 mo prior over the left corona radiata,bilateral frontal lobe,and parietal lobe with right hemiplegia and Broca’s aphasia.She had a history of hypertension for 5 years,hyperlipidemia for 4 years,hyperthyroidism for 3 years,and T1DM for 31 years.The first brain magnetic resonance imaging not only revealed the aforementioned ischemic lesions but also bilateral internal carotid artery occlusion.She was admitted to our ward for rehabilitation due to prior stroke sequalae.DKA took place on hospital day 2.On hospital day 6,she had a new massive infarction over the bilateral anterior cerebral artery and middle cerebral artery territory.After weeks of aggressive treatment,she remained in a coma and on mechanical ventilation due to respiratory failure.After discussion with her family,compassionate extubation was performed on hospital day 29 and she died.CONCLUSION DKA can lead to cerebral infarction due to several mechanisms.In people with existing BICAO and several stroke risk factors such as hypertension, T1DM,hyperlipidemia, DKA has the potential to cause more serious ischemic strokes.

Exacerbated VEGF up-regulation accompanies diabetes-aggravated hemorrhage in mice after experimental cerebral ischemia and delayed reperfusion

Reperfusion therapy is the preferred treatment for ischemic stroke,but is hindered by its short treatment window,especially in patients with diabetes whose reperfusion after prolonged ischemia is often accompanied by exacerbated hemorrhage.The mechanisms underlying exacerbated hemorrhage are not fully understood.This study aimed to identify this mechanism by inducing prolonged 2-hour transient intraluminal middle cerebral artery occlusion in diabetic Ins2Akita/+mice to mimic patients with diabetes undergoing delayed mechanical thrombectomy.The results showed that at as early as 2 hours after reperfusion,Ins2Akita/+mice exhibited rapid development of neurological deficits,increased infarct and hemorrhagic transformation,together with exacerbated down-regulation of tight-junction protein ZO-1 and upregulation of blood-brain barrier-disrupting matrix metallopeptidase 2 and matrix metallopeptidase 9 when compared with normoglycemic Ins2+/+mice.This indicated that diabetes led to the rapid compromise of vessel integrity immediately after reperfusion,and consequently earlier death and further aggravation of hemorrhagic transformation 22 hours after reperfusion.This observation was associated with earlier and stronger up-regulation of pro-angiogenic vascular endothelial growth factor(VEGF)and its downstream phospho-Erk1/2 at 2 hours after reperfusion,which was suggestive of premature angiogenesis induced by early VEGF up-regulation,resulting in rapid vessel disintegration in diabetic stroke.Endoplasmic reticulum stress-related pro-apoptotic C/EBP homologous protein was overexpressed in challenged Ins2Akita/+mice,which suggests that the exacerbated VEGF up-regulation may be caused by overwhelming endoplasmic reticulum stress under diabetic conditions.In conclusion,the results mimicked complications in patients with diabetes undergoing delayed mechanical thrombectomy,and diabetes-induced accelerated VEGF up-regulation is likely to underlie exacerbated hemorrhagic transformation.Thus,suppression of the VEGF pathway could be a potential approach to allow reperfusion therapy in patients with diabetic stroke beyond the current treatment window.Experiments were approved by the Committee on the Use of Live Animals in Teaching and Research of the University of Hong Kong[CULATR 3834-15(approval date January 5,2016);3977-16(approval date April 13,2016);and 4666-18(approval date March 29,2018)].

汉黄芩素干预糖尿病脑梗死模型大鼠的神经损伤

背景:汉黄芩素是黄芩根中提取的一种黄酮类化合物,既往研究表明汉黄芩素对脑缺血再灌注损伤有保护作用,还能降低糖尿病小鼠的血糖及其并发症,但其在糖尿病脑梗死中的作用及机制还不清楚。目的:探究汉黄芩素对糖尿病脑梗死大鼠神经损伤的影响,并探究其作用机制。方法:将SD大鼠随机分为6组:对照组、模型组、汉黄芩素低、中、高剂量组和汉黄芩素高剂量+RhoA激活剂组,每组10只。除对照组外,其余组通过腹腔注射链脲佐菌素和大脑中动脉闭塞法构建糖尿病脑梗死大鼠模型,汉黄芩素低、中、高剂量组分别灌胃10,20,40 mg/kg汉黄芩素,汉黄芩素高剂量+RhoA激活剂组灌胃40 mg/kg汉黄芩素并腹腔注射10 mg/kg溶血磷脂酸,对照组和模型组给予等量生理盐水,1次/d,连续7 d。末次给药结束后,各组大鼠进行神经功能缺损评分,检测血糖水平,TTC染色检测脑梗死体积,苏木精-伊红染色观察脑组织病理变化,ELISA试剂盒检测脑组织中肿瘤坏死因子α、白细胞介素6和丙二醛、超氧化物歧化酶水平,Western blot检测脑组织中RhoA、ROCK2蛋白表达。结果与结论:(1)与对照组相比,模型组大鼠神经元结构严重受损,细胞坏死、变性;神经功能缺损评分、血糖水平、脑梗死体积升高(P<0.05);脑组织中肿瘤坏死因子α、白细胞介素6、丙二醛水平升高(P<0.05),超氧化物歧化酶水平下降(P<0.05);脑组织中RhoA、ROCK2蛋白表达升高(P<0.05);(2)与模型组相比,汉黄芩素低、中、高剂量组神经元损伤改善,细胞变性和坏死减少;神经功能缺损评分、血糖水平、脑梗死体积下降(P<0.05);脑组织中肿瘤坏死因子α、白细胞介素6、丙二醛水平下降(P<0.05),超氧化物歧化酶水平升高(P<0.05);脑组织中RhoA、ROCK2蛋白表达下降(P<0.05);(3)与汉黄芩素高剂量组相比,汉黄芩素高剂量+RhoA激活剂组明显抑制糖尿病脑梗死大鼠上述指标的改善(P<0.05)。结果表明:汉黄芩素能够改善糖尿病脑梗死大鼠血糖水平,减轻脑梗死和神经损伤,其作用机制可能与抑制RhoA/ROCK信号通路有关。

尤瑞克林联合依达拉奉治疗2型糖尿病合并急性脑梗死患者的效果

目的:观察尤瑞克林联合依达拉奉治疗2型糖尿病合并急性脑梗死患者的效果。方法:选取2021年6月至2023年1月该院收治的120例2型糖尿病合并急性脑梗死患者进行前瞻性研究,按照随机数字表法将其分为对照组和观察组各60例。两组均给予常规降糖治疗,在此基础上,对照组给予依达拉奉治疗,观察组在对照组基础上联合尤瑞克林治疗。比较两组临床疗效、治疗前后糖脂代谢指标[空腹血糖(FPG)、总胆固醇(TC)、三酰甘油(TG)]水平、炎性因子[白细胞介素-6(IL-6)、可溶性血管细胞黏附分子-1(sVCAM-1)、高敏C反应蛋白(hs-CRP)]水平、血管内皮指标[血栓素B2(TXB2)、血管内皮生长因子(VEGF)、内皮素(ET-1)]水平及不良反应发生率。结果:观察组治疗总有效率为93.33%,高于对照组的75.00%,差异有统计学意义(P<0.05);治疗后,两组FPG、TC、TG水平均低于治疗前,且观察组低于对照组,差异有统计学意义(P<0.05);两组IL-6、sVCAM-1、hs-CRP水平均低于治疗前,且观察组低于对照组,差异有统计学意义(P<0.05);两组TXB2、VEGF、ET-1水平均低于治疗前,且观察组低于对照组,差异有统计学意义(P<0.05);两组不良反应发生率比较,差异无统计学意义(P>0.05)。结论:尤瑞克林联合依达拉奉治疗2型糖尿病合并急性脑梗死患者,可提高临床疗效,改善糖脂代谢指标水平,减轻机体炎症反应,降低血管内皮指标水平,效果优于单纯依达拉奉治疗。

急性脑梗死老年患者轻度认知障碍发生的影响因素

目的:探讨老年急性脑梗死(ACI)患者轻度认知障碍(MCI)发生情况及影响因素.方法:选取2023年1月至2024年1月本院收治的106例老年ACI患者为研究对象.依据简易智力状态(MMSE)评分,将其分为MCI组(n=22)与无MCI组(n=84).收集两组患者临床资料,采用多因素非条件Logistic回归法分析老年ACI患者发生MCI的影响因素.结果:本研究纳入的106例老年ACI患者中,发生MCI者为22例,MCI发生率为20.75%(22/106).两组患者年龄,合并糖尿病、原发性高血压及高脂血症占比比较,差异均有统计学意义(P<0.05).采用多因素非条件Logistic回归分析结果显示,年龄,合并原发性高血压、糖尿病及高脂血症,均是导致老年ACI患者发生MCI的独立危险因素(OR>1,P<0.05).结论:年龄、合并原发性高血压、合并糖尿病及高脂血症是老年ACI患者MCI发生的独立危险因素,应重点关注高龄和合并基础疾病患者,并尽早制定对症治疗措施,降低ACI患者MCI发生率.

急性脑梗死伴2型糖尿病的临床及治疗进展

急性脑梗死与糖尿病均是临床常见疾病,二者息息相关,常伴随发生,近年来其共病率呈现逐年上升趋势,因而日益受到医学界重视。高血糖不仅增加急性脑梗死的发病率,而且加剧脑损伤症状,极不利于患者预后。对急性脑梗死伴2型糖尿病临床及治疗的研究将有助于病情评估、治疗方案优化。本文就急性脑梗死伴2型糖尿病的发病机制、临床特征及治疗进展作一综述,旨在为临床提供参考。

2型糖尿病合并急性脑梗死患者血清ADA、 SERPINE1水平及临床意义

目的 探讨2型糖尿病(T2DM)合并急性脑梗死(ACI)患者血清腺苷脱氨酶(ADA)、纤溶酶原激活物抑制因子1(SERPINE1)水平及预后预测价值。方法 选择2019年3月至2023年3月西安工会医院收治的195例T2DM合并ACI患者为ACI组和174例单纯T2DM患者为对照组。比较ACI组、对照组及不同神经缺损程度及预后患者血清ADA、SERPINE1水平,分析T2DM合并ACI患者预后不良影响因素,以及各指标预测预后不良的价值。结果 ACI组血清ADA、SERPINE1水平高于对照组(P<0.05)。随着T2DM合并ACI患者神经缺损程度加重,血清ADA、SERPINE1水平升高(P<0.05)。预后不良组血清ADA、SERPINE1水平高于预后良好组(P<0.05)。重度神经缺损及高水平ADA、SERPINE1、HbA1c是T2DM合并ACI患者预后不良的危险因素(P<0.05)。ADA、SERPINE1联合预测T2DM合并ACI患者预后的曲线下面积为0.896,高于单独预测(P<0.05)。结论 T2DM合并ACI患者血清ADA、SERPINE1水平升高与神经缺损程度较重和预后不良有关,联合检测可预测T2DM合并ACI患者预后不良。

探讨系统化护理在脑梗死合并糖尿病患者中的应用效果

目的 分析系统化护理在脑梗死合并糖尿病患者中的应用效果。方法 选取2022年12月—2023年12月兰陵县人民医院收治的78例脑梗死合并糖尿病患者作为研究对象,根据不同的护理方法分为对照组、观察组,各39例。对照组实施传统护理,观察组实施系统化护理,比较两组转归情况[肢体运动功能(Fugelmeyer Assessment, FMA)、日常生活活动能力(Activities of Daily Living, ADL)]、血糖指标、生活质量评分、护理满意度。结果 观察组FMA、ADL、生活质量评分均高于对照组,空腹血糖、餐后2 h血糖水平均低于对照组,护理满意率高于对照组,差异有统计学意义(P均<0.05)。结论 系统化护理可控制脑梗死合并糖尿病患者疾病发作,改善其血糖水平,提高其生活质量和护理满意度。

刍议脑梗死合并糖尿病患者实施综合康复护理的应用价值

目的分析针对脑梗死合并糖尿病患者开展基于综合康复护理的应用价值。方法选取2022年10月—2023年10月兰陵县人民医院收治的78例脑梗死合并糖尿病患者作为研究对象,采用随机数表法分为两组,各39例。参照组实施常规护理,研究组行综合康复护理,比较两组患者健康知识掌握程度相关评分、血糖指标、焦虑自评量表评分、抑郁自评量表评分。结果研究组健康知识掌握程度相关评分高于参照组,血糖指标低于参照组,焦虑、抑郁自评量表评分低于参照组,差异有统计学意义(P均<0.05)。结论实施综合康复护理效果好,对脑梗死合并糖尿病患者较为适用。

利拉鲁肽联合二甲双胍缓释片在脑梗死合并糖尿病患者中的效果及对血液流变学的影响研究

目的分析在脑梗死合并糖尿病患者中应用利拉鲁肽联合二甲双胍缓释片的治疗效果及对血液流变学的影响。方法选择2023年1—12月昌乐县人民医院收治的88例脑梗死合并糖尿病患者为研究对象,按照治疗方案不同,分为对照组(在脑梗死治疗的基础上给予二甲双胍缓释片治疗)和观察组(在对照组基础上联合利拉鲁肽治疗),各44例,比较两组的治疗总有效率、血糖(空腹血糖、餐后2 h血糖)水平与血液流变学指标(D-二聚体、纤维蛋白原)。结果观察组治疗总有效率高于对照组,差异有统计学意义(P<0.05)。治疗后,观察组血糖水平低于对照组,差异有统计学意义(P均<0.05)。治疗后,观察组的纤维蛋白原与D-二聚体水平均低于对照组,差异有统计学意义(P均<0.05)。结论利拉鲁肽联合二甲双胍缓释片对糖尿病合并脑梗死患者具有较好的治疗效果,同时具有改善血液流变学的作用。但在临床上,还需要针对患者的个体差异,对其进行定期监测,才能保证患者取得较好的疗效。

综合护理对脑梗死合并糖尿病患者的护理效能分析

目的分析脑梗死并糖尿病实施综合护理的影响。方法选取2022年12月—2023年12月兰陵县人民医院收治的72例脑梗死合并糖尿病患者为研究对象,以奇偶数分为两组,各36例,普通组为传统护理,综合组为综合护理,比较两组护理效能、不良情绪评分、血糖指标、护理满意率。结果施护后,两组护理效能评分高于施护前,且综合组高于普通组,差异有统计学意义(P<0.05)。施护后,两组不良情绪评分均降低,且综合组低于普通组,差异有统计学意义(P<0.05)。施护后,两组血糖指标均降低,且综合组低于普通组,差异有统计学意义(P<0.05)。综合组护理满意率为97.22%,高于普通组的77.78%,差异有统计学意义(χ^(2)=6.222,P<0.05)。结论综合护理对提升自我效能有正面影响,可减轻情绪问题,使患者血糖得到控制,利于稳定脑梗死合并糖尿病患者的病情,提高护理满意率。

血清NT-pro-BNP、MMP-2水平与糖尿病合并急性脑梗死患者冠状动脉病变程度的关系

目的探讨血清N末端脑钠肽前体(NT-pro BNP)、基质金属蛋白酶-2(MMP-2)水平与糖尿病合并急性脑梗死(ACI)患者冠状动脉病变程度的关系。方法选择首都医科大学电力教学医院2021年1月—2022年12月收治的126例糖尿病合并ACI患者为观察组,其中单支病变62例,双支病变33例,三支病变31例,轻度狭窄37例,中度狭窄43例,重度狭窄46例。另将同期于我院体检的60例单纯糖尿病患者纳为对照组以及60例健康体检者设为正常组。比较三组心肌肌钙蛋白I(cTnI)、肌酸激酶同工酶MB(CK-MB)、NT-pro BNP、MMP-2、I型胶原交联羧基末端肽(ICTP)水平;以ROC分析NT-pro BNP、MMP-2诊断糖尿病患者并发ACI的价值;比较不同冠状动脉病变支数及不同冠状动脉狭窄程度患者NT-pro BNP、MMP-2、ICTP水平;以Spearman秩相关分析NT-pro BNP、MMP-2、ICTP水平与冠状动脉病变支数、冠状动脉狭窄程度之间的相关性。结果观察组cTnI、CK-MB、NT-pro BNP、MMP-2、ICTP水平显著高于对照组(P<0.05),对照组cTnI、CK-MB、NT-pro BNP、MMP-2、ICTP水平显著高于正常组(P<0.05)。ROC结果显示,NT-pro BNP、MMP-2诊断糖尿病患者并发ACI训练集的曲线下面积为0.953、0.872,测试集的曲线下面积为0.902、0.842(P均<0.05)。NT-pro BNP、MMP-2、ICTP水平随着冠状动脉病变支数的增加及冠状动脉狭窄程度的加重而上升(P<0.05)。NT-proBNP、MMP-2、ICTP水平与糖尿病合并ACI患者冠状动脉病变支数、冠状动脉狭窄程度呈正相关(均有P<0.05)。结论NT-pro BNP、MMP-2、ICTP水平与糖尿病合并ACI患者冠状动脉病变支数、冠状动脉狭窄程度呈正相关,临床关注以上指标可对糖尿病合并ACI患者冠状动脉病变程度进行评估。

糖尿病合并急性脑梗死患者采取胰岛素强化治疗的效果及对血糖水平的影响

目的分析糖尿病合并急性脑梗死患者采取胰岛素强化治疗的疗效。方法回顾性选取2022年6月—2023年12月福建医科大学附属龙岩第一医院收治的102例糖尿病合并急性脑梗死患者的临床资料,根据治疗方法不同分为两组,各51例。对照组采用常规治疗,研究组采用胰岛素强化治疗。比较两组临床疗效、血糖水平、胰岛功能。结果研究组治疗总有效率高于对照组,差异有统计学意义(P<0.05)。治疗后,研究组空腹血糖、餐后2 h血糖水平均低于对照组,差异有统计学意义(P均<0.05)。治疗后,研究组空腹胰岛素、胰岛素抵抗指数低于对照组,胰岛β细胞功能指数高于对照组,差异有统计学意义(P均<0.05)。结论糖尿病合并急性脑梗死患者采取胰岛素强化治疗能够降低血糖水平、改善胰岛功能,提高临床疗效。

个体化饮食指导结合运动疗法在糖尿病合并脑梗死患者治疗中的应用效果研究

目的分析个体化饮食指导结合运动疗法在糖尿病合并脑梗死患者中的作用。方法选取2023年2—7月泉州市第一医院收治的212例糖尿病合并脑梗死患者为研究对象,采用随机数表法将患者分为研究组和对照组,每组106例。对照组患者实施常规干预,研究组结合个体化饮食指导与运动疗法。比较两组血糖指标、日常生活能力及生活质量评分。结果研究组各项血糖指标水平均低于对照组,日常生活能力评分低于对照组,生活质量评分高于对照组,差异有统计学意义(P均<0.05)。结论个体化饮食指导联合运动疗法能够帮助糖尿病合并脑梗死患者降低血糖水平,提高日常生活能力及生活质量。

普罗布考联合瑞舒伐他汀治疗T2DM并脑梗死的效果及对血清内脂素及Hcy的影响研究

目的:探讨普罗布考对2型糖尿病(Type 2 diabetes mellitus,T2DM)并脑梗死患者血清内脂素及同型半胱氨酸(Homocysteine,Hcy)的影响。方法:选取2021年1月至2022年12月于我院治疗的82例T2DM并脑梗死患者作为研究对象。按随机数字表法将患者分为对照组和研究组,各41例。对照组采用瑞舒伐他汀治疗;观察组在对照组的基础上联合普罗布考治疗。分析比较两组的临床疗效、血清内脂素、Hcy、颈动脉内膜斑块面积、颈动脉内膜中膜厚度(Carotid intima-media thickness,CAIMT),及不良反应。结果:观察组的治疗总有效率明显高于对照组(P<0.05)。治疗后,两组内脂素和Hcy水平、斑块面积和CAIMT均明显低于治疗前,且观察组明显低于对照组(P<0.05)。两组的不良反应发生率无明显差异(P>0.05)。结论:T2DM并脑梗死患者采用普罗布考联合瑞舒伐他汀治疗能够控制患者病情,缩小颈动脉斑块面积、CAIMT,降低血清内脂素及Hcy水平,改善患者神经功能,且并未增加明显不良反应。

Expression and significance of angiostatin, vascular endothelial growth factor and matrix metalloproteinase-9 in brain tissue of diabetic rats with ischemia reperfusion

Objective: To discuss the expression and significance of angiostatin, vascular endothelial growth factor and matrix metalloproteinase-9 in the brain tissue of diabetic rats with ischemia reperfusion. Methods: A total of 60 male Wistar rats were randomly divided into the normal group, sham group, diabetic cerebral infarction group and single cerebral infarction group according to the random number table, with 15 rats in each group. The high sucrose diet and intraperitoneal injection of streptozotocin were performed for the modeling of diabetic rats, while the thread-occlusion method was employed to build the model of cerebral ischemia reperfusion. The immunohistochemical staining was performed to detect the expression of angiostatin, vascular endothelial growth factor(VEGF) and matrix metalloproteinase-9(MMP-9) in the brain tissue. Results: The expression of angiostatin after the reperfusion in the brain tissue of rats in the single cerebral infarction group and diabetic cerebral infarction group was increased 6 h after the reperfusion, reached to the peak on 1 d and then decreased gradually. The expression of angiostatin in the diabetic cerebral infarction group 6 h, 1 d, 3 d and 7 d after the reperfusion was significantly higher than that in the single cerebral infarction group(P<0.05). VEGF began to be increased 1 h after the reperfusion in the single cerebral infarction group and diabetic cerebral infarction group, reached to the peak at 6 h and then decreased gradually. The expression of VEGF in the diabetic cerebral infarction group at each time point after the reperfusion was significantly lower than that in the single cerebral infarction group(P<0.05). MMP-9 began to be be increased 1 h after the reperfusion in the single cerebral infarction group and diabetic cerebral infarction group, reached to the peak on 1 d and then decreased gradually. The expression of MMP-9 in the diabetic cerebral infarction group at each time point after the reperfusion was significantly higher than that in the single cerebral infarction group(P<0.05). Conclusions: The high glucose environment in which the diabetic cerebral infarction is occurred is to induce the formation of MMP-9 at first and then activate and increase the expression of angiostatin. Afterwards, the expression of VEGF is inhibited, resulting in the poor angiogenesis after cerebral infarction, which thus makes the injury of brain tissue after cerebral infarction even worse than the non-diabetes mellitus.

Pathogenesis of diabetic cerebral vascular disease complication

Diabetes mellitus is one of the most potent independent risk factors for the development of diabetic cerebral vascular disease(CVD). Many evidences suggested that hyperglycemia caused excess free fatty acids, the loss of endothelium-derived nitric oxide, insulin resistance, the prothrombotic state, endothelial dysfunction, the abnormal release of endothelial vasoactivators,vascular smooth muscle dysfunction, oxidative stress, and the downregulation of mi Rs participated in vessel generation and recovery as well as the balance of endotheliocytes. In turn, these abnormalities, mainly via phosphatidylinositol 3 kinase, mitogen-activated protein kinase, polyol, hexosamine, protein kinase C activation, and increased generation of advanced glycosylation end products pathway, play an important role in inducing diabetic CVD complication. A deeper comprehension of pathogenesis producing diabetic CVD could offer base for developing new therapeutic ways preventing diabetic CVD complications, therefore, in the paper we mainly reviewed present information about the possible pathogenesis of diabetic CVD complication.