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红细胞膜中的血小板活化因子乙酰水解酶。活性降低是否会损害缺血性中风患者的红细胞变形能力?

Platelet-activating factor acetylhydrolase in red cell membranes. Does decreased activity impair erythrocyte deformability in ischemic stroke patients?

作者信息

Yoshida H, Satoh K, Takamatsu S

机构信息

Department of Pathologic Physiology, Hirosaki University School of Medicine, Japan.

出版信息

Stroke. 1993 Jan;24(1):14-8. doi: 10.1161/01.str.24.1.14.

Abstract

BACKGROUND AND PURPOSE

Platelet-activating factor acetylhydrolase hydrolyzes platelet-activating factor (1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine). It also hydrolyzes oxidized derivatives of phosphatidylcholine that have a short-chain acyl residue at the sn-2 position. This enzyme may act mainly in the degradation of oxidized phospholipids and may play a role in maintaining erythrocyte deformability. Therefore, we assessed the activity of red cell membrane platelet-activating factor acetylhydrolase in patients with ischemic stroke and studied the relation of the enzyme activity to red cell deformability.

METHODS

Enzyme activity was measured in the detergent extract of red cell membranes from 38 patients with cerebral thrombosis and 38 age-matched healthy volunteers. Red cell filterability, an index of red cell deformability, was also measured.

RESULTS

The enzyme activity in patients and control subjects was 100 +/- 74 and 148 +/- 128 nmol/g protein per minute (2.68 +/- 2.11 and 3.79 +/- 2.46 pmol/10(9) cells per minute) (mean +/- SD), respectively, and the difference was significant (p < 0.05 by the Mann-Whitney U test, two-sided test). Enzyme activity was correlated positively with red cell filterability in the patients (n = 20, r = 0.565, p < 0.01).

CONCLUSIONS

Red blood cells from stroke patients have lower levels of platelet-activating factor acetylhydrolase activity when compared with those from healthy subjects. This may result in the accumulation of oxidized lipids in the cell membrane and lead to impaired red cell deformability in patients with cerebral thrombosis.

摘要

背景与目的

血小板活化因子乙酰水解酶可水解血小板活化因子(1-O-烷基-2-乙酰-sn-甘油-3-磷酸胆碱)。它还能水解在sn-2位带有短链酰基残基的磷脂酰胆碱氧化衍生物。该酶可能主要作用于氧化磷脂的降解,并可能在维持红细胞变形性方面发挥作用。因此,我们评估了缺血性中风患者红细胞膜血小板活化因子乙酰水解酶的活性,并研究了该酶活性与红细胞变形性的关系。

方法

测定了38例脑血栓形成患者和38例年龄匹配的健康志愿者红细胞膜去污剂提取物中的酶活性。还测量了红细胞滤过率,这是红细胞变形性的一个指标。

结果

患者和对照组的酶活性分别为每分钟100±74和148±128 nmol/g蛋白质(每分钟2.68±2.11和3.79±2.46 pmol/10⁹细胞)(均值±标准差),差异有统计学意义(曼-惠特尼U检验,双侧检验,p<0.05)。患者的酶活性与红细胞滤过率呈正相关(n = 20,r = 0.565,p<0.01)。

结论

与健康受试者相比,中风患者的红细胞血小板活化因子乙酰水解酶活性较低。这可能导致细胞膜中氧化脂质的积累,并导致脑血栓形成患者的红细胞变形性受损。

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