The Level Changes Of M2 Macrophage In CHD Peripheral Blood And Its Polarization Signal Pathway

Objective: To detect the expression of M2 macrophage specific marker CD163 in coronary heart disease patients and normal control group and analysis the correlation between these different groups, and explore the probable signal pathway that adjust M2 macrophage polarization,to provide a theoretical basis for further improving the stability of atherosclerotic plaques in patients with coronary heart disease and thus improve coronary ischemic events’ s occurrence.Methods: The research objects include 110 patients with coronary heart disease from September 2014 to August 2015 in hospital in the cardiovascular medicine of the Second Affiliated Hospital of Nanhua University, the normal control amount 32 cases from the same stage of the Physical Examination Center, the checks showed no significant biochemical abnormalities, among the enrolled patients were divided into stable angina pectoris(SAP) group of 38 patients, with non-ST segment elevation acute coronary syndrome(NSTEACS) 37 cases, ST segment elevation acute myocardial infarction(STEMI) 35 cases. Western blot method was used to detect the expression levels of CD163 and p-STAT3, STAT3 protein expression. Another control group of normal blood samples was centrifuged to obtain a purified monocytes, macrophages culture formed and then treated with IL-4 and IL-13 to induce the formation of M2 macrophage, in the experimental groups different concentrations of STAT3 inhibitor Stattic was used( 30μmol/L, 15μmol/L, 10μmol/L, 5μmol/L),named a, b, c, d group, adding a set of blank control group e, for the process of M2 macrophage formation induced by IL4/IL13 with no Stattic join in, after each group of cells cultured then centrifugation and Western blot analysis M2 macrophage cell marker CD163 levels.Results:(1) Compared with β-Actin, the relative CD163 levels in normal control group(2.34±0.083), stable angina pectoris goup(2.28±0.096), non-ST segment elevation acute coronary syndrome group(1.49±0.071), ST segment elevation acute myocardial infarction group(0.85±0.041), by analysis of variance between groups was statistically significant difference(P<0.05). Further pairwise comparison, in addition to the SAP and control group, the difference between the other groups were statistically significant(P<0.05).(2) Compared with β-Actin, the relative p-STAT3 levels in the control group(2.66±0.066), stable angina pectoris goup(2.58±0.052), non-ST segment elevation acute coronary syndrome group(0.98 ± 0.035), ST segment elevation acute myocardial infarction group(0.36± 0.021), by analysis of variance between groups was statistically significant difference(P<0.05). Further pairwise comparison, in addition to the SAP and control group, the difference between the other groups were statistically significant(P<0.05); and STAT3 protein in normal control group and CHD groups showed no significant difference(P>0.05).(3) By adding different concentrations of inhibitor Stattic on the polarization of M2 macrophage, compared with β-Actin, CD163 expression lever was detected, its relative value in a, b, c, d, e group were 0.56 ± 0.018, 0.85 ± 0.022, 1.12 ± 0.026, 1.18 ± 0.017, 2.65 ± 0.025, by analysis of variance, in addition to the c, d group, the difference between the other groups are statistically significant(P<0.05).Conclusion:(1) M2 Macrophage have a role in stabilizing atherosclerotic plaques;(2) Activation of STAT3 signaling pathway may contribute to M2 macrophage’ polarization.