2-O-β-D-Glucopyranosyl-L-ascorbic acid,an ascorbic acid derivative isolated from the fruits of Lycium barbarum L.,ameliorates high fructose-induced neuroinflammation in mice:involvement of gut microbiota and leaky gut

Western diet(rich in highly refined sugar and fat)can induce a range of metabolic dysfunctions in animals and humans,including neuroinflammation and cognitive function decline.Neuroinflammation and cognitive impairment,two critical pathological characteristics of Alzheimer’s disease,have been closely associated with microbial alteration via the gut-brain axis.Thus,the present study aimed to investigate the influence of 2-O-β-D-glucopyranosyl-L-ascorbic acid(AA-2βG)isolated from the fruits of Lycium barbarum on preventing the high-fructose diet(HFrD)induced neuroinflammation in mice.It was found that AA-2βG prevented HFr D-induced cognitive deficits.AA-2βG also predominantly enhanced the gut barrier integrity,decreased lipopolysaccharide entry into the circulation,which subsequently countered the activation of glial cells and neuroinflammatory response.These beneficial effects were transmissible by horizontal fecal microbiome transplantation,transferring from AA-2βG fed mice to HFr D fed mice.Additionally,AA-2βG exerted neuroprotective effects involving the enrichment of Lactobacillus and Akkermansia,potentially beneficial intestinal bacteria.The present study provided the evidence that AA-2βG could improve indices of cognition and neuroinflammmation via modulating gut dybiosis and preventing leaky gut.As a potential functional food ingredient,AA-2βG may be applied to attenuate neuroinflammation associated with Western-style diets.

S4B-2 Bushen-Yizhi Formula Inhibits the NLRP3/NFκB Mediated Neuroinflammation and Improves the Motor Dysfunction in a Mouse Model of Parkinson’s Disease

Objective:Parkinson’s disease(PD)is the second largest neurodegenerative disease following Alzheimer’s disease(AD),which associated with aging.There are many similarities in pathology and pathogenesis,even in the TCM theory understanding,so we can learn from each other in the process of drug discovery.The clinical results showed that Bushen-Yizhi formula(BSYZ)could effectively improve the neurological function score of senile dementia patients and had a better anti-dementia effect.Further pharmacological studies showed that BSYZ had neuroprotective effects,such as anti-inflammatory,anti-oxidation,anti-apoptosis and neurotrophic effects.In this study,the therapeutic effect of BSYZ on PD was evaluated in vivo and in vivo,and its molecular mechanism was discussed in order to expand the scope of application of BSYZ and to provide strategies for drug discovery of related neurodegenerative diseases.Methods:C57 BL/6 mice were injected intraperitoneally with MPTP to construct a PD mouse model.BSYZ(1.46,2.92,5.84 mg·kg-1)was administered for two weeks,and the positive control group was given a NSAID,piroxicam(12.5 mg·kg-1).After 1 week of pretreatment,MPTP was used to construct a PD mouse model.The mice were subjected to Rotation test on days 1,3 and 5,6th day.and the movement coordination and exercise ability of the drug on PD mice were observed on theThe number of TH-positive cells,Iba1 and CD68-labeled microglial cells in SNpc region were observed by immunofluorescence to observe the proliferation and activation of microglial cells and GFAP-labeled astrocytes.Western blotting was used to detect the nuclear transfer of NLRP3,Caspase-1,ASC,pro-IL-1β,IL-1βand NF-κB in the midbrain.Results:1.BSYZ could significantly improve the expression of MPTP model mice in the experiment of fatigue and Y-maze,increase the number of neurons in SNpc region and the positive expression of TH protein.2.BSYZ significantly inhibited the number of Iba1/CD68-positive microglial cells in MPTP-model mice and decreased the number of GFAP-positive astrocytes.3.BSYZ significantly inhibited the expression of NLRP3-associated protein in BV2 microglial cells induced by LPS+ATP and inhibited the nuclear transfer of NF-κB.Conclusion:BSYZ can effectively relieve the motor dysfunction of PD model mice,improve the damage of dopaminergic neurons,inhibit the proliferation and activation of microglial cells and astrocytes,and have good anti-MPTPinduced neuroinflammation and neuroinflammation mediated by nuclear transfer of NF-κB.The results show that BSYZ has a good prospect of anti-Parkinson’s disease and provides valuable drug discovery strategies for the related neurodegenerative diseases.

Biochanin A and CPe-Ⅲ Peptide Improved Hepatic Infl ammation by Regulating the Hepatic Lipid Metabolic Pathways in Diet-Induced Obese Mice

Biochanin A(BCA) and CPe-Ⅲ peptide, which both exist in chickpea(Cicer arietinum L.), possess significant antihyperlipidemic properties. However, the actualmechanisms ofthose compounds in inhibiting the dysregulation oflipid metabolism and complicated inflammation have not been wellcharacterized. This study investigated the effects ofBCA, CPe-Ⅲ peptide, and combined BCA and CPe-Ⅲ peptide(BC) on the expression ofgenes involved in hepatic lipid and inflammation metabolism. Results demonstrated that BCA, CPe-Ⅲ peptide, and BC significantly attenuated hepatitis and hyperlipidemia by downregulating those genes involved in pro-inflammatory cytokines(TNF-α), hepatic fatty acid(FA) synthesis(ACC1 and FAS), cholesterolmetabolism(SREBP2, HMGCR, and PCSK9), and upregulating key regulators involved in FA oxidation(PPARα and FABP1), lipolysis(ATGL), LDLR, reverse cholesteroltransport(ABCA1, SR-B1, and LXRα), and cholesterolcatabolism(CYP7 A1). Moreover, they also altered the expression oflipid metabolism-related proteins, including SREBP2, PCSK9, LDLR, ABCA1, and CYP7 A1. Finally, these results revealed that the combination treatment ofBCA and CPe-Ⅲ peptide resulted in greater antihyperlipidemic activity compared with individualcompounds.

Moringa oleifera Lam. leaf extract mitigates carbon tetrachloride-mediated hepatic inflammation and apoptosis via targeting oxidative stress and toll-like receptor 4/nuclear factor kappa B pathway in mice

Carbon tetrachloride(CCl4)is a hepatotoxin that triggers liver damage.This study aimed to evaluate the protective effect of phytochemicals detected in Moringa oleifera Lam.leaf extract(MOLE)on CCl4-induced hepatotoxicity in mice.Phytochemicals,total phenolics,and total fl avonoids were detected in MOLE.MOLE markedly decreased the elevation of serum alanine aminotransferase(ALT)and aspartate aminotransferase(AST)in consistence with the ameliorating effect on CCl4-induced histopathological abnormalities.Moreover,MOLE significantly alleviated the decrease in the antioxidant defense mechanism induced by CCl4.The suppressing effect of MOLE on the boosted inflammatory pathway triggered by CCl4 was detected by measuring the protein levels of nuclear factor kappa-light-chain-enhancer of activated B-cells(NF-κB-p65),toll-like receptor 4(TLR4),tumor necrosis factor-α(TNF-α),interleukin(IL)-6,IL-1β,and IL-8 as well as the relative expressions of nuclear factor kappa B(NF-κB),TNF-α,IL-1β,and TLR4 genes.Apoptosis and genotoxicity induced by CCl4 were signifi cantly alleviated by MOLE.MOLE co-administration modulated TLR4/NF-κB pathway as presented by the suppressed gene expression of TLR4 and NF-κB as well as by the reduced protein expression of TLR4 and NF-κB-p65.In conclusion,MOLE has a multifarious protective role against hepatotoxicity through control of oxidative stress and modulation of TLR4/NF-κB.

Cholic acid mitigates osteoarthritis by inhibiting the NF-κB/PERK/ SIRT1 signaling pathway

Introduction:Cholic acid(CA)is a natural steroid useful in treating chronic bronchitis and cholecystitis.On the other hand,its potential impact on osteoarthritis(OA)is unknown.Objective:Using an in vitro and in vivo osteoarthritis model,we sought to assess the chondroprotective properties of CA.Methods:We employed the Cell Counting Kit-8 to measure the impact of CA on chondrocyte activity to assess the toxicity of the cells.Multiple molecular biology experimental techniques were used to investigate potential signaling pathways that CA may use to prevent inflammation and give chondrocytes protection.Furthermore,how CA affects the OA model in Sprague-Dawley(SD)rats was evaluated.Results:CA significantly suppressed the up-regulation of the interleukin-1β(IL-1β),cyclooxygenase-2(COX-2),and matrix metalloproteinase 13(MMP-13)and the downregulation of aggrecan and type II collagen A1(COL2A)in chondrocytes treated tumor necrosis factor-alpha(TNF-α).Differentially expressed genes(DEG)enrichment revealed IL-17,TNF,chemokine,cytokine-cytokine receptor,toll-like receptor,and nucleotide oligomerization domain-like receptor were the primary signaling pathways.The enriched DEGs included CXCL6,CCL20,MMP3,CXCL3,CXCL11,CCL5,CXCL10,MMP9,MMP13,and CXCL2;these DEGs are involved in inflammatory responses and their expression induced by TNF-αwas reversed by CA treatment.CA inhibits p65 nuclear translocation and inhibitory subunit kappa B alpha(IκBα)phosphorylation induced by TNF-α.Furthermore,CA attenuated protein expression of protein kinase RNA-like endoplasmic reticulum kinase(PERK),inositol-requiring transmembrane kinase/endoribonuclease 1α(IRE1α),glucose regulatory protein 78(GRP78),and sirtuin 1(SIRT1),and down-regulation of phosphorylation of AMP-activated protein kinase-α(p-AMPKα)in TNF-α-treated chondrocytes.Conclusions:CA significantly ameliorated cartilage degradation in the OA rat model.CA alleviated the inflammatory response through the nuclear factor kappa B/PERK/SIRT1 axis and ameliorated cartilage degradation.

硅胶制品在瘢痕防治中的作用机制及应用进展

病理性瘢痕包括增生性瘢痕和瘢痕疙瘩,多认为起源于修复和再生失调引起的异常创伤愈合过程,其发病机制尚不清楚,常引起患者机体功能和心理障碍,治疗方法虽然很多,但没有一种疗效确切且简单易行。硅胶制品预防和治疗瘢痕的效果明显,且由于其具有方便及无创的特点,在临床上被广泛应用。本文就目前硅胶制品防治瘢痕的机制,硅胶制品联合其他药物治疗瘢痕的临床案例进行总结和阐述,并展望其应用前景。

炎症研究现状与进展

炎症是自身免疫系统对外界刺激的防御反应,能够在各种有害条件下维持组织稳态。然而,炎症反应会导致暂时性的组织功能下降,这反过来也是许多疾病发生的机制之一。因此,当炎症反应过度或持续存在时,会促进多种慢性疾病的发展,例如心血管疾病、恶性肿瘤、糖尿病、慢性肾病以及代谢相关脂肪性肝病(MAFLD)等。从生命的早期阶段起,炎症在我们伤口愈合和感染康复中扮演着至关重要的角色,而到了老年时,我们可能会遭受各种慢性炎症性疾病的折磨。人类生命过程与炎症息息相关,炎症不仅是一种保护因素,同时也可能是一种致病因素,贯穿了整个生命周期。因此,全面了解炎症并尝试采取措施来减轻炎症对健康的影响十分重要。本文旨在系统介绍炎症相关进展。通过系统性地探讨炎症理论发展史、炎症发生模式、炎症分类、炎症作用以及炎症调控等内容,以期为炎症相关疾病的干预和治疗提供新的思路和方向。

微炎症状态及肠道菌群与老年2型糖尿病患者并发糖尿病肾病的关系探讨

目的探讨微炎症状态及肠道菌群与老年2型糖尿病(T2DM)患者并发糖尿病肾病的关系。方法选取2022年1月至2023年12月四川省广元市中心医院收治的154例老年T2DM患者为研究对象,根据是否并发糖尿病肾病将研究对象分为发生组(并发糖尿病肾病,41例)与未发生组(未并发糖尿病肾病,113例)。比较分析两组患者的微炎症状态[肿瘤坏死因子-α(TNF-α)、C反应蛋白(CRP)、白介素-6(IL-6)]及肠道菌群[双歧杆菌、肠球菌、乳杆菌、肠杆菌、双歧杆菌与肠杆菌比值(B/E)]。分析老年T2DM患者并发糖尿病肾病的影响因素以及B/E与微炎症状态的交互作用。结果发生组患者的TNF-α、CRP、IL-6、肠杆菌水平均高于未发生组,双歧杆菌、乳杆菌、B/E均低于未发生组,差异均有统计学意义(P<0.05)。多因素logistic回归分析结果显示,TNF-α、CRP、IL-6均为老年T2DM患者并发糖尿病肾病的独立危险因素(P<0.05),B/E为老年T2DM患者并发糖尿病肾病的独立保护因素(P<0.05)。相乘交互作用分析结果显示,B/E与TNF-α、CRP、IL-6之间不存在相乘交互作用(P>0.05);相加交互作用分析结果显示,相对超额危险度和归因交互效应百分比的可信区间均>0,交互作用指数的可信区间>1,表明B/E与TNF-α、B/E与CRP、B/E与IL-6之间均存在相加交互作用。结论老年T2DM患者并发糖尿病肾病后伴有不同程度的微炎症状态及肠道菌群失调,TNF-α、CRP、IL-6均为老年T2DM患者并发糖尿病肾病的独立危险因素,B/E为老年T2DM患者并发糖尿病肾病的独立保护因素,且B/E与微炎症状态相关指标存在相加交互作用。

腹腔镜胆囊切除术后不放置引流管治疗急性化脓性胆囊炎的效果及影响

目的 探讨腹腔镜胆囊切除术(laparoscopic cholecystectomy,LC)后放置引流管与不放置引流管治疗急性化脓性胆囊炎的效果及影响。方法 选取2022年1月至2023年9月北京市通州区中医医院收治的86例急性化脓性胆囊炎患者,均接受腹腔镜下胆囊切除术治疗,按照术后置管与否分组,A组43例患者术后不放置引流管,B组43例患者术后放置引流管,比较两组围手术期指标、炎症指标及术后并发症发生情况。结果 A组患者术后肛门排气时间、下床活动时间、住院时间均短于B组,差异有显著性(P<0.05)。两组患者术前C反应蛋白、白细胞计数、白介素-6水平无明显差异(P> 0.05);术后3d,A组患者上述指标水平均优于B组,差异有显著性(P <0.05)。A组患者术后切口疼痛、感染、胆漏、肩部疼痛等发生率显著低于B组(P <0.05)。结论 急性化脓性胆囊炎患者采用腹腔镜胆囊切除术后不放置引流管,能缩短患者术后恢复时间,降低并发症发生风险。

Antrodia Cinnamomea ameliorates neointimal formation by inhibiting infl ammatory cell infi ltration through downregulation of adhesion molecule expression in vitro and in vivo

The increased vascular infl ammation is a key event in the development of atherosclerotic lesions.Antrodia cinnamomea has been shown to promote anticancerogenic activity through decreasing infl ammation.However,the potential role of A.cinnamomea in cardiovascular diseases remains unexplored.Herein,using carotid arterial ligation models,we found that ethanol extract from A.cinnamomea(EEAC)signifi cantly inhibited neointimal hyperplasia in a dose-dependent manner,accompanied with the reduced expression of activated p65 and infl ammatory cytokines.We also show that EEAC ameliorated TNF-α-induced phosphorylation of p65 and pro-infl ammatory cytokine expression in both vascular smooth muscle cells(VSMCs)and macrophages in vitro.Mechanistically,EEAC suppressed expression levels of intercellular adhesion molecule-1(ICAM-1)and vascular cell adhesion molecule(VCAM-1)in VSMCs,which attenuates the ability of monocytes/macrophages adhesion to VSMCs.Furthermore,the expression level of these adhesion molecules and infi ltration of monocytes/macrophages were also decreased in neointimal VSMCs of arteries pretreated with EEAC.Altogether,our results reveal a novel function of A.cinnamomea in suppressing vascular infl ammation upon ligation injury during neointimal formation,likely through inhibition of infl ammatory cell infi ltration via downregulating the adhesion molecules in VSMCs.Thus,A.cinnamomea may offer a pharmacological therapy to slow down disease progression in patients with vascular injury.

Lunasin protease inhibitor concentrate decreases pro-infl ammatory cytokines and improves histopathological markers in dextran sodium sulfate-induced ulcerative colitis

Lunasin protease inhibitor concentrate(LPIC)is a novel combination of soy bioactive peptide lunasin,Kunitz and Bowman-Birk protease inhibitors.The reported anti-inflammatory and anticancer properties of each one of them suggest LPIC as a promising candidate for the treatment of infl ammatory-related diseases.Our objective was to assess the in vivo anti-infl ammatory properties of LPIC.First,an in vitro test was performed in lipopolysaccharide(LPS)-activated RAW264.7 murine macrophages by measuring the production of nitric oxide(NO),interleukin-6(IL-6),and tumor necrosis factorα(TNF-α)as infl ammatory markers.For the in vivo model,ulcerative colitis(UC)was induced in mice via oral administration of dextran sodium sulfate(DSS).LPIC treatment was performed via daily intraperitoneal injection of 50 mg/kg body weight.Body weight,visible blood in stool and stool consistency were scored daily as macroscopic indicators of disease progression.Occult blood was evaluated by the presence of hemoglobin in stool every third day.Colon length,caecum weight,colonic myeloperoxidase activity(MPO),presence of pro-inflammatory cytokines in blood and colon,changes in the architecture,and expression of inducible nitric oxide synthase(i NOS)in colonic tissue were evaluated.In vitro,LPIC induced production of NO and maintained cytokine levels in comparison to activated untreated macrophages.In vivo,LPIC increased colonic bleeding and did not improve macroscopic markers of the disease,but reduced colonic IL-1βand IL-6,decreased systemic circulation of TNF-α,attenuated neutrophils infi ltration and i NOS expression in colonic tissue,and diminished the damage in colonic architecture.Our results suggest that combinations of peptides in LPIC may counteract the antiinfl ammatory properties in vitro;while in vivo,LPIC can signifi cantly reduce the histopathological damage,hence is a possible therapeutic strategy to attenuate UC.

5-氨基酮戊酸光动力疗法对中重度痤疮炎症性皮损和炎症后红斑的影响

目的:探讨5-氨基酮戊酸光动力疗法(5-aminolevulinic acid photodynamic therapy,ALA-PDT)治疗中重度痤疮患者的临床疗效。方法:采用随机数字表法将2021年1月-2022年1月笔者医院收治的中重度痤疮患者80例分为对照组(n=40)和治疗组(n=40),对照组予以红蓝光照射治疗,治疗组采取ALA-PDT治疗,均持续治疗4周。比较两组临床疗效,治疗前后痤疮严重程度分级系统评分(Global Acne grading system,GAGS)、痤疮特异性生活质量量表评分(The acne-specific quality of life questionnaire,Acne-QOL)、皮损情况、炎症后红斑情况及不良反应发生情况。结果:治疗组临床总有效率为95.00%,高于对照组的72.50%(P<0.05);与治疗前相比,治疗后两组GAGS评分均降低(P<0.05),两组Acne-QOL量表评分均升高(P<0.05),两组炎性皮损和非炎性皮损数量均减少(P<0.05),两组红斑指数和红斑主观评分均降低(P<0.05),且治疗组GAGS评分、炎性皮损和非炎性皮损个数、红斑指数和红斑主观评分均低于对照组(P<0.05),Acne-QOL量表评分高于对照组(P<0.05);治疗组不良反应总发生率低于对照组(P<0.05)。结论:中重度痤疮患者采用ALA-PDT治疗效果显著,可降低患者痤疮严重程度,提高生活质量,改善皮损情况及炎症后红斑,值得推广。

温阳强心颗粒对大鼠心肌缺血-再灌注损伤的保护作用研究

目的 探讨温阳强心颗粒对大鼠心肌缺血-再灌注损伤(MIRI)的保护作用。方法 通过结扎左冠状动脉前降支阻断心脏供血,再恢复血液供应建立心肌缺血再灌注损伤模型,分成假手术组、模型组、阳性对照组和温阳强心组,每组20只。全程监测各组术中血流动力学以及心电图,用于评价心脏功能的变化。再灌注2 h后采集血清,检测血清氧化应激损伤标志物SOD、MDA、CAT,血清心肌酶活性CK、CK-MB、AST和LDH等,血清炎性细胞因子IL-6和TNF-α水平。结果 与模型组相比较,在各个时间点上,阳性对照组和温阳强心组大鼠T波幅高度均显著降低(P <0.01),LVSP和+dp/dtmax显著升高(P <0.01),-dp/dtmax显著降低(P <0.01)。与模型组比较,阳性对照组与温阳强心组大鼠血清SOD和CAT显著升高(P <0.01),同时MDA水平显著降低(P <0.01),血清各项心肌酶活性均显著降低(P <0.01),血清IL-6和TNF-α均显著降低(P <0.01)。结论温阳强心颗粒预处理减缓了心肌缺血-再灌注损伤中的氧化应激反应,抑制了心肌缺血-再灌注损伤对组织细胞的损伤,增强了大鼠心肌细胞膜的稳定性,抑制伴随的炎性反应,发挥对心肌缺血-再灌注损伤大鼠心脏的保护作用。

Over-expression of programmed death-ligand 1 and programmed death-1 on antigen-presenting cells as a predictor of organ dysfunction and mortality during early sepsis: a prospective cohort study

BACKGROUND:This study aimed to explore the changes of programmed death-ligand 1(PDL1)and programmed death-1(PD-1)expression on antigen-presenting cells(APCs)and evaluate their association with organ failure and mortality during early sepsis.METHODS:In total,40 healthy controls and 198 patients with sepsis were included in this study.Peripheral blood was collected within the first 24 h after the diagnosis of sepsis.The expression of PDL1 and PD-1 was determined on APCs,such as B cells,monocytes,and dendritic cells(DCs),by flow cytometry.Cytokines in plasma,such as interferon-γ(IFN-γ),tumor necrosis factor-α(TNF-α),interleukin-4(IL-4),IL-6,IL-10,and IL-17A were determined by Luminex assay.RESULTS:PD-1 expression decreased significantly on B cells,monocytes,myeloid DCs(mDCs),and plasmacytoid DCs(pDCs)as the severity of sepsis increased.PD-1 expression was also markedly decreased in non-survivors compared with survivors.In contrast,PD-L1 expression was markedly higher on mDCs,pDCs,and monocytes in patients with sepsis than in healthy controls and in non-survivors than in survivors.The PD-L1 expression on APCs(monocytes and DCs)was weakly related to organ dysfunction and infl ammation.The area under the receiver operating characteristic curve(AUC)of the PD-1 percentage of monocytes(monocyte PD-1%)+APACHE II model(0.823)and monocyte PD-1%+SOFA model(0.816)had higher prognostic value than other parameters alone.Monocyte PD-1%was an independent risk factor for 28-day mortality.CONCLUSION:The severity of sepsis was correlated with PD-L1 or PD-1 over-expression on APCs.PD-L1 in monocytes and DCs was weakly correlated with infl ammation and organ dysfunction during early sepsis.The combination of SOFA or APACHE II scores with monocyte PD-1%could improve the prediction ability for mortality.

甘草酸苷对对乙酰氨基酚所致小鼠急性肝损伤的保护作用

目的探究甘草酸苷对对乙酰氨基酚所致急性肝损伤(ALI)小鼠的肝脏保护作用。方法对乙酰氨基酚腹腔注射建模。随机分为模型组、联苯双酯组(60 mg/kg联苯双酯灌胃)、甘草酸苷低、中、高剂量组[分别以50、100、150 mg/mL甘草酸苷灌胃(剂量均为1 mL/100 g小鼠体质量)],另设置对照组。酶标仪检测小鼠血清肝功能、炎性因子水平;苏木素-伊红(HE)染色法观察小鼠肝组织病理学变化;酶标分析仪检测肝组织匀浆氧化应激。结果与对照组相比,模型组肝组织损伤,血清ALT、AST、LDH水平上升,TNF-α、IL-6含量增加,肝组织GSH、SOD活性下降,MDA活性上升;与模型组相比,联苯双酯组和甘草酸苷低、中、高剂量组均改善。联苯双酯组与甘草酸苷中剂量组比较,差异均无统计学意义(P>0.05),其余每2组比较,差异均有统计学意义(P<0.05)。结论甘草酸苷可减轻对乙酰氨基酚引起的肝损害,还可减轻炎性反应及氧化应激。

动画产业人才需求与动画教育现状的反思

本文对我国动画教育发展现状和动漫产业的人才需求结构进行了分析和反思。

左西孟旦对猪冠状动脉微栓塞后心肌细胞炎症反应的影响

目的探讨左西孟旦对猪急性冠状动脉微栓塞(CME)后心肌细胞炎症反应的影响及意义。方法将健康巴马系小型猪随机分为CME+左西孟旦组、假手术组及CME组,每组5只。采用经皮冠状动脉介入治疗法,于左前降支中段(发出第一对角支)处,经微导管在40 min内注入42μm的微栓塞球45 ml(假手术组注射等量生理盐水),再用10 ml生理盐水冲洗微导管并注入冠状动脉内。CME+左西孟旦组在CME建立前以左西孟旦预处理[从耳缘静脉以0.05μg/(kg·min)使用24 h,术前60 min再以0.2μg/(kg·min)负荷使用]。术后12 h采用超声心动图检测心功能包括左心室舒张末期内径(LVEDd)、左心室射血分数(LVEF)、心排血量(CO)及左心室短轴缩短率(FS),以Western blot检测活化肿瘤坏死因子α(TNF-α)表达水平。结果 CME组术后12 h FS[(24.49±2.86)%比(41.28±2.86)%,P=0.023]、LVEF[(49.83±4.64)%比(66.86±3.97)%,P=0.035]、CO[(2.58±0.42) L/min比(4.32±0.89) L/min,P=0.042]与假手术组比较均显著下降,而LVEDd[(38.26±1.93) mm比(32.39±1.52) mm,P=0.043]比假手术组显著增加,差异均具有统计学意义。CME+左西孟旦组FS[(32.42±3.98)%比(24.49±2.86)%,P=0.029]、LVEF[(58.42±5.28)%比(49.83±4.64)%,P=0.043]、CO[(3.58±0.92) L/min比(2.58±0.42)L/min,P=0.038]与CME组比较均呈现升高趋势,LVEDd [(33.92±1.56)mm比(38.26±1.93) mm,P=0.037]比CME组呈现降低趋势,差异均有统计学意义。Western blot定量分析显示,CME组与对照组比较,心肌组织TNF-α蛋白表达水平较高(P=0.039);CME+左西孟旦组与CME组比较,心肌组织TNF-α蛋白表达水平较低(P=0.042),差异均有统计学意义。结论左西孟旦预处理可明显减少CME后心肌细胞炎症反应并改善心功能,其机制可能是通过抑制心肌细胞促炎蛋白TNF-α表达来实现。

1.25-二羟维生素D3与皮肤病

1.25-二羟维生素D3是维生素D的活性形式,参与机体钙磷代谢、免疫反应、应激、炎症以及肿瘤的调控等。大量研究表明,1.25-二羟维生素D3能与T淋巴细胞、树突状细胞、巨噬细胞等发生作用,通过抗光老化、抑制自身免疫细胞的增生及细胞因子的合成和分泌在炎症性皮肤病、自身免疫性皮肤病及皮肤肿瘤中发挥作用。1.25-二羟维生素D3和类似物将在皮肤病治疗方面发挥重要的作用。

脂肪因子在银屑病发病机制中的研究进展

银屑病是一种慢性炎症性皮肤病,患者多伴有系统性代谢性疾病。脂肪组织作为内分泌器官可分泌多种脂肪因子参与多种代谢性疾病和炎症性疾病的发病。目前的研究证实一些脂肪因子可能参与银屑病的发病过程,并且为将来的诊断治疗提供新的生物学标志。

炎症性肠病患者营养状况与生活质量的相关性研究

目的探讨炎症性肠病患者营养状况的影响因素及与生活质量的关系。方法选取2019年1月—2020年6月在南通大学第二附属医院住院的73例炎症性肠病(IBD)患者,收集患者的一般资料、营养状况分级资料、疾病活动指数、生活质量等数据,通过单因素和多因素分析影响炎症性肠病患者生活质量的主要因素,并分析营养状况与生活质量的相关性。结果IBD患者中多发营养不良,多因素分析显示,疾病类型、疾病状态、营养状况为影响患者生活质量的主要影响因素。相关性分析显示,营养不良与生活质量呈负相关。结论IBD患者生活质量下降与营养受损存在相关性,改善营养状况,可为改善患者整体状况提供基础。