Expression of Monocyte Chemoattractant Protein-1 in Monocytes and Effects of Native and Oxidized Very Low Density Lipoproteins

Monocyte chemoattractant protein-1(MCP-1), a potent chemoattractant, is thought to play an important role in migration of monocytes into atherosclerotic lesions. The present study was designed to investigate the capacity of human peripheral blood monocytes to express MCP-1 and effects of native very low density lipoprotein (VLDL) and oxidized VLDL(OX-VLDL) on the expression. The total RNA was extracted from cultured monocytes, which were exposed to VLDL and OX-VLDL, and the media conditioned by monocytes were collected. MCP-1 mRNA expression was examined by Northern blot analysis. MCP-1 protein in conditioned media was determined by using sandwich ELISA. The results showed that monocytes can express MCP-1 after a 24 h incubation at 37℃，and the expression was markedly increased by a exposure to OX-VLDL, whereas the expression was slightly increased when exposed to VLDL. It suggests that the capacity of monocytes to produce MCP-1 that recruits and activates circulating monocytes may be of considerable importance in atherogenesis, and oxidation of VLDL enhances its potential to promote atherogenesis.

Effect of Danzhijiangtang capsule on monocyte chemoattractant protein-1 mRNA expression in newly diagnosed diabetes subclinical vascular lesions

AIM:To investigate the effect of Danzhijiangtang capsule(DJC) on monocyte chemoattractant protein-1(MCP-1) mRNA expression in newly diagnosed type 2 diabetes mellitus(T2DM) subclinical vascular lesions.METHODS:Sixty-two patients with newly diagnosed T2DM subclinical vascular lesions were randomly divided into a control group and treatment group of 31 cases each.Oral antidiabetic therapy with routine western medicine was conducted in both groups,and the treatment group was additionally treated with DJCs.The treatment course for both groups was 12 wk.Before and after treatment,the total efficiency and traditional Chinese medicine(TCM) syndrome score were calculated.The fasting plasma glucose(FPG),2-h plasma glucose(2hPG),fasting insulin(FINS),insulin resistance index(IRI),hemoglobin(Hb)A1c,blood lipids,and hemorheology indices were determined.In addition,the levels of vascular endothelial growth factors including thrombomodulin(TM),von Willebrand factor(vWF),P-selectin and MCP-1 mRNA were determined.RESULTS:After 12 wk of treatment,the TCM syndrome score was significantly decreased compared to before treatment in both groups.After treatment,FPG,2hPG,HbA1c,FINS,IRI,total cholesterol,triglycerides,low-density lipoprotein,high-density lipoprotein,whole blood low shear specific viscosity,plasma specific viscosity,TM,vWF,P-selectin and MCP-1 mRNA were significantly improved compared to before treatment in both groups.After treatment,the total efficiency and TCM syndrome score in the treatment group were better than in the control group.FINS,IRI,whole blood high shear specific viscosity,plasma specific viscosity,TM,vWF,P-selectin and MCP-1 mRNA level in the treatment group were significantly reduced after treatment compared with control group.CONCLUSION:DJCs are efficacious in supplementing qi,nourishing yin and invigorating blood circulation,and upregulate MCP-1 mRNA expression in patients with T2DM subclinical vascular lesions.

Interleukin-1β,Tumor Necrosis Factor-α and Lipopolysaccharide Induce Expression of Monocyte Chemoattractant Protein-1 in Calf Aortic Smooth Muscle Cells

Summary: To investigate whether interleukin-1β(IL-1β), tumor necrosis factor-α (TNF-α) and lipopolysaccharide (LPS) induce expression of monocyte chemoattractant protein-1 (MCP-1 ) mRNA and protein in calf aortic smooth muscle cells(SMCs), calf aortic SMCs were cultured by a substrate-attached explant method. The cultured SMCs were used between the third to the fifth passage. After the cells became confluent, the SMCs were exposed to 2 ng/ml IL-1β, 20ng/ml TNF-1α and 100 ng/ml LPS respectively, and the total RNA of SMCs which were incubated for 4 h at 37℃ were extracted from the cells by using guanidinium isothiocyanate method. The expres- ion of MCP-1 mRNA in SMCs was detected by using dot blotting analysis using a probe of γ-32 P- end-labelled 35-mer oligonucleotide. After a 24-h incubation, the media conditioned by the cul- tured SMCs were collected. The MCP-1 protein content in the conditioned media was determined by using sandwich ELISA. The results were as follows: Dot blotting analysis showed that the cul- tured SMCs could express MCP-1 mRNA. After a 4-h exposure to IL-1β, TNF-α and LPS, the MCP-1 mRNA expression in SMCs was increased (3.6-fold, 2. 3-fold and 1. 6-fold, respectively). ELISA showed that the levels of MCP-1 protein in the conditioned media were also increased (2.9- fold, 1.7-fold and 1.1-fold, respectively). The results suggest that calf aortic SMCs could ex- press MCP-1 mRNA and protein. IL-1β and TNF-α can induce strong expression of MCP-1 mRNA and protein, and the former is more effective than the latter.

Effects of Simvastatin on NF-κB-DNA Binding Activity and Monocyte Chemoattractant Protein-1 Expression in a Rabbit Model of Atherosclerosis

To observe the effects of simvastatin on nuclear factor kappaB （NF-kB）-DNA binding activity and on the expression of monocyte chemoattractant protein-1 （MCP-1） in atherosclerotic plaque in rabbits and to explore the anti-atherosclerotic properties beyond its lipid-lowering effects. Thirty-six New Zealand male rabbits were randomly divided into low-cholesterol group （LC）, high- cholesterol group （HC）, high-cholesterol＋ simvastatin group （HC＋S） and then were fed for 12 weeks. At the end of the experiment, standard enzymatic assays, electrophoretic mobility shift as- say （EMSA）, immunohistochemical staining, and morphometry were performed to observe serum lipids, NF-kB-DNA binding activity, MCP-1 protein expression, intirna thickness and plaque area of aorta respectively in all three groups. Our results showed that the serum lipids, NF-kB-DNA binding activity, expression of MCP-1 protein, intima thickness, and plaque area of aorta in the LC and HC＋S groups were significantly lower than those in the HC group （P〈0.05）. There was no significant difference in the serum lipids between the LC and HC＋S groups （P〉0.05）, but the NF-kB-DNA binding activity, the expression of MCP-1 protein and the intirna thickness and plaque area of aorta in the HC＋S group were significantly decreased as compared to the LC group （P〈0. 05）. This study demonstrated that simvastatin could decrease atherosclerosis by inhibiting the NF-kB-DNA binding activity and by reducing the expression of MCP-1 protein.

The enhancement of astrocytic-derived monocyte chemoattractant protein-1 induced by the interaction of opiate and HIV tat in HIV-associated dementia

HIV-associated dementia(HAD)is a public health problem and is particularly prevalent in drug abusers.The neuropathogenesis of human immunodeficiency virus(HIV)infection involves a complex cascade of inflammatory events,including monocyte/macrophage infiltration in the brain,glial immune activation and release of neurotoxic substances.In these events,astrocytic-derived monocyte chemoattractant protein-1(MCP-1)plays an important role,whose release is elevated by HIV transactivator of transcription(HIV tat)and could be further elevated by opiates.This review will also consider some critical factors and events in MCP-1 enhancement induced by the interactions of opiate and HIV tat,including the mediating role of mu opioid receptor(MOR)and CCR2 as well as the possible signal transduction pathways within the cells.Finally,it will make some future perspectives on the exact pathways,new receptors and target cells,and the vulnerability to neurodegeneration with HIV and opiates.

Variation of Serum Monocyte Chemoattractant Protein-1 in Patients with Diabetes and Metabolic Syndrome

This study investigated the variation of serum monocyte chemoattractant protein-1（MCP-1） in patients with both diabetes mellitus（DM） and metabolic syndrome（MS）.Based on the International Diabetes Federation（IDF） diagnostic criteria,93 patients enrolled in this study were divided into four groups：normal control（NC）,simple DM,simple MS,and DM plus MS（DM-MS） groups.The main measures included height,weight,waist circumference（WC）,hip circumference,blood pressure,fasting blood glucose,insulin resistance index（HOMA-IR）,serum triglyceride（TG）,HDL-ch,LDL-ch,and MCP-1.The results showed that the serum levels of MCP-1 in the DM-MS group were significantly increased as compared with those in the DM and MS groups（P0.05）,and the increase in the MCP-1 level in the DM group was much higher than in the MS group（P0.05）.The DM-MS group had the highest HOMA-IR levels,followed by MS,DM and NC groups（P0.05）.Correlation tests showed that the association of MCP-1 with age,HDL-ch,or LDL-ch was insignificant,whereas that of MCP-1 with body mass index（BMI）,waist hip rate（WHR）,WC,systolic blood pressure（SBP）,diastolic blood pressure（DBP）,TG,and HOMA-IR was significantly positive.It was concluded that circulating MCP-1 was substantially increased in patients with both DM and MS as compared with that in the patients with DM or MS alone,and the central obese state may contribute to a more vicious proinflammatory condition and insulin resistance in patients with diabetes.

Monocyte chemoattractant protein-1 plays a key role in type 1 diabetes

Type 1 diabetes is an autoimmune dise as e resulting from the selective destruction of β cells in the pa ncreatic islets. In both human and rodent models of type 1 diabetes, the clinica l disease is preceded by a progressive mononuclear cell invasion of the pancreat ic islets (insulitis). In the early stage of insulitis,the major components are monocyte/macrophages, and the recruitment of mononuclear cells is a critical st ep in the pathogenesis of the type 1 diabetes. Studies have revealed that Monocy te chemoattractant protein-1(MCP-1) specifically recruits monocytes/ macrophag es into pancreas and plays an important role in the development of insulitis and diabetes.

Role of monocytes and macrophages in experimental and human acute liver failure

Acute liver failure (ALF) is a devastating clinical syndrome characterised by progressive encephalopathy, coagulopathy, and circulatory dysfunction, which commonly leads to multiorgan failure and death. Central to the pathogenesis of ALF is activation of the immune system with mobilisation of cellular effectors and massive production of cytokines. As key components of the innate immune system, monocytes and macrophages are postulated to play a central role in the initiation, progression and resolution of ALF. ALF in humans follows a rapidly progressive clinical course that poses inherent difficulties in delineating the role of these pivotal immune cells. Therefore, a number of experimental models have been used to study the pathogenesis of ALF. Here we consider the evidence from experimental and human studies of ALF on the role of monocytes and macrophages in acute hepatic injury and the ensuing extrahepatic manifestations, including functional monocyte deactivation and multiple organ failure.

Urotensin Ⅱ promotes monocyte chemoattractant protein-1 expression in aortic adventitial fibroblasts of rat

Background Urotensin Ⅱ （Ull）,a potent vasoconstrictive peptide,is able to stimulate phenotypic differentiation of adventitial fibroblasts.This study aimed to determine the effect of UII on monocyte chemoattractant protein-1 （MCP1） expression in rat aortic adventitial fibroblasts,so as to explore possible mechanisms in the development of vascular inflammation.Methods Growth-arrested adventitial fibroblasts were incubated in serum-free medium with UII （1010-10-7 mol/L） and inhibitors of signal transduction pathways for 1 to 24 hours.MCP-1 mRNA and protein expression and secretion were determined by RT-PCR,Western blotting analysis and enzyme-linked immunosorbent assay （ELISA）,respectively.Results UII dose-and time-dependently promoted MCP-1 mRNA and protein expression and secretion in cells,with maximal effect at 10-8 mol/L at 3 hours for mRNA expression,24 hours for protein expression in the cells,and 12 hours for protein secretion from the cells.Furthermore,the UII effects were significantly inhibited by treatment with its receptor antagonist SB710411,Rho kinase inhibitor Y27632,protein kinase C （PKC） inhibitor H7,mitogen-activated protein kinase inhibitor PD98059,calcineurin inhibitor cyclosporine A,and the Ca2＋channel blocker nicardipine.Conclusion UII may stimulate MCP-1 expression in rat aortic adventitial fibroblasts through its receptor and Rho kinase,PKC,mitogen-activated protein kinase,calcineurin and Ca2＋ channel signal transduction,thus contributing to adventitial inflammation.

Calcitonin gene-related peptide induces proliferation and monocyte chemoattractant protein-1 expression via extracellular signal-regulated kinase activation in rat osteoblasts

Background Calcitonin gene-related peptide （CGRP）, a sensory neuropeptide, affects osteoblast proliferation and bone formation. However, the mechanisms are not fully understood. Monocyte chemoattractant protein-1 （MCP-1） is a chemokine that stimulates the migration of monocytes and plays important roles in regulating bone remolding during fracture repair. In this study, we investigated the effects of CGRP on proliferation and MCP-1 expression in cultured rat osteoblasts. Methods Primary rat osteoblasts were isolated from fetal rats calvariae. Cells were exposed to gradient concentrations （10^-9 to 10^-7 mol/L） of CGRP. Protein and mRNA levels of MCP-1 were quantified by Western blotting and semiquantitative reverse transcdption-polymerase chain reaction, respectively. The protein level of MCP-1 was investigated and compared in cell culture media by enzyme linked immunosorbent assay （ELISA）. Phospho-extracellular signal-regulated kinase （ERK） expression was detected by Western blotting. Cell proliferative activity was measured by 3-（4,5-dimethylthiazol-2-yl）-2, 5-diphenyl tetrazolium bromide （MTT） and BrdU assay. The effects of MAPK/ERK kinase （MEK）-inhibitor U0126 on CGRP-induced MCP-1 expression in primary rat osteoblasts were examined. Results CGRP effectively enhanced primary rat osteoblast proliferation and led to significant increases in the expression of MCP-1 mRNA and protein in time- and dose-dependent manners. CGRP activated the ERK pathway. Pretreatment of cultured rat osteoblasts with MEK inhibitor U0126 resulted in dose-dependent inhibitions of CGRP-induced MCP-1 mRNA and protein levels. Thus, CGRP promoted cell proliferation and stimulated MCP-1 expression in cultured rat osteoblasts. Conclusion These studies document novel links between CGRP and MCP-1 and illuminate the effects of CGRP in regulating bone remodeling.

Monocyte chemoattractant protein 1 expression in renal tissue is associated w ith monocyte recruitment and tubulo-interstitial lesions in patients with lup us nephritis

Objective To investigate the pattern of monocyte chemoattractant prolein-1 (MCP-1) distribution in the renal interstitium and evaluate its pathogenic role in tubulo-interstitial lesions in patients with lupus nephritis, the distribution of MCP-1 in renal tissue was observed.Methods Eighteen female patients with biopsy-proven lupus nephritis were enrolled in this study. No intensive immunosuppresive therapy was used in these patients during the 3 months prior to renal biopsy. The distribution of MCP-1, infiltration of CD68+ (macrophage/monocyte), CD4+ and CD8+ cells in the tubulo-interstitium of patients with lupus nephritis was detected using immunohistochemical staining with specific antibodies. Renal specimens from patients with minimal change glomerulonephritis were used as controls. Results MCP-1 protein was widely distributed in the renal tissue of patients with lupus nephritis, mainly located at the baso-lateral surface of tubular epithelial cells (16/18 biopsies), and on the wall of interstitial blood vessels (9/18 biopsies). In contrast, tubular MCP-1 staining was weak and rare in renal tissue from controls (7.4±6.2% vs 26.7±22.8%, P<0.01). Tubulo-interstitial infiltration of CD68+, CD4+ and CD8+ cells was markedly increased in patients with lupus nephritis as compared to controls. The tubular expression of MCP-1 was strongly associated with the amount of CD68+ cell infiltration in the interstitium (r=0.5420, P<0.05) and the extent of interstitial fibrosis. There was no correlation between MCP-1 production in tubules and the degree of urinary protein excretion in patients with lupus nephritis (r=0.0547, P>0.05).Conclusions The expression of MCP-1 in the renal tubules and vascular wall was markedly increased in patients with lupus nephritis. The overproduction of MCP-1 in renal tissue may contribute to monocyte recruitment in the interstitium and thus result in tubulo-interstitial damage in lupus nephritis.

内异方联合米非司酮片治疗子宫内膜异位症临床研究

目的:观察内异方联合米非司酮片治疗子宫内膜异位症(EMT)的临床疗效。方法:选取108例EMT患者作为研究对象,按随机数字表法分为对照组和观察组各54例。对照组给予米非司酮片治疗,观察组在对照组基础上联合内异方治疗,治疗3个月经周期。比较2组治疗前后中医证候评分、疼痛介质、血液黏度、血清相关因子水平。结果:治疗后,2组小腹胀痛、经血量少、经血夹血块评分均较治疗前降低(P<0.05),且观察组小腹胀痛、经血量少、经血夹血块评分均低于对照组(P<0.05)。治疗后,2组神经生长因子(NGF)、前列腺素F_(2α)(PGF_(2α))、前列腺素E2 (PGE2)水平均较治疗前降低(P<0.05),且观察组NGF、PGF_(2α)、PGE2水平均低于对照组(P<0.05)。治疗后,2组血浆黏度、高切全血黏度、低切全血黏度均较治疗前降低(P<0.05),且观察组血浆黏度、高切全血黏度、低切全血黏度均低于对照组(P<0.05)。治疗后,2组血清视黄醇结合蛋白4 (RBP4)、单核细胞趋化蛋白1 (MCP-1)、细胞间黏附相关因子(ICAM-1)水平均较治疗前降低(P<0.05),且观察组血清RBP4、MCP-1、ICAM-1水平均低于对照组(P<0.05)。结论:内异方可改善EMT患者临床症状,调节疼痛介质及血液黏度,调控血清相关因子水平。

依达拉奉右莰醇联合丁苯酞氯化钠注射液对急性脑梗死患者血清单核细胞趋化蛋白-1、内皮素-1表达的影响

目的探讨依达拉奉右莰醇联合丁苯酞氯化钠注射液对急性脑梗死患者血清单核细胞趋化蛋白-1(MCP-1)、内皮素-1(ET-1)表达及动脉粥样硬化斑块的影响。方法选取河北省邯郸市中医院2020年12月至2022年8月收治的急性脑梗死患者140例,按随机数字表法分为联合组和对照组,各70例。两组患者均予丁苯酞氯化钠注射液,联合组患者加用依达拉奉右莰醇注射液,均治疗14 d。结果联合组总有效率为91.43%,显著高于对照组的68.57%(P<0.05)。治疗后,两组患者的颈动脉内中膜厚度、斑块面积、美国国立卫生研究院卒中量表(NIHSS)评分、改良Rankin量表(MRS)评分及血清MCP-1、ET-1、丙二醛、超氧化物歧化酶水平均显著降低(P<0.05),且联合组均显著低于对照组(P<0.05);联合组和对照组患者治疗期间不良反应发生率相当(12.86%比14.29%,P>0.05)。结论依达拉奉右莰醇联合丁苯酞氯化钠注射液治疗急性脑梗死的临床疗效良好,可有效改善患者的神经功能缺损情况、颈动脉粥样硬化斑块稳定性及内皮功能,降低氧化应激水平,提高生活质量,且安全性良好。

NapA蛋白诱导巨噬细胞分泌趋化因子单核细胞趋化蛋白1和白细胞介素8的机制

目的:研究幽门螺杆菌NapA蛋白诱导巨噬细胞分泌趋化因子单核细胞趋化蛋白1(monocyte chemoattractant protein-1,MCP-1)和白细胞介素8(interleukin-8,IL-8)的机制。方法:利用NapA蛋白处理巨噬细胞,然后使用ELISA法检测上清中MCP-1和IL-8的表达量。使用C29、ST2825、SB203580、SP600125以及PDTC和巨噬细胞预先共孵育1 h,分别抑制Toll样受体2(toll-like receptors 2,TLR2)、髓样分化因子(myeloid differentiation factor 88,MyD88)、核糖核酸酶p蛋白亚基p38(ribonuclease p-protein subunit p38,p38)、应激活化蛋白激酶(c-Jun N-terminal kinase,c-Jun)和核因子κB(nuclear factor kappa B,NF-κB)的活性,然后再加入NapA蛋白孵育4 h,收集上清并检查其中MCP-1和IL-8的表达量。结果:NapA蛋白刺激巨噬细胞后,MCP-1和IL-8的表达量明显高于未处理组。利用抑制剂C29抑制TLR2的活性,NapA蛋白诱导的MCP-1和IL-8表达量降低。使用ST2825、PDTC以及SB203580分别抑制MyD88、NF-κB以及p38的活性,能够降低NapA蛋白诱导巨噬细胞分泌MCP-1和IL-8的能力,但是抑制c-Jun不影响NapA蛋白诱导巨噬细胞分泌MCP-1和IL-8。结论:幽门螺杆菌NapA蛋白通过TLR2/MyD88/NF-κB通路诱导巨噬细胞分泌MCP-1和IL-8。

miR-17-5p、IL-6及MCP-1联合检测对卵巢子宫内膜异位症患者术后复发的预测价值

目的 分析研究血清微小RNA-17-5p(miR-17-5p)、白细胞介素-6(IL-6)及单核细胞趋化蛋白1(MCP-1)联合检测对卵巢子宫内膜异位症(OEM)患者术后复发的预测价值。方法 选取郑州大学第三附属医院2019年1月至2022年12月收治的OEM患者作为研究对象,将其命名为OEM组(n=100),另选同期在本院进行体检的健康女性为对照组(n=60)。比较两组血清miR-17-5p、IL-6及MCP-1水平;OEM组患者在入院后均进行手术与药物对症治疗,在治疗结束后对患者随访12个月。以多因素Logistic回归分析OEM患者术后复发的影响因素,并绘制ROC曲线分析血清miR-17-5p、IL-6、MCP-1水平对OEM患者术后复发的预测价值。结果 OEM组的血清miR-17-5p水平低于对照组,IL-6、MCP-1水平均高于对照组,差异有统计学意义(t=11.015、59.651、38.199,均P<0.05);多因素Logistic回归分析显示,囊肿直径>5 cm(OR=1.828)、ASRM分期为Ⅲ~Ⅳ期(OR=1.815)、血清miR-17-5p水平降低(OR=2.042)、IL-6水平升高(OR=2.136)及MCP-1水平升高(OR=1.966)均是OEM患者术后复发的独立危险因素(P<0.05);ROC曲线分析显示,血清miR-17-5p、IL-6、MCP-1水平及联合检测的曲线下面积(AUC)分别为0.816、0.781、0.745、0.933,联合检测优于单一检测(P<0.05)。结论 miR-17-5p、IL-6及MCP-1联合检测对OEM患者术后复发具有一定预测价值。

温胆汤加减治疗气虚血瘀痰阻型缺血性脑卒中急性期的疗效及对NT-proBNP、ICAM-1和MCP-1的影响研究

目的:探讨温胆汤加减治疗气虚血瘀痰阻型缺血性脑卒中急性期患者的疗效,以及对N末端脑钠肽前体(NT-proBNP)、细胞间黏附分子-1(ICAM-1)和单核细胞趋化蛋白-1(MCP-1)水平的影响。方法:以2021年5月至2022年5月该院收治的气虚血瘀痰阻型缺血性脑卒中急性期患者100例为研究对象,根据随机数字表法分为对照组和观察组,每组50例。对照组患者给予常规治疗,观察组患者在对照组的基础上给予温胆汤加减治疗。比较两组患者的临床疗效,NT-proBNP、ICAM-1和MCP-1水平,美国国立卫生院卒中神经功能缺损评分量表(NIHSS)评分、改良Rankin量表(mRS)评分及中医证候积分。结果:治疗1个月后,观察组患者的总有效率为94.00%(47/50),显著高于对照组的80.00%(40/50),差异有统计学意义(P<0.05)。治疗1个月后,观察组患者NT-proBNP、ICAM-1和MCP-1水平显著低于对照组,血液流变学各指标(血浆黏度、血低切黏度、血高切黏度、纤维蛋白原和红细胞压积)水平显著低于对照组,差异均有统计学意义(P<0.05)。治疗7 d、1个月后,观察组患者的NIHSS评分低于对照组;治疗1个月后,观察组患者的mRS评分、中医证候积分低于对照组,差异均有统计学意义(P<0.05)。结论:温胆汤加减治疗气虚血瘀痰阻型缺血性脑卒中急性期患者的效果较好,可显著降低NT-proBNP、ICAM-1和MCP-1水平,促进血液流通和疾病的恢复,提高患者的生活质量。

Advanced oxidation protein products induce monocyte chemoattractant protein-1 expression via p38 mitogen-activated protein kinase activation in rat vascular smooth muscle cells

Background Advanced oxidation protein products （AOPPs） are new uremic toxins reported by Witko-Sarsat in 1996, which are associated with the pathogenesis of atherosclerosis. However, the mechanisms by which AOPPs enhance atherosclerosis have not been fully understood. Monocyte chemoattractant protein-1 （MCP-1） is a chemokine which stimulates migration of monocytes and plays a critical role in the development of atherosclerosis. In this study, we investigated the effect of AOPPs on MCP-1 expression in cultured vascular smooth muscle cells （VSMCs）.

单磷酸阿糖腺苷治疗毛细支气管炎

目的探讨单磷酸阿糖腺苷治疗毛细支气管炎患儿的效果。方法选择122例毛细支气管炎患儿,根据入院顺序随机分为观察组与对照组,各61例。对照组接受吸入用布地奈德混悬液、复方异丙托溴铵溶液治疗,观察组在对照组基础上接受注射用单磷酸阿糖腺苷治疗。2组均治疗7 d。观察2组治疗7 d后的疗效,记录2组临床指标变化情况,比较2组治疗前、治疗7 d后肺功能指标、血清淀粉蛋白A(SAA)、白三烯E4(LTE4)、单核细胞趋化蛋白-1(MCP-1)水平及治疗期间不良反应发生率。结果治疗7 d后,观察组总有效率(93.44%,57/61)高于对照组(80.33%,49/61)(P<0.05)。观察组喘息、湿啰音、咳嗽消失及住院时间短于对照组(P<0.05)。治疗7 d后,2组达峰时间比(TPTEF/TE)、潮气量(TV)水平高于治疗前,且观察组高于对照组;2组血清SAA、LTE4、MCP-1、吸呼时间比(TI/TE)水平低于治疗前,观察组低于对照组(P均<0.05)。治疗期间,2组不良反应发生率比较,差异无统计学意义(P>0.05)。结论毛细支气管炎患儿在布地奈德、复方异丙托溴铵治疗后给予单磷酸阿糖腺苷联合治疗可降低血清SAA、LTE4、MCP-1水平,明显改善患儿肺功能及临床症状,提高疗效,缩短住院时间,安全性良好。

体积描记法联合血清单核细胞趋化蛋白-1水平预测急性下呼吸道感染患者合并哮喘的效能分析

目的探究体积描记法联合血清单核细胞趋化蛋白-1(MCP-1)对急性下呼吸道感染患者合并哮喘的预测价值。方法回顾性分析2019年6月—2022年12月青海省人民医院收治的188例急性下呼吸道感染患者的病历资料。根据患者住院期间是否并发哮喘分为合并组(48例)和非合并组(140例)。收集并整理所有受试者的人口学资料和实验室检测指标(体积描记法相关参数:肺总量、残气量、残气率,血清MCP-1水平)。比较两组患者临床资料的差异,分析肺总量、残气量与功能残气量(FRC)、MCP-1的相关性,分析影响急性下呼吸道感染患者并发哮喘的相关因素,以及FRC、MCP-1对急性下呼吸道感染患者并发哮喘的预测价值。结果合并组FRC、肺总量、残气量、残气率、MCP-1水平均高于非合并组(P<0.05)。FRC与肺总量、残气量水平均呈正相关(r=0.681和0.671,均P=0.001);MCP-1与肺总量、残气量水平均呈正相关(r=0.669和0.654,均P=0.001)。多因素逐步Logistic回归分析结果显示:FRC[O^R=2.450(95%CI:1.239,4.840)]、MCP-1[O^R=2.995(95%CI:1.516,5.918)]是急性下呼吸道感染患者并发哮喘的危险因素(P<0.05)。受试者工作特征曲线结果分析显示,FRC、MCP-1及联合预测急性下呼吸道感染患者并发哮喘的敏感性分别为72.92%(95%CI:0.579,0.842)、83.33%(95%CI:0.692,0.920)、79.17%(95%CI:0.645,0.890),特异性分别为81.43%(95%CI:0.737,0.873)、70.71%(95%CI:0.623,0.779)、81.43%(95%CI:0.737,0.873)。结论体积描记法和血清MCP-1水平可用于评估急性下呼吸道感染患者肺功能,且血清MCP-1与体积描记法检测的FRC对急性下呼吸道感染患者并发哮喘的预测效能良好。