Association of the Platelet Glycoprotein Ia C807T Gene Polymorphism With Risk of Myocardial Infarction in Chinese

Objectives To investigate the relationship of the GPIa C807T dimorphism to the risk of myocardial infarction （MI） in Chinese. Methods We did a case-control study including 100 patients and 110 controls with same race. An allele-specific polymerase chain reaction （PCR） was used for genotyping of C807T polymorphism. Results An apparent association was found between the T807 allele and MI among individuals younger than the mean age of 60 years （odds ratio, 2. 49 ; 95 % confidence interval, 1.08 - 6.22 ）. The T807 allele remained an independent risk factor for MI when age, sex, smoking, hypertension, diabetes, bodymass index, LDL-cholesterol and HDL-cholesterol were adjusted by logistic regression. Conclusions GPIa T807 appears to be an independent risk factor for MI.

Effect of Xiaoyu Zhixue Tablet (消瘀止血片) on Expression ofPlatelet Membrane Glycoproteins in Patients withHemorrhagic Thrombopathy

Objective: To observe the effect of Xiaoyu Zhixue tablet (消瘀止血片,XYZXT) on the expression of platelet membrane glycoproteins in patients with hemorrhagic thrombopathy, and to explore its possible mechanism. Methods: The total of 148 patients with hemorrhagic thrombopathy were randomly divided into two groups, the traditional Chinese medicicne (TCM) group (n=98) treated with XYZXT and the Western medicine (WM) group (n=50) treated with adrenosin, vitamins C, K and P, both for 6 months. The therapeutic effect and the recovery rate of platelet aggregation in the two groups were observed. And platelet membrane glycoprotein (GP) Ⅰb/Ⅸ, GPⅡb/Ⅲa complexes, GPⅠb, GPⅡb, GP Ⅲa and P-selectin were analyzed by flow cytometry in both groups before and after treatment and also in 34 normal healthy subjects. Results: The total effective rate of hemostasis was 89. 8% in TCM group and 54. 0% in the WM group (x2=45.83, P<0.01), and the recovery rate of platelet aggregation was 72.4% and 4.0% respectively (x2=62.06, P<0.01). The fluorescence intensity of GP Ⅰ b/Ⅸ, GPⅡb/Ⅲa complexes, GPⅠb, GPⅢa and P-selectin were lower in both groups before treatment than those in the healthy subjects. Expression of above-mentioned marks was elevated in TCM group after 6 months' therapy, which was insignificantly different as compared with the healthy subjects (P>0.05) and higher than those in the WM group (P<0.05). Conclusion: One of the mechanisms in treating hemorrhagic thrombopathy with XYZXT is that it could regulate the expression of GP Ⅰb/Ⅸ, GPⅡ b/Ⅲa complexes, GPⅠb, GPⅢa and P-selectin at the level of receptor protein.

Expression of Platelet Membrane Glycoprotein Ib/Ⅸ/Ⅴ Complex,a Receptor of Thrombin,in Patients with Hemorrhagic Thrombopathy

To investigate the role of platelet membrane glycoprotein （GP） Ib/Ⅸ/Ⅴ complex and its subunit GP Ibα in patients with hemorrhagic thrombopathy （HT）, the expressions of GP Ib/Ⅸ/Ⅴ complex and GP Ibα,defined as mean fluorescence intensity （MFI）, were assessed by flow cytometry. The maximum aggregation of platelet was determined by turbidity method. These indicators were compared among 68 HT patients with the presenting complaint of hemorrhage, 33 well-controlled HT patients and 32 normal healthy subjects. The results showed that the MFI of GP Ib/Ⅸ /Ⅴ complex and GP Ibα was markedly lower in HT patients with current hemorrhage than that in the healthy subjects, with difference being statistically significant （P〈0.05）. There was no significant difference in the expressions of GP Ib/ Ⅸ/ Ⅴ complex and GP Ibα between well-controlled HT patients and normal healthy subjects （P〉0.05）. It was concluded that the expression of GP Ib/Ⅸ /Ⅴ complex, the receptor of thrombin and von Willebrand factor, was down-regulated in HT patients with current hemorrhage, which might result in the dysfunction of platelet aggregation and recurrence of HT.

Association of the Platelet Membrane Glycoprotein Ⅰa C807T Gene Polymorphism with Aspirin Resistance

To explore the correlation between the C807T polymorphism of platelet membrane glycoprotein Ⅰa （GP Ⅰa） gene and aspirin resistance in Chinese people, 200 patients with high-risk of atherosclerosis took aspirin （100 mg/d） for 7 days. Platelet aggregation function was detected using adenosine diphosphate （ADP） and arachidonic acid （AA） before and after the administration of aspirin. Then the subjects were divided into three groups according to the results of platelet aggregation function： an aspirin resistant （AR） group, an aspirin semi-responder （ASR） group and an aspirin-sensitive （AS） group. Platelet GP Ⅰa gene 807CT polymorphism was examined by means of polymerase chain reaction-sequence specific primers （PCR-SSP）. The results showed that T allelic frequency in AR group and ASR group were higher that of AS group （P〈0.005）, and the prevalence of genotypes （TT＋TC） of these two groups was significantly higher than that in AS group （P〈0.05）. Platelet GP Ⅰa T allele was significantly associated with aspirin resistance as revealed by multiple logistic regression （OR=3.76, 95% CI： 2.87-9.58）. The results suggest that inherited platelet GP Ⅰa variations may have an important impact on aspirin resistance and the presence of GP Ⅰa T allele may be a marker of genetic susceptibility to aspirin resistance.

Redistribution of Platelet Membrane Glycoprotein IV and Release of Intracellular α-granule Thrombospondin in Patients with Chronic Myelogenous Leukemia

The redistribution of platelet membrane glycoprotein IV (GPIV) and the release of intracellular Q-granule thrombospondin (TSP) were examined and the inhibition of 5-thromboglobulin (&TG) and platelet factor 4 (PF4) in patients with chronic myelogenous leukemia (CML) was observed and quantitation of β-TG and PF4 in sera was conducted. GPIV in inactive platelet from CML was 36080±17010 molecules/platelet as compared with 13190±4810 from the controls (P<0,01), No abnormality was found in the distribution of platelet membrane GPIb and GPIIb/III.(P>0. 05). The GPIV redistribution on active platelet membrane induced thrombin (1U/ml) from CML and healthy donors was 44320132310 and 228001 12700 molecules/platelet respectively (P<0. 01 ). The difference in the release of intracellular Q-granule TSP between CML and the control group was not found (P>0.05). There was no direct correlation between GPIV expression and TSP binding after platelet activation. The high leveIs of β-TG and PF4 in sera inhibited release of intracellular a-granule TSP in vitro. These results indicate that the abnormality of platelet membrane GPIV is a common marker in CML, therefore the specific increase of platelet GPIV in patients with CML may be a useful tool for the diagnosis and monitoring of the platelet dysfunction. The release of interna1 TSP pools is hindered by either β-TG or PF4 in sera.

Relationship and significance between anti-b2-glycoproteinⅠantibodies and platelet activation state in patients with ulcerative colitis

AIM:To study the relationship between anti-b2-glycoprotein Ⅰ (ab2GPⅠ) antibodies and platelet activation state in patients with ulcerative colitis (UC) and its significance. METHODS:Peripheral blood samples were collected from 56 UC patients (34 males and 22 females, aged 43.5 years, range 21-66 years), including 36 at active stage and 20 at remission stage, and 25 sex-and age-matched controls. The level of ab2GPⅠ was measured by ELISA. The platelet activation markers, platelet activation complex-Ⅰ (PAC-Ⅰ) and P-selectin (CD62P) were detected by flow cytometry. RESULTS:The A value for IgG ab2GPⅠ in the active UC group was 0.61 ± 0.13, significantly higher than that in the remittent UC and control groups (0.50 ± 0.13 and 0.22 ± 0.14, P < 0.01). There was a significant difference between the two groups (P < 0.01). The A value for IgM ab2GPⅠ in the active and remittent UC groups was 0.43 ± 0.13 and 0.38 ± 0.12, significantly higher than that in the control group (0.20 ± 0.12, P < 0.01). However, there was no significant difference between the two groups (P > 0.05). The PAC-Ⅰ positive rate for the active and remittent UC groups was 30.6% ± 7.6% and 19.6% ± 7.8% respectively, significantly higher than that for the control group (6.3% ± 1.7%, P < 0.01). There was a significant difference between the two groups (P < 0.01). The CD62P positive rate for the active and remittent UC groups was 45.0% ± 8.8% and 31.9% ± 7.8% respectively, significantly higher than that for the control group (9.2% ± 2.7%, P < 0.01). There was a significant difference between the two groups (P < 0.01). In the active UC group, the more severe the state of illness was, the higher the A value for IgG ab2GPⅠ was, and the positive rate for PAC-I and CD62P was positively correlated with the state of illness (Fab2GPⅠ = 3.679, P < 0.05;FPAC-I (%) = 5.346, P < 0.01;and FCD62P (%) = 5. 418, P < 0.01). Meanwhile, in the same state of illness, the A value for IgG ab2GPⅠ was positively correlated to the positive rates for PAC-I and CD62P. CONCLUSION:ab2GPⅠ level, platelet activation state and their relationship of them are closely correlated with the pathogenesis and development of UC.

原发与继发免疫性血小板减少症患者血小板膜糖蛋白特异性抗体及其与出血评分关系的研究

目的探讨原发与继发免疫性血小板减少症(ITP)患者抗GPⅡb/Ⅲa及GPΙb/Ⅸ抗体的表达、抗体阳性表达与出血评分的关系,以及不同抗体类型出血评分的差异,为原发与继发ITP患者的诊治和出血严重程度提供临床依据。方法选取2013年10月—2020年8月在新疆医科大学第一附属医院诊断为原发ITP患者(42例)及继发ITP患者(42例)为研究对象,所有患者入院时采用ITP出血评分量表行出血评分。应用改良MAIPA法检测患者抗GPⅡb/Ⅲa和抗GPΙb/Ⅸ抗体。结果原发与继发组患者抗GPⅡb/Ⅲa抗体、抗GPΙb/Ⅸ抗体阳性率比较,差异无统计学意义(P>0.05),原发组患者抗体表达以抗GPⅡb/Ⅲa抗体为主,继发组抗体表达以抗GPΙb/Ⅸ抗体为主,两者抗体阳性构成比较,差异有统计学意义(P<0.05)。继发组患者整体出血程度较原发组重(P<0.05)。抗体阳性表达与出血程度的关系:(1)抗GPⅡb/Ⅲa抗体阳性患者出血程度较抗体阴性患者重(P<0.05)。(2)抗GPΙb/Ⅸ抗体阳性患者出血程度较抗体阴性患者重(P<0.05),双抗体阳性患者出血程度较抗体阴性患者重(P<0.05)。结论抗GPⅡb/Ⅲa抗体、抗GPΙb/Ⅸ抗体阳性表达对原发与继发ITP无鉴别意义,但原发ITP患者抗体表达以抗GPⅡb/Ⅲa抗体为主,继发ITP患者抗体表达以抗GPΙb/Ⅸ抗体为主。继发ITP患者临床出血程度较原发ITP患者重。抗GPⅡb/Ⅲa抗体、抗GPΙb/Ⅸ抗体及抗体双阳性患者出血程度较抗体阴性患者重。

慢性非缺血性心力衰竭患者血小板PAC-1和CD62p的表达及其与心功能的关系

目的探讨慢性非缺血性心力衰竭患者血小板膜糖蛋白纤维蛋白原受体(PAC-1)和P选择素(CD62p)的表达及其与心功能的关系。方法选取2019年1月至2022年1月天津市南开医院收治的185例慢性非缺血性心力衰竭患者作为观察组,根据纽约心脏病学会(NYHA)心功能分级将观察组患者分为心功能Ⅱ级组58例、心功能Ⅲ级组88例和心功能Ⅳ级组39例,根据左室射血分数(LVEF)将观察组患者分为射血分数保留心衰组(HFpEF)123例、射血分数临界值心衰组(HFmrEF)25例和射血分数下降心衰组(HFrEF)37例,再以B型钠尿肽(BNP)中位数为界将观察组患者分为高BNP组109例和低BNP组76例;另选取同期心功能正常的就诊者55例作为对照组。比较各组患者的基本临床信息、生化、BNP指标和PAC-1、CD62p的表达水平,采用Pearson相关分析法分析PAC-1、CD62p水平与BNP、LVEF的关系。结果观察组患者的PAC-1、CD62p水平分别为(23.67±16.54)%、(10.43±9.19)%,明显高于对照组的(9.33±9.63)%、(4.24±5.49)%,差异均有统计学意义(P<0.05);不同心功能分级患者对比发现,PAC-1、BNP水平为Ⅳ级>Ⅲ级>Ⅱ级>对照组,CD62p水平为Ⅳ级>Ⅲ级、Ⅱ级>对照组,差异均有统计学意义(P<0.05);不同LVEF分级患者对比发现,PAC-1水平为HFrEF组>HFmrEF组、HFpEF组>对照组,BNP水平为HFrEF组>HFmrEF组>HFpEF组>对照组,HFpEF组、HFmrEF组、HFrEF组CD62p水平分别为(10.72±9.17)%、(9.87±11.19)%、(9.84±7.88)%,明显高于对照组的(4.24±5.49)%,差异均有统计学意义(P<0.05);高BNP组患者的PAC-1、CD62p分别为(26.97±16.94)%、(11.05±9.62)%,明显高于低BNP组的(13.80±12.82)%、(6.97±7.54)%,差异均有统计学意义(P<0.05);经Pearson相关分析结果显示,PAC-1、CD62p与BNP呈正相关(r=0.363、0.182,P<0.05),PAC-1与LVEF呈负相关(r=-0.297,P<0.05)。结论慢性非缺血性心力衰竭患者的PAC-1、CD62p水平均明显增高,且与心功能有关,检测其水平有助于为患者的病情评估及临床治疗提供参考依据。

替罗非班辅助血管内治疗急性缺血性脑卒中的疗效评估研究进展

急性缺血性脑卒中(AIS)是脑组织缺血缺氧而引起神经功能损伤的临床综合征。抗血小板治疗是缺血性脑卒中预防及治疗的基础。目前,AIS血管内治疗主要方法有机械取栓、血栓抽吸、动脉溶栓、支架植入等,可有效改善血运及临床症状。但血管内治疗可能会损伤血管内皮细胞,导致血小板聚集及血栓形成。血管内治疗的围手术期使用抗血小板药物是降低手术期间和术后发生血栓形成、栓塞和缺血等并发症风险的常用治疗方法。近年来,有关AIS血管内治疗中抗血小板药物的应用,特别是血小板糖蛋白Ⅱb/Ⅲa(GPⅡb/Ⅲa)受体拮抗剂,使AIS血管内治疗的发展前景充满希望。目前,美国食品药品监督管理局发布的GPⅡb/Ⅲa受体拮抗剂有3种,分别为替罗非班、阿昔单抗和依替巴肽。替罗非班是国内临床中主要应用的GPⅡb/Ⅲa受体拮抗剂,GPⅡb/Ⅲa受体作为血小板聚集、血栓形成的最终通路,其拮抗剂通过直接与GPⅡb/Ⅲa受体结合,从而快速发挥抗血小板聚集的作用。替罗非班作为的新型抗血小板药物,在心血管疾病中的应用已经基本成熟,但是在脑血管疾病中的应用仍处于探索阶段,具体用法、用量及安全性仍有较多争议,且属于超说明书用药。该文就替罗非班在急性缺血性脑卒中血管内治疗中的应用及研究进展进行综述。

GPIa C807T和G873A基因多态性对血小板聚集抑制率的影响

目的:探讨GPIa C807T和G873A基因多态性对血小板聚集抑制率的影响,为临床个体化抗血小板聚集治疗提供实验数据支持。方法:收集正在使用阿司匹林抗血小板聚集治疗的住院患者80例,采用血栓弹力图仪检测血小板聚集抑制率,根据聚集抑制率检测结果分为阿司匹林抵抗(aspirin resistance,AR)组(共10例)和阿司匹林敏感(aspirin sensitivity,AS)组(共70例),分析GPIa C807T、G873A基因型及其等位基因在两组分布状况以及两者患者临床资料与实验检测指标关系。结果:AR组807T、873G等位基因高于AS组(χ^(2)=4.039、4.354,P=0.044、0.037);AR组高血压病史患病率、卒中史高于AS组(χ^(2)=4.612、4.737,P=0.032、0.030);AR组血浆D-二聚体(D-D)、血清甘油三酯(TG)高于AS组(t=2.499、2.276,P=0.016、0.033),而AR组血小板聚集抑制率、血清葡萄糖低于AS组(t=15.352、3.076,P<0.001、0.005)。结论:GPIa C807T和G873A基因多态性与AR存在相关性,建议联合检测两基因位点的多态性并结合血小板聚集抑制率,共同指导临床个体化抗血小板聚集治疗。

Platelet activation and the protective effect of aprotinin in hepatolithiasis patients

OBJECTIVE: To explore platelet activation and the protective effect of aprotinin in patients with hepatolithiasis. METHODS: The count of plaletets and levels of CD_(62P) and CD_(63) were measured by flow cytometry in 38 patients with hepatolithiasis. Several measurements were carried out after treatment with aprotinin. RESULTS: The levels of CD_(62P), CD_(63) in patients with hepalolithiasis were higher than those in patients with cholecystolithiasis (P<0.05), but the count of platelets was lower (P<0.05). After operation, the levels of CD_(62P), CD_(63) were significantly increased in patients with hepatolithiasis, but the count of platelets was lower (P<0.05). Postoperative levels of CD_(62P), CD_(63) were significantly lower in patients treated with aprotinin than in normal controls (P<0.05); but there was no significant change in the count of platelets in the two groups. CONCLUSION: Platelet activation occurs in patients with hepatolithiasis, and may be inhibited by aprotinin.

Pharmacological actions of miltirone in the modulation of platelet function

OBJECTIVE Salvia miltiorrhiza bunge contains various active constituents,some of which have been developed as commercially available medicine.Moreover,some other ingredients in Salvia miltiorrhiza play great roles in anti-platelet activity.The aim of the present study was to investigate the effects and the underlying mechanism of miltirone,a lipophilic compound of Salvia miltiorrhiza Bunge.METHODS The ability of miltirone to modulate platelet function was investigated by a variety of in vitro and in vivo experiments.Platelet aggregation and dense granule secretion induced by various agonists were measured with platelet aggregometer.Clot retraction and spreading were imaged by digital camera and fl uorescence microscope.Ferric chloride-induced carotid injury model and pulmonary thromboembolism model were used to check miltirone effect in vivo.To elucidate the mechanisms of anti-platelet activity of miltirone,flow cytometry and Western blotting were performed.RESULTS Miltirone(2,4,8 μmol·L^(-1)) was shown to suppress platelet aggregation,dense granule and α granule secretion in a dose-dependent manner.Meanwhile,miltirone inhibited the clot retraction and spreading of washed platelets.It reduced the phosphorylation of PLCγ2,PKC,Akt,GSK3β and ERK1/2 in the downstream signal pathway of collagen receptor.It also reduced the phosphorylation of Src and FAK in the integrin αⅡbβ3 mediated "outside-in" signaling,while it did not suppress the phosphorylation of β3.In addition,miltirone prolonged the occlusion time and reduced collagen/epinephrine induced pulmonary thrombi.CONCLUSION Miltirone suppresses platelet "inside-out" and "outside-in" signaling by affecting PLCγ2/PKC/ERK1/2,PI3K/Akt and Src/FAK signaling.Therefore,miltirone might represent a potential anti-platelet candidate for the prevention of thrombotic disorders.

Diagnosis of Disorders of Platelet Function by Flow Cytometry

The platelet membrane glycoprotein (GP)Ⅱ b/Ⅲ a, GPIX were detected by immunogold assay and flow cytometry, respectively, in two cases of Glannzmann's thrombasthenia (GT). The immunogold assay showed that the GPⅡ b/Ⅲ a gold granules in GT were decreased obviously, compared with that in normal controls. Flow cytometry results showed that GPⅡ b/Ⅲ a in two cases of GT was 0.1 % and 0.5 % of normal control, respectively. While GPIX showed no difference between the GT and normal control. The patients' father showed no bleeding symptoms, whose GPⅡ b/Ⅲ a accounted for 36.99 % of normal control. The experiment results suggested that flow cytometry is a quick, simple and sensitive method for the diagnosis of GP disorders.

Effect of the platelet membrane GPⅠa gene polymorphism in the pathogenesis of unstable angina pectoris

Objective: To investigate the effect of platelet membrane glycoprotein(GP) Ⅰa gene polymorphism in the pathogenesis of unstable angina pectoris (UAP) in Chinese people. Methods: Collagen type Ⅰ-induced platelet aggregation was measured in 33 healthy subjects in vitro. Plasma level of α-granule membrane protein (GMP-140) was measured in both the above 33 healthy subjects during fasting and 35 patients with recent onset effort anina during rest onset within 24 h after hospitalization. Furthermore, the platelet membrane GP Ⅰa gene 807C/T polymorphism was checked in all subjects with polymerase chain reaction-sequence specific primers(PCR-SSP) technique. Results: The lag time before 30% platelet aggregation was significantly longer in healthy subjects with CC genotype than with TC genotype (P<0.01). However, there was no significant difference in the maximal platelet aggregation between healthy subjects with the above two genotypes. Plasma level of GMP-140 was significantly higher in TC genotypic patients with recent onset effort angina than in CC genotypic patients with the same type of UAP(P<0.05) and healthy subjects (P<0.01), furthermore, there was also significant difference between the latter two groups(P<0.05). Conclusion: The rapid initiation of collagen-induced platelet aggregation may be associated with platelet membrane GP Ⅰa T (807) allele, which may play an important role in the pathogenesis of UAP.

MECHANISM OF PRESERVING EFFECT OF APROTININ ON PLATELET FUNCTION DURING CARDIOPULMONARY BYPASS

The deficiency of platelet function is the main defect of hemostatic mechanism during cardiopulmonary bypass (CPB), which attributed to the postoperative bleeding complication to a great extent. The proteinase inhibitor aprotinin was reported to have preserving effect on platelet adhesion during CPB. In this clinical reserch we found that CPB caused plasma alpha 2-antiplasmin decreasing, indicating the fibrinolytic system activation. Meanwhile, the ristocetin-induced aggregation declined to 39.6% and platelet GPIb decreased to 50% of preoperative value. However, by treatment with aprotinin, the plasma alpha 2-antiplasmin during CPB did not change, platelet aggregation was improved and platelet GPIb was preserved, and consequently resulted in a 46% lower blood loss postoperatively. These results confirmed that aprotinin could inhibit the fibrinolysis during CPB, and thus relieve the platelet damage and improve the postoperative hemostatic mechanism.

血小板膜糖蛋白特异性抗体在ITP患儿中的表达及其与疗效、出血程度的关系分析

目的分析血小板膜糖蛋白(GP)特异性抗体在免疫性血小板减少症(ITP)患儿中的表达情况及其与疗效、出血程度的关系。方法选取2018年2月至2020年12月于唐山市妇幼保健院儿科就诊的102例ITP患儿为研究对象,并将其纳入病例组,另选取同期同院进行体检的110例健康儿童纳入健康组。病例组患儿均接受糖皮质激素冲击疗法,以4周为1个疗程,共治疗5个疗程,并随访3个月。检测并比较两组GP特异性抗体表达情况,统计ITP患儿出血部位并分析不同GP特异性抗体出血程度、疗效及预后。结果病例组抗GPⅠb/Ⅸ抗体、抗GPⅡb/Ⅲa抗体表达水平高于健康组,差异有统计学意义(t值分别为16.521、51.718,P<0.05);102例ITP患儿抗GPⅠb/Ⅸ抗体阳性、抗GPⅡb/Ⅲa抗体阳性、双抗体阳性、双抗体阴性检出率分别为15.69%、4.90%、30.39%、49.02%,0级、1级、2级出血率分别为16.67%、50.00%、33.33%;且0级出血以双抗体阳性占比(0)最低,1级出血以抗GPⅡb/Ⅲa抗体阳性占比(80.00%)最高,2级出血以抗GPⅠb/Ⅸ抗体阳性、双抗体阳性占比(62.50%、48.39%)较高,差异有统计学意义(H=38.237,P<0.05);102例ITP患儿治疗5个疗程后有效率为78.43%,随访3个月后完全缓解率为68.63%;双抗体阴性ITP患儿有效率、完全缓解率均高于抗GPⅠb/Ⅸ抗体阳性、抗GPⅡb/Ⅲa抗体阳性、双抗体阳性ITP患儿,差异有统计学意义(χ^(2)值分别为19.866、27.709,P<0.05)。结论ITP患儿抗GPⅠb/Ⅸ抗体、抗GPⅡb/Ⅲa抗体表达水平较高,且其不同表达水平与患儿出血程度、疗效及预后均有密切关系,临床可通过监测GP特异性抗体来对ITP患儿进行早期诊断,并对其出血程度、疗效、预后等进行预测。

丹参饮对高脂血症模型大鼠血小板生理特性和功能的影响机制

目的基于血小板膜糖蛋白4(CD36)/磷脂酰肌醇3-激酶(PI3K)/蛋白激酶B(Akt)信号通路探讨丹参饮对高脂血症模型大鼠血小板生理特性和功能的影响机制。方法通过喂养高脂饮食复制高脂血症模型大鼠,将其随机分为模型组、辛伐他汀组(0.004 g/kg)和丹参饮高、低剂量组(3.6、0.9 g/kg),另设空白组(喂养基础饲料),每组10只。各给药组大鼠每天灌胃相应药物,其余组灌胃等体积生理盐水,连续4周。末次给药后,检测大鼠血脂生化指标[总胆固醇(TC)、三酰甘油(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)]含量,全血黏度、血浆黏度和血浆中纤维蛋白原(FIB)含量,血小板相关参数[血小板计数(PLT)、血小板分布宽度(PDW)和血小板平均体积(MPV)],血小板生理特性和功能相关因子[血管性血友病因子(vWF)、纤维连接蛋白(Fn)、磷脂酶A2(PLA2)、血栓素B2(TXB2)、6-酮-前列腺素F1α(6-keto-PGF1α)、血栓素A2(TXA2)、前列腺素(PGI2)、环磷酸腺苷(cAMP)、环磷酸鸟苷(cGMP)、β-血小板球蛋白(β-TG)]水平,血小板聚集率(最大聚集率、60 s聚集率、180 s聚集率)和纤溶系统相关因子[组织型纤溶酶原活化剂(t-PA)、纤溶酶原激活物抑制剂1(PAI-1)]水平,血小板中CD36/PI3K/Akt信号通路相关蛋白[CD36、黏着斑激酶(FAK)、磷脂酰肌醇4-磷酸5-激酶(PIP5K)、PI3K、磷酸化Akt(p-Akt)、p-Akt1/2/3]表达水平。结果与空白组比较,模型组大鼠血浆中TC、TG、LDL-C含量,全血黏度、血浆黏度、血浆中FIB含量,血浆中PLT、MPV、vWF、Fn、PLA2、TXB2、TXA2、cGMP、β-TG水平,血小板最大聚集率、60 s聚集率,血浆中PAI-1水平,CD36、FAK、PIP5K、PI3K、p-Akt、p-Akt1/2/3蛋白表达水平均显著升高(P<0.05);HDL-C含量和6-keto-PGF1α、PGI2、t-PA水平均显著降低(P<0.05)。经丹参饮干预后,上述大部分指标均显著逆转(P<0.05)。结论丹参饮可改善高脂血症模型大鼠血小板生理特性和功能,其作用机制可能与下调CD36/PI3K/Akt信号通路活性、降低血小板活化程度有关。

复方丹参滴丸联合氯吡格雷治疗门诊冠心病患者的效果

目的探讨复方丹参滴丸联合氯吡格雷用于门诊冠心病患者治疗的效果研究。方法选取济南市第二人民医院2018年1月至2020年11月收治的122例门诊冠心病患者作为研究对象,进行前瞻性研究,根据随机数字表法将其分为联合组和对照组。对照组61例,男30例、女31例,年龄32~81(55.67±7.21)岁,予以氯吡格雷治疗;联合组61例,男31例、女30例,年龄39~76(57.36±8.85)岁,在对照组基础上联合复方丹参滴丸治疗。两组患者均于治疗前、治疗1个月后评估临床疗效、血小板功能[血小板膜糖蛋白GpⅡb/Ⅲa复合物(PAC-1)、血小板最大聚集率]、凝血功能[D-二聚体(D-D)水平,抗凝血酶Ⅲ(AT-Ⅲ)水平]。组间比较采用t检验、χ^(2)检验、秩和检验。结果治疗前,两组PAC-1、血小板最大聚集率比较,差异均无统计学意义(均P>0.05)。治疗后,两组PAC-1、血小板最大聚集率较治疗前均降低(均P<0.05),且联合组PAC-1、血小板最大聚集率低于对照组(均P<0.05)。联合组临床疗效(95.08%,58/61)优于对照组(77.05%,47/61),差异有统计学意义(P<0.05)。治疗1个月,两组D-D水平高于治疗前(P<0.05),联合组高于对照组(P<0.05);AT-Ⅲ水平低于治疗前(P<0.05),且联合组低于对照组(P<0.05)。结论复方丹参滴丸联合氯吡格雷能提高门诊冠心病患者的治疗效果,改善患者血小板功能、凝血功能。

抗凝血酶Ⅲ和膜糖蛋白CD62P对特发性膜性肾病发生栓塞风险的研究

据研究统计,慢性疾病给人们造成巨大的经济损失,长期遗留的并发症也严重影响着人们的生活质量。肾脏病也逐渐增加,现在已成为常见慢性疾病,肾病综合征是其中常见类型。原发性肾病综合征的发病病理类型有20%是特发性膜性肾病,近年仍有上升的趋势。特发性膜性肾病常见且严重的并发症是血栓栓塞,血栓栓塞一旦发生会危及患者的生命安全并且严重影响预后与未来生活质量,因此预防血栓栓塞的发生有重要作用。本文探讨抗凝血酶Ⅲ与血小板膜糖蛋白CD62P这两个指标对发生血栓栓塞的风险预测。