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<p><b>Background</b>Acute coronary syndrome (ACS) is closely related to unstable plaques and secondary thrombosis. The inflammatory cells in plaques and their inflammatory products may be the cause for plaque instability and ruptures. The study aimed to disclose the changes of inflammatory factors including serum intracellular adhesion molecule-1 (ICAM-1), chitinase-3-like protein 1 (YKL-40), and lipoprotein-associated phospholipase A2 (Lp-PLA2) in patients with ACS and its clinical significance.</p><p><b>Methods</b>A total of 120 patients with coronary heart disease (CHD) were categorized into 2 groups: 69 with ACS and 51 with stable angina pectoris (SAP); 20 patients with chest pain and normal angiography served as a control group. The 120 patients with CHD were categorized into single-vessel disease group, double-vessel disease group, and three-vessel disease group based on the number of coronary artery stenosis. The severity of coronary artery stenosis was quantified based on coronary angiography using Gensini score. They were further divided into mild CHD group with its Gensini score <26 (n = 36), moderate CHD group with its Gensini score being 26-54 (n = 48) and severe CHD group with its Gensini score >54 (n = 36). Serum levels of ICAM-1, YKL-40, and Lp-PLA2 of different groups were determined by enzyme-linked immunosorbent assay. Correlation between ICAM-1, YKL-40, Lp-PLA2, and Gensini score was analyzed.</p><p><b>Results</b>The levels of serum inflammatory factors ICAM-1, YKL-40, and Lp-PLA2 were significantly higher in the ACS group than those in control group and SAP group (all P < 0.05); and compared with control group, no significant difference was observed in terms of the serum ICAM-1, YKL-40, and Lp-PLA2 levels in the SAP group (P > 0.05).The levels of serum ICAM-1, YKL-40, and Lp-PLA2 were not significantly different among control group, single-vessel disease group, double-vessel disease group, and three-vessel disease group (all P > 0.05). The levels of serum ICAM-1, YKL-40, and Lp-PLA2 were not significantly different among control group, mild CHD group (Gensini score <26), moderate CHD group (Gensini score 26-54), and severe CHD group (Gensini score >54) (all P > 0.05). Nonparametric Spearman correlation analysis showed that the levels of serum ICAM-1, YKL-40, and Lp-PLA2 were not correlated with the Gensini score in CHD patients (r = 0.093, r = -0.149, and r = -0.085, all P > 0.05; respectively).</p><p><b>Conclusions</b>The serum levels of ICAM-1, YKL-40, and Lp-PLA2 were correlated with different clinical types of CHD, but not well correlated the severity and extent of artery stenosis, suggesting that ICAM-1, YKL-40, and Lp-PLA2 might be involved in occurrence of instability of atherosclerotic plaque, and might reflect the severity of CHD mostly through reflecting the plaque stability.</p>
Subject(s)
Adult , Aged , Humans , Middle Aged , 1-Alkyl-2-acetylglycerophosphocholine Esterase , Metabolism , Acute Coronary Syndrome , Blood , Allergy and Immunology , Metabolism , Chitinase-3-Like Protein 1 , Metabolism , Coronary Angiography , Coronary Disease , Blood , Allergy and Immunology , Metabolism , Intercellular Adhesion Molecule-1 , MetabolismABSTRACT
<p><b>OBJECTIVE</b>To investigate the relationship between inflammatory factors and two Chinese medicine (CM) syndrome types of qi stagnation and blood stasis (QSBS) and qi deficiency and blood stasis (QDBS) in patients with acute coronary syndrome (ACS).</p><p><b>METHODS</b>Sixty subjects with ACS, whose pathogenesis changes belongs to qi disturbance blood stasis syndrome, were divided into 2 groups: 30 in the QSBS group and 30 in the QDBS group. The comparative analysis on them was carried out through comparing general information, coronary angiography and inflammatory factors including intracellular adhesion molecule-1 (ICAM-1), chitinase-3-like protein 1 (YKL-40) and lipoprotein-associated phospholipase A2 (Lp-PLA2).</p><p><b>RESULTS</b>Compared with the QSBS group, Lp-PLA2 and YKL-40 levels in the QDBS group showed no-significant difference (P>0.05); ICAM-1 was significantly higher in the QDBS group than in the QSBS group in the pathological processes of qi disturbance and blood stasis syndrome of ACS (P<0.05).</p><p><b>CONCLUSIONS</b>Inflammatory factor ICAM-1 may be an objective basis for syndrome typing of QSBS and QDBS, which provides a research direction for standardization research of CM syndrome types.</p>
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Objective: To investigate the correlations between aqueous concentrations of vascular endothelial growth factor (VEGF), monocyte chemoattractant protein-1 (MCP-1), soluble intracellular adhesion molecule-1 (sICAM-1) and diabetic macular edema (DME). Materials and Methods: VEGF, MCP-1 and sICAM-1 concentrations in aqueous humor samples of 22 patients with DME and 23 patients with cataract of a control group were measured with solid-phase chemiluminescence immunoassay. Results: Aqueous VEGF (89.2 ± 58.5 pg/ml versus 48.5 ± 27.8 pg/ml, P = 0.006), MCP-1 (684.2 ± 423.4 pg/ml versus 432.4 ± 230.4 pg/ml, P = 0.019) and sICAM-1 (3213.8 ± 2581.6 pg/ml versus 260.2 ± 212.2 pg/ml, P < 0.001) all vary significantly between DME group and control group. Maximum height of submacular fluid measured by Optical coherence tomography (OCT) was significantly associated with aqueous sICAM-1 (r = -0.45, P = 0.034). The maximum height of macular thickness measured by OCT was not significantly associated with either VEGF (P = 0.300), MCP-1 (P = 0.320) or sICAM-1 (P = 0.285). Conclusions: Our results suggest that sICAM-1 may majorly contribute to the formation of subretinal fluid in DME patients and imply that MCP-1 and sICAM-1 may be the potential therapy targets, besides VEGF.
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Background The impact of statins on inflammation are independent of cholesterol-lowering effect.Recent studies showed that Toll-like receptor 4(TLR4),a mediator of innate immune responses,is involved in the initiation and progression of atherosclerosis.Objective To investigate the effects of atorvastatin on LPS-induced TLR4 expression and downstream signals and to explore the molecular mechanisms of anti-inflammation by statins.Methods Human umbilical vein endothelial cells(HUVEC)were pretreated with atorvastatin(1 or 10 ?mol/L)or NF-?B inhibitor CAPE for 30 min,then incubated by purified LPS for 24 hours.TLR4,ICAM-1 and E-selectin mRNA were measured by RT-PCR;the percentage of TLR4 positive cells were detected by flow cytometry.The activation of NF-?B(p65)were detected by Western blot.Results Atorvastatin(1-10 ?mol/L)prevented LPS-induced increases in TLR4,ICAM-1 and E-selectin expression [TLR4 mRNA(1.24?0.21)vs LPS(1.82?0.27),P
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AIM To investigate if the protective effect of baicalin on cerebral injury induced by transient focal ischemia is related to modulation of expressions of inflammatory cytokines or adhesive molecules. METHODS Transient focal cerebral ischemia injury model in rats was induced by occlusion of the right middle cerebral artery for 2 h, followed by 24 h reperfusion. The infarct volume and neurological deficit were determined by TTC staining and the scoring method of Longa et al. The expression of intracellular adhesion molecule-1 (ICAM-1), neutrophils infiltration, and myeloperoxidase (MPO) activity in brain were measured by immunohistochemistry, hematoxylin-eosin staining, and spectrophotometer, respectively. Semiquantitative RT-PCR was employed to assess the expression of inducible nitric oxide synthase (iNOS) mRNA. The level of interleukin-1 (IL-1) in brain was assayed by radioimmunoassay. The expression of nuclear factor-κB (NF-κB) protein was evaluated by Western blot. RESULTS After transient cerebral ischemia, MPO activity and the expression of ICAM-1 in the periphery of ischemic cortex were significantly increased. Increase in iNOS mRNA and NF-κB protein expression was also shown in the ischemic area. Treatment with baicalin markedly reduced brain infarct volume and neurological deficit induced by ischemic insult, inhibited MPO activity, inflammatory cell infiltration, as well as expression of ICAM-1, iNOS and NF-κB, and decreased IL-1 level. CONCLUSION Baicalin may play a protective effect on cerebral ischemic injury through inhibiting the expression and release of the inflammatory mediators after cerebral ischemia.
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Objectives:To investigate the level of soluble intracellular adhesion molecule 1 (sICAM 1) concentrations in the serum and peritoneal fluid from the patients with or without endometriosis.To discuss the relationship within sICAM 1 and pelvic endometriosis. Methods:35 serum and 30 peritoneal fluid of patients with endometriosis (test group) and 26 serum and 4 peritoneal fluid without endometriosis (control group) were studied.Soluble intracellular adhesion molecule 1 levels were detected by an enzyme linked immunoassay(ELISA).The results were analysed by T test. Results: The serum concentration of sICAM 1 was significantly higher in test group than controll group. However,There was no significant difference in between two groups. Conclusions: These results suggest that sICAM 1 could play some role in the persistence of endometriotic lesions.
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Objective To study the intercellular adhesion molecule-1(ICAM-1)and fat metabolism in the contribution of the incidence of steroid avascular necrosis of femoral head(ANFH).Methods 32 New Zealand rabbits were randomly divided into two groups:animals in experiment group(n=24)were given an injection of hydrocortisone acetate(8.0mg/kg)two times per week,and animals in control group(n=8)were given an injection with the same volume of normal saline.Serum total cholesterol(TC),triglyceride(TG)and ICAM-1 were quantitated before and 2,4,6,8 weeks after the treatment.2,4,6 and 8 weeks after treatment,6 animals of the experiment group and 2 of the control group were randomly chosen and sacrificed.ICAM-1 expression in soft tissue around hip was determined immunohistochemically,and pathohistological changes in femoral head were observed by light microscopy.Results Serum TC and TG levels of the animals in experimental group were significantly higher than those before treatment and those in control group in the 6th week after treatment(P
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To determine the effects of Remifentanil on the expression of adhesive factors during acute lung injury, we used immunohistochemistry and reverse transcription polymerase chain reaction (RT PCR) technics to measure the expression levels of ICAM 1, and P Selectin in the lung in a rat model of hemorrhagic shock. We duplicated modified Wigger hemorrhagic shock model in healthy SD rats. The rats were divided into three groups: control group, resuscitation group, resuscitation and drug using group. The positive ratios of ICAM 1 and P Selectin in the lungs at different time points, namely preshock, shock, resuscitation 2 hours, and resuscitation 4 hours were determined. There were 6 rats in each group and each time point. The degree of pulmonary injury in the drug using group was less than that in other two groups. Resuscitation with lactated Ringer's solution led to most serious injury in the resuscitation group. In drug using group, the expression of ICAM 1 and P Selectin was far less than that in the other two groups ( P