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Objective To study the activation of cytosolic PLA2 and hypertensive cardiac remodeling relations, in this study the use of electron microscopy 4,8,16,24-week-old SHR left ventricular myocardial cells ultrastructural changes around the regulation of ERK1 / 2 pathway, immune staining different week-old SHR left ventricular wall (inner longitudinal layer, Central layer, outer oblique layer), ventricular septal ERK1 / 2 downstream regulator of cPLA2 expression, Western-blotting assay p-of cPLA2, p-MEK, p -ERK1 / 2 expression, transduction from the cell signaling pathway analysis hypertensive state cPLA2 is involved in hypertensive cardiac remodeling, to further clarify the ERK1 / 2 may adjust the mechanism involved in hypertensive cardiac remodeling. Animal grouping method: ① essential hypertension (Spontaneously Hypertensive Rats, SHR) group: 4-week-old group (SHR4), 8-week-old group (SHR8 of), 16-week-old group (SHR16), 24-week-old group (SHR24) n = 6; ② WKY (Wistar-Kyoto) rats were used as the control group: 4-week-old group (WKY4), 8-week-old group (WKY8), 16-week-old group (WKY16), 24-week-old group (WKY24) n = 6. HE staining, light microscopy measurements micrometer measurements of 4, 8, 16, 24-week-old SHR cardiac remodeling change observed histological changes SHR myocardial ultrastructure change of all ages using transmission electron microscopy and immunohistochemical methods to detect different weeks age of SHR left ventricular wall (inner longitudinal layer, Central layer, outer oblique layer), ventricular septal p-cPLA2 expression, Western-blotting assay cPLA2, p-MEK, p-ERK1 / 2 expression. 1, changes in blood pressure: WKY blood pressure maintained at normal levels (107.65 ± 6.55mmHg). SHR group from 8 weeks of age, high blood pressure, SHR8 SHR16, SHR24 group systolic blood pressure were significantly higher than the same week-old WKY group (P lt; 0.05); 2, heart / body weight ratio change: With the rat-week-old increase in SHR and WKY rats heart / body weight ratio gradually increased to 16, 24-week-old SHR heart / body weight ratio was significantly higher than the 4-week-old SHR (P lt; 0.05) ratio comparing with the same week-old WKY rats 16, 24-week-old SHR heart / body weight ratio was significantly higher than WKY rats (P lt; 0.05); heart relative thickness of the chamber changes: SHR group relative left ventricular wall thickness with the week-old, gradually increasing to the left ventricular muscle inner and increased media thickness, 16 and 24 weeks SHR relative left ventricular wall thickness was significantly higher than the 16 and 24 weeks WKY rats (P lt; 0.05). Relative left ventricular wall thickness of 16, 24-week-old SHR group was significantly higher than SHR4 group (P lt; 0.05); histological changes: HE sections of myocardial tissue observation, control group of normotensive WKY rats myocardial neat and clear, the basic structure. Correspondingly, the basic structure of the heart of the SHR group, myocardial arranged overall neat individual regional myocardial disorganized, myocardial cell volume generally increases, increase in the length of the myocardial cells, occasionally dual-core. The SHR group myocardial interstitial vessel wall was significantly thicker than the WKY group. 3 myocardial ultrastructure of change: the WKY group myocardial sarcolemma smooth, mitochondria, Run disk no significant pathological manifestations of normal stromal vascular. 8,16 weeks old SHR cardiomyocytes comparison, visible within the ridge structure in the expansion increases mitochondrial matrix blur, part of the mitochondria was feathery dissolved necrosis. The sarcoplasmic reticulum cell expansion uneven was bubbly highlights a small number of mitochondria dissolved, the above to SHR24 myocardial cells change becomes more apparent. SHR24 Run disk is significantly reduced, Run disk local gap expansion, visible abnormal spherical enlargement Run disk running disorder flexion; SHR myocardial capillary endothelial cell proliferation, vascular wall thickening and vascular stenosis deformation; myocardial interstitial perivascular Visible fibroblast hyperplasia, collagen increased. 4, the phosphorylation of cPLA2 histochemical positive performance in the test results of the various parts of the heart: phosphorylated cPLA2 immunohistochemistry for myocardial cell cytoplasm brownish yellow or light yellow particles composure, week-old rats with experimental heart area, its range of different expression, rat cardiac left ventricular wall and interventricular septum, phosphorylation of cPLA2 expression of SHR with the birds grew gradually increased expression of the layers of the ventricular wall: the inner layer of the left ventricular wall SHR16, SHR24 the positive expression rate 76.38%, 78.56%, significantly higher than WKY16, WKY24 positive rate of 51.52%, 53.74%; the middle SHR16 in the left ventricular wall, the positive expression rate of SHR24 were 75.03%, 82.03%, significantly higher than WKY16, WKY24 rat The positive rate of 46.51%, 55.67%; in left ventricular wall the outer layer SHR24 the positive expression rate of 78.53%, significantly higher than WKY24 rats positive rate of 56.74%; phosphorylation of cPLA2 In the interventricular septum in the expression pattern of the left ventricular wall: phosphorylated cPLA2 expression of SHR24 rats ventricular septal left ventricular surface positive rate was 50.12%, significantly higher than WKY24 group expression positive rate of 29.87%; ventricular septal right ventricular surface phosphorylated cPLA2 expression groups no significant difference; phosphorylation of cPLA2 in SHR4 the inner and middle of the left ventricular wall was significantly higher than the the ventricular septal left and right ventricular surface expression (P lt; 0.05). Within in SHR24 left ventricular wall, the outer layer of positive expression rate was significantly higher than the ventricular septal right ventricular surface positive rate (P lt; 0.05), ventricular septal left ventricle surface expression of the right ventricular surface expression There was no significant difference. 5, Western blot detection with weeks of age increased phosphorylation in the SHR heart cPLA2 protein content gradually increased results. 6, the phosphorylation of MEK test results of the rat heart: SHR24 heart phosphorylation of MEK1 / 2 protein content higher than SHR8 phosphorylation of MEK1 / 2 protein content of than WKY24 rats high SHR24 heart. Phosphorylated ERK detection results of rat heart: SHR24 heart of phosphorylated ERK1 / 2 protein content higher than SHR8, SHR24 heart of phosphorylated ERK1 / 2 protein content than WKY24 rats. Conclusion (1) SHR hypertensive rats cardiac remodeling in left ventricular hypertrophy. (2) myocardial cell proliferation / apoptosis imbalance, the myocardial vascular remodeling and myocardial fibrosis participation SHR cardiac remodeling. (3) MEK1/2-ERK1/2-cPlA2 pathway involved in SHR cardiac remodeling, cardiomyocyte proliferation / apoptosis imbalance.
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