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Objective To study the relationship between serum salusin-α and lipoprotein associated phospholipase A2(Lp-PLA2) in carotid unstable plaque with cerebral infarction. Methods One hundred patients with carotid unstable plaque confirmed by carotid ultrasound, divided into two groups as follows:cerebral infarction group (CI group, n = 50) or without cerebral infarction (plaque group, n = 50). We took 50 health subjects in the same period as control. The levels of serum salusin-α, Lp-PLA2 were detected by ELISA. Results Serum salusin-αlevel was significantly lower in the CI group than in the control group (P<0.01), and was also significantly lower in the CI group than in the plaque group (P < 0.01); Serum Lp-PLA2 level was obviously higher in CI group than in control group (P<0.05), and was also significantly higher in CI group than in plaque group (P < 0.05); The correlation between serum salusin-α level(OR = 0.140, 95% CI: 0.054-0.368, P<0.01) and cerebral infarction was significant in patients with unstable plaque. Conclusions The decrease of serum salusin-α level is significantly in patients with unstable plaque; the increase of Lp-PLA2 is significantly in patients with unstable plaque. The serum salusin-αlevel is a possible risk factor for cerebral infarction.
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Objective: To explore the changes and signiifcance of serum level of salusins in patients with essential hypertension (EH), obstructive sleep apnea hypopnea syndrome (OSAHS) and OSAHS complicated hypertension. Methods: Our research included 4 groups: EH+OSAHS group,n=50, EH group,n=60, OSAHS group,n=35 and Control group,n=31 healthy subjects. Blood pressure, AHI index, body weight, height and routine biochemical examination were conducted and recorded in all subjects, serum levels of salusin-α and salusin-β were detected by ELISA, the relationship between each variable and OSAHS complicated hypertension was studied by multivariate Logistic regression analysis. Results:①Serum levels of salusin-α were reduced accordingly as in Control group (7.438±1.626) pg/ml, in OSAHS group (6.186±1.200) pg/ml, in EH group (5.938±1.287) pg/ml and in EH+OSAHS group (5.299±1.398) pg/ml; for difference between OSAHS group and EH group,P>0.05 and for differences between other groups, allP0.05 and fordifferences between other groups, allP Conclusion: Low serum levels of salusin-α and salusin-β were related to OSAHS complicated hypertension.
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Objective: To explore the relationship of plasma salusin-α level with the stability, severity, and other risks of coronary atherosclerosis. Methods: The patient group included 122 hospitalized patients with coronary artery disease (CAD), whose diagnoses were confirmed by coronary angiography (CAG). The CAD group was further divided into subgroups according to the clinical types, the number of diseased coronary branches, and Gensini's scores. Control group inlcuded 60 healthy subjects who underwent physical examination in our hospital. Salusin-α level and other general biochemical indicators were determined, and the general clinical data were obtained before CAG in all subjects. Results: The peripheral blood salusin-α level in CAD patients was significantly lower than that in the controls ([0.50±0.18] ng/ml vs [0.69±0.23 ng/ml], P<0.01), and that in the acute coronary syndrome patients was significantly lower than that in the stable angina pectoris patients ([0.46±0.17] ng/ml vs [0.56±0.19] ng/ml, P<0.01). Salusin-α levels were not significantly different between patients with different Gensini's scores or between patients with 1, 2 and 3 diseased branches. Conclusion: Peripheral blood salusin-α level might be associated with stability of the CAD, but not with the severity of coronary atherosclerosis.