ABSTRACT
Objectives: To investigate the relationships between the stability of carotid plaque and serum Lp-PLA2, A-FABP levels in hypertensive postmenopausal women. Methods: 195 postmenopausal women with hypertension were selected and divided into non-plaque group, stable plaque group and unstable plaque group according to the results of carotid intima-media thickness (IMT) and plaque types derived from color doppler ultrasonography. In addition, 40 healthy postmenopausal women were recruited as normal control group. The serum Lp-PLA2 and A-FABP levels of all subjects were measured. Lp-PLA2 and A-FABP levels were compared among four groups by One-Way ANOVA. Spearman correlation analysis and multiple logistic regression analysis were also performed. Results: Plaque group included 123 subjects (unstable plaque group: 29 cases; stable plaque group: 94 cases), and non-plaque group included 72 subjects. The average serum A-FABP level was significantly higher in unstable plaque group [(172.60±33.70) ng/L] than in non-plaque group[(133.04±29.49) ng/L], P<0.05. Serum Lp-PLA2 level was similar between the four groups, P>0.05. Serum A-FABP level was positively correlated with the carotid plaque (r=0.3446, P=0.0049);serum Lp-PLA2 level was not correlated with the carotid plaque (r=0.2058, P=0.0996). Multiple logistic regression analysis showed that high A-FABP level was associated with stable plaque in hypertensive postmenopausal women (P=0.040, OR=1.017, 95%CI: 1.001~1.033), which was also associated with unstable plaque in this population (P=0.003, OR=1.031, 95%CI: 1.010~1.052). Conclusions: The level of A-FABP is a determinant responsible for the occurrence and stability of carotid plaque among hypertensive postmenopausal women. There was no correlation between Lp-PLA2 level and the stability of carotid plaque in this patient cohort.
ABSTRACT
The mechanisms of exercise-induced fatigue have not been investigated using proteomic techniques, an approach that could improve our understanding and generate novel information regarding the effects of exercise. In this study, the proteom alterations of rat skeletal muscle were investigated during exercise-induced fatigue. The proteins were extracted from the skeletal muscle of SD rat thigh, and then analyzed by two-dimensional electrophoresis and PDQuest software. Compared to control samples, 10 significantly altered proteins were found in exercise samples, two of them were upregulated and eight of them were downregulated. These proteins were identified by MALDI TOF-MS. The two upregulated proteins were identified as MLC1 and myosin L2 (DTNB) regulatory light-chain precursors. The eight decreased proteins are Glyceraldehyde-3-phosphate Dehydrogenas (GAPDH); Beta enolase; Creatine kinase M chain (M-CK); ATP-AMP Transphosphorylase (AK1); myosin heavy chain (MHC); actin; Troponin I, fast-skeletal muscle (Troponin I fast-twitch isoform), fsTnI; Troponin T, fast-skeletal muscle isoforms (TnTF). In these proteins, four of the eight decreased proteins are related directly or indirectly to exercise induced fatigue. The other proteins represent diverse sets of proteins including enzymyes related to energy metabolism, skeletal muscle fabric protein and protein with unknown functions. They did not exhibit evident relationship with exercise-induced fatigue. Whereas the two identified increased proteins exhibit evident relationship with fatigue. These findings will help in understanding the mechanisms involved in exercise-induced fatigue.