Diagnostic significance of serum levels of serum amyloid A,procalcitonin,and high-mobility group box 1 in identifying necrotising enterocolitis in newborns

BACKGROUND Necrotising enterocolitis(NEC)is a critical gastrointestinal emergency affecting premature and low-birth-weight neonates.Serum amyloid A(SAA),procalcitonin(PCT),and high-mobility group box 1(HMGB1)have emerged as potential biomarkers for NEC due to their roles in inflammatory response,tissue damage,and immune regulation.AIM To evaluate the diagnostic value of SAA,PCT,and HMGB1 in the context of NEC in newborns.METHODS The study retrospectively analysed the clinical data of 48 newborns diagnosed with NEC and 50 healthy newborns admitted to the hospital.Clinical,radiological,and laboratory findings,including serum SAA,PCT,and HMGB1 Levels,were collected,and specific detection methods were used.The diagnostic value of the biomarkers was evaluated through statistical analysis,which was performed using chi-square test,t-test,correlation analysis,and receiver operating characteristic(ROC)analysis.RESULTS The study demonstrated significantly elevated levels of serum SAA,PCT,and HMGB1 Levels in newborns diagnosed with NEC compared with healthy controls.The correlation analysis indicated strong positive correlations among serum SAA,PCT,and HMGB1 Levels and the presence of NEC.ROC analysis revealed promising sensitivity and specificity for serum SAA,PCT,and HMGB1 Levels as potential diagnostic markers.The combined model of the three biomarkers demonstrating an extremely high area under the curve(0.908).CONCLUSION The diagnostic value of serum SAA,PCT,and HMGB1 Levels in NEC was highlighted.These biomarkers potentially improve the early detection,risk stratification,and clinical management of critical conditions.The findings suggest that these biomarkers may aid in timely intervention and the enhancement of outcomes for neonates affected by NEC.

Inhibition of high-mobility group box 1 expression by siRNA in rat hepatic stellate cells

AIM:To explore the role of high-mobility group box 1 (HMGB1) protein during liver fibrogenesis and investigate the functional effects of HMGB1 gene silencing in hepatic stellate cells (HSCs) using siRNA.METHODS:Hepatic fibrosis in rats was induced through serial subcutaneous injections of dimethylnitrosamine,and expression of HMGB1 was detected by immunohistochemistry.HMGB1 siRNAs were developed and transiently transfected into HSC-T6 cells using Lipofectamine 2000.HMGB1 expression was evaluated by real-time polymerase chain reaction (PCR) and Western blotting analysis.Expression of α-smooth muscle actin (α-SMA) and collagen typesⅠand Ⅲ was evaluated by real-time PCR.Cell proliferation and the cell cycle were determined using the methyl thiazolyl tetrazolium method.Finally,collagen content in HSC supernatant was evaluated by an enzyme-linked immunosorbent assay.RESULTS:The results showed that HMGB1 was upregulated during liver fibrosis and that its expression was closely correlated with the deposition of collagen.siRNA molecules were successfully transfected into HSCs and induced inhibition of HMGB1 expression in a time-dependent manner.Moreover,HMGB1 siRNA treatment inhibited synthesis of α-SMA and collagen types Ⅰ and Ⅲ in transfected HSCs.CONCLUSION:This study suggests a significant functional role for HMGB1 in the development of liver fibrosis.It also demonstrates that downregulation of HMGB1 expression might be a potential strategy to treat liver fibrosis.

Inhibition of LOX-1 alleviates the proinflammatory effects of high-mobility group box 1 in Aspergillus fumigatus keratitis

AIM: To investigate the inflammatory amplification effect of high-mobility group box 1(HMGB1) in Aspergillus fumigatus(A. fumigatus) keratitis and the relationship between lectin-like oxidized low-density lipoprotein receptor 1(LOX-1) and HMGB1 in keratitis immune responses.METHODS: Phosphate buffer saline(PBS), and Boxb were injected into BALB/c mice subconjunctivally before the corneas were infected with A. fumigatus. RAW264.7 macrophages and neutrophils were pretreated with PBS and Boxb to determine the HMGB1 inflammatory amplification effects. Abdominal cavity extracted macrophages were pretreated with Boxb and Poly(I)(a LOX-1 inhibitor) before A. fumigatus hyphae stimulation to prove the the relationship between the two molecules. LOX-1, interleukin-1β(IL-1β), tumor necrosis factor-α(TNF-α), macrophage inflammatory protein-2(MIP-2) and IL-10 were assessed by polymerase chain reaction and Western blot.RESULTS: Pretreatment with Boxb exacerbated corneal inflammation. In macrophages and neutrophils, A. fumigatus induced LOX-1, IL-1β, TNF-α and MIP-2 expression in Boxb group was higher than those in PBS group. Poly(I) treatments before infection alleviated the proinflammatory effects of Boxb in abdominal cavity extracted macrophages. Pretreatment with Boxb did not influence Dectin-1 mRNA levels in macrophages and neutrophils.CONCLUSION: In fungal keratitis, HMGB1 is a proinflammatory factor in the first line of immune response. HMGB1 mainly stimulates neutrophils and macrophages to produce inflammatory cytokines and chemokines during the immune response. LOX-1 participates in HMGB1 induced inflammatory exacerbation in A. fumigatus keratitis.

Scolopendra subspinipes mutilans protected the ceruleininduced acute pancreatitis by inhibiting high-mobility group box protein-1

AIM:To evaluate the inhibitory effects of Scolopendra subspinipes mutilans(SSM) on cerulein-induced acute pancreatitis(AP) in a mouse model.METHODS:SSM water extract(0.1,0.5,or 1 g/kg) was administrated intraperitoneally 1 h prior to the first injection of cerulein.Once AP developed,the stable cholecystokinin analogue,cerulein was injected hourly,over a 6 h period.Blood samples were taken 6 h later to determine serum amylase,lipase,and cytokine levels.The pancreas and lungs were rapidly removed for morphological examination,myeloperoxidase assay,and real-time reverse transcription polymerase chain reaction.To specify the role of SSM in pancreatitis,the pancreatic acinar cells were isolated using collagenase method.Then the cells were pre-treated with SSM,then stimulated with cerulein.The cell viability,cytokine productions and high-mobility group box protein-1(HMGB-1) were measured.Furthermore,the regulating mechanisms of SSM action were evaluated.RESULTS:The administration of SSM significantly attenuated the severity of pancreatitis and pancreatitis associated lung injury,as was shown by the reduction in pancreatic edema,neutrophil infiltration,vacuolization and necrosis.SSM treatment also reduced pancreatic weight/body weight ratio,serum amylase,lipase and cytokine levels,and mRNA expression of multiple inflammatory mediators such as tumor necrosis factor-α and interleukin-1β.In addition,treatment with SSM inhibited HMGB-1 expression in the pancreas during AP.In accordance with in vivo data,SSM inhibited the cerulein-induced acinar cell death,cytokine,and HMGB-1 release.SSM also inhibited the activation of c-Jun NH2-terminal kinase,p38 and nuclear factor(NF)-κB.CONCLUSION:These results suggest that SSM plays a protective role during the development of AP and pancreatitis associated lung injury via deactivating c-Jun NH2-terminal kinase,p38 and NF-κB.

Clinical signification of high-mobility group box 1protein(HMGB1) expression in infiltrating ductalcarcinoma breast tissue

Objective: Exploring the clinical signification of high-mobility group box 1 protein(HMGB1) expression in infiltrating ductal carcinoma(IDC) breast tissue. Methods: The expression of HMGB1 protein in IDC breast tissue was detected by immunohistochemistry, and the relations among size of tumour, lymph node metastasis, clinical staging, estrogen receptor(ER), progesterone receptor(PR) and human epidermal growth factor receptor 2(HER-2) were also analyzed. Results: Fortysix cases out of 60 cases of IDC breast tissue showed positive or strong positive HMGB1 expression(76.67%), statistical significance was observed between HMGB1 expression with clinical staging(P < 0.01), lymph node metastasis(P < 0.01), breast cancer ER(P < 0.05) and HER-2(P < 0.05), however same conclusion can not be drawn between HMGB1 with either size of tumour or PR expression(P > 0.05) in IDC breast tissue. Spearman analysis showed negative correlation between HMGB1 expression and ER, and positive correlation between HMGB1 expression and clinical staging, lymph node metastasis together with HER-2. Conclusion: It's promising that HMGB1 expression in IDC tissue can be one of biological indicators of poor prognosis.

Effect on proliferation and apoptosis of retinoblastoma cell by RNA inhibiting high mobility group protein box-1 expression

AIM： To investigate the effect of high mobility group protein box-1 （HMGB1） siRNA on proliferation and apoptosis of retinoblastoma （Rb） cells.METHODS： The expression of HMGB1 in Rb cells were detected by real-time polymerase chain reaction （RT-PCR） and Western blot. Chemically synthesized HMGB1 siRNA was transfected into Y79 cells. The inhibitory rate was also examined by RT-PCR and Western blot. After HMGB1 siRNA transfection, the cell proliferation was analyzed by MTT, and cell apoptosis was detected by Caspase-3 active detection kit. Cell cycle distribution and apoptosis were detected by flow cytometry. RESULTS： The expression of HMGB1 significantly elevated in Rb cells （P〈0.01）. After transfected by siRNA, the HMGB1 protein level of Y79 cells was significantly reduced （P〈0.01）. After siRNA interference HMGB1, the proportion of proliferating cells reduced, and the proportion of quiescent cells increased （P〈0.05）. In addition, apoptosis rate of Y79 cells increased from 2.03% to 9.10% after interfering with HMGB1 siRNA （P〈0.05）.CONCLUSION： Specific HMGB1 siRNA can inhibit the expression of HMGB1. The effect may be attributed to inhibit the proliferation and promote cell apoptosis.

Boxb mediate BALB/c mice corneal inflammation through a TLR4/MyD88-dependent signaling pathway in Aspergillus fumigatus keratitis

AIM： To investigate whether high-mobility group box 1（HMGB1） Boxb exacerbates BALB/c mice corneal immune responses and inflammatory through the Toll-like receptor 4（TLR4）/myeloid differentiation primary response 88（My D88）-dependent signaling pathway in Aspergillus fumigatus（A. fumigatus） keratitis.METHODS： The mice corneas were pretreated with phosphate buffer saline（PBS）, Boxb before A. fumigatus infection. The abdominal cavity extracted macrophages were pretreated with PBS, Boxb, TLR4 inhibitor（CLI-095）, Dimethyl sulfoxide（DMSO） separately before A. fumigatus hyphae stimulation. HMGB1 was detected in normal and infected mice corneas and macrophages by real-time reverse transcriptase polymerase chain reaction（RT-PCR）, the TLR4, My D88, interleukin-1β（IL-1β）, tumor necrosis factor-α（TNF-α） were detected by Western blot and PCR.RESULTS： In BALB/c mice corneas, the expressions of TLR4, HMGB1, IL-1β, TNF-α were increased after A. fumigatus infection. While pretreatment with Boxb significantly increased the expressions of TLR4, HMGB1, My D88, IL-1β, TNF-α compared with PBS control after infection. In BALB/c mice abdominal cavity extracted macrophages, pretreatment with Boxb increased the expressions of TLR4, HMGB1, My D88, IL-1β, TNF-α, while pretreatment with CLI-095 and Boxb significantly decreased the expressions of TLR4, HMGB1, My D88, IL-1β, TNF-α. CONCLUSION： In A. fumigatus keratitis, Boxb play a proinflammatory role in corneal anti-fungi immune response through the HMGB1-TLR4-My D88 signal pathway.

RNA干扰抑制HMGB1基因表达对宫颈癌HeLa细胞生物学行为的影响

背景与目的:高迁移率族蛋白1(high mobility group box-l,HMGB1)是一种非组蛋白染色体蛋白质,在多种高转移性肿瘤中高表达。前期研究结果证实,HMGB1在宫颈鳞癌组织及宫颈癌HeLa细胞中高表达,并与肿瘤临床分期、侵袭、转移密切相关。本研究通过RNA干扰(RNA interference,RNAi)抑制HMGB1基因表达,观察其对HeLa细胞增殖、侵袭和迁移的影响。方法:将HMGB1 siRNA真核表达质粒PGCsi3.0-1在脂质体介导下转染HeLa细胞,G418筛选阳性克隆,以转染PGCsi3.0-Neg(无关序列siRNA)质粒的细胞和未转染HeLa细胞作为对照。采用RT-PCR和Western blot检测HMGB1 mRNA和蛋白表达,通过MTT实验、细胞划痕实验和Transwell实验分别检测HeLa细胞增殖、侵袭和迁移能力。结果:PGCsi3.0-1组HMGB1 mRNA和蛋白表达水平分别为0.38±0.12和0.10±0.44,PGCsi3.0-Neg组分别为1.19±0.25和1.90±0.35,未转染组分别为1.42±0.14和2.55±0.32,前组HMGB1 mRNA及蛋白表达水平与后两组比较,差异均有统计学意义(P<0.05)。MTT和细胞划痕实验显示,PGCsi3.0-1组细胞生长受到明显抑制,细胞迁移率降低(P<0.05)。Transwell实验显示PGCsi3.0-1组穿膜细胞数为18.0±4.2,低于PGCsi3.0-Neg组的62.0±3.5和未转染组的58.0±4.9(P<0.05)。结论:应用RNAi能有效抑制HMGB1基因表达,进而抑制HeLa细胞增殖、侵袭和迁移,为宫颈癌的基因治疗提供了新思路。

胃癌组织中HMGB1表达与幽门螺杆菌L型感染的相关性研究

目的探讨人胃癌组织中高迁移率族蛋白B1(HMGBl)的表达以及与幽门螺杆菌L型(Hp-L)感染的相关性。方法采用RT-PCR技术检测30例新鲜胃癌组织及远端正常组织中HMGB1的mRNA表达,免疫组化采用SP法检测80例胃癌和50例切缘正常对照组织HMGB1及Hp-L型抗原的表达;并应用革兰氏染色法检测上述组织的Hp和Hp-L型的感染情况。结果胃癌组织HMGB1阳性率为77.5%(62/80),显著高于对照组24%(12/50)(P<0.01),其表达与肿瘤大小、临床分期、胃癌的淋巴结转移相关(P<0.05),而与肿瘤组织分级无关(P>0.05);胃癌组Hp-L型阳性组HMGB1阳性率为87.7%(50/57),明显高于Hp-L型阴性组52.2%(12/23),差异极显著(P<0.01)。Hp-L型阳性与HMGB1的表达呈正相关(P<0.01)。结论 HMGB1在肿瘤组织中表达水平较高,可能与胃癌的浸润和转移有密切关系。

Glycyrrhizin attenuates HMGB1-induced hepatocyte apoptosis by inhibiting the p38-dependent mitochondrial pathway

AIM： To examine how High-mobility group box I （HMGB1） regulates hepatocyte apoptosis and, furthermore, to determine whether glycyrrhizin （GL）, a known HMGB1 inhibitor, prevents HMGBl-induced hepatocyte apoptosis.

Severity of sepsisis is correlated with the elevation of serum high-mobility group box 1 in rats

Background Sepsis is a leading cause of death in the intensive care units. The late inflammatory cytokine, high-mobility group box 1 （HMGB1）, plays a critical role in sepsis. In the present study, we investigated the association between the serum HMGB1 levels and the severity of organ injury in the lipopolysaccharide-induced sepsis in rats. Methods To produce an animal model of sepsis with different degree of organ injury, animals were treated with three different doses of lipopolysaccharide （4, 8 and 16 mg/kg）, and the animals in control group were treated with the same volume of the vehicle （saline）. The levels of serum HMGB1 were measured at 0, 2, 4, 8, 16, 24, 32 and 48 hours after lipopolysaccharide （LPS） or vehicle injection, meanwhile the biochemical and histopathological indicators for the severity of organ injury were assessed. Results The level of HMGB1 had a positive, high correlation with the abnormal changes of serum cardiac troponin I, alanine aminotransferase, aspartate aminotransferase, creatinine and blood urea nitrogen, as well as the pathologic scores of heart, lung, liver and kidney. Conclusions The level of serum HMGB1 is highly correlated with the severity of sepsis in rats, suggesting that HMGB1 could serve as a valuable adjunct in the diagnosis and management of sepsis.

M2-like Kupffer cells in fibrotic liver may protect against acute insult

AIM To investigate the mechanism of hepatoprotection conferred by liver fibrosis through evaluating the activation phenotype of kupffer cells.METHODS Control and fibrotic mice were challenged with a lethal dose of D-Gal N/lipopolysaccharide(LPS),and hepatic damage was assessed by histology,serum alanine transferase(ALT)levels,and hepatic expression of HMGB1,a potent pro-inflammatory mediator.The localization of F4/80(a surrogate marker of KCs),HMGB1,and type I collagen(Col-1)was determined by immunofluorescence staining.The phenotype of KCs was characterized by real-time PCR.KCs isolated from control or fibrotic mice were challenged with LPS or HMGB1 peptide,and HMGB1 translocation was analyzed.RESULTS Liver fibrosis protected mice against D-Gal N/LPS challenge,as shown by improved hepatic histology and reduced elevation of ALT compared with the normal mice treated in the same way.This hepatoprotection was also accompanied by inhibition of HMGB1 expression in the liver.Co-localization of F4/80,HMGB1,and Col-1 was found in fibrotic livers,indicating the close relationship between KCs,HMGB1 and liver fibrosis.KCs isolated from fibrotic mice predominantly exhibited an M2-like phenotype.In vitro experiments showed that HMGB1 was localized in the nucleus of the majority of M2-like KCs and that the translocation of HMGB1 was inhibited following stimulation with LPS or HMGB1 peptide,while both LPS and HMGB1 peptide elicited translocation of intranuclear HMGB1 in KCs isolated from the control mice.CONCLUSION M2-like Kupffer cells in fibrotic liver may exert a protective effect against acute insult by inhibiting the translocation of HMGB1.

Decreased serum platelet derived growth factor BB levels in acute and increased in chronic pancreatitis

AIM: To examine circulating growth factor concentrations in patients with acute pancreatitis (AP) and chronic pancreatitis (CP), and walled-off pancreatic necrosis (WOPN).

CT引导下脉冲射频联合连续神经阻滞治疗顽固性带状疱疹后神经痛的临床疗效研究

目的探究CT引导下脉冲射频联合连续神经阻滞治疗顽固性带状疱疹后神经痛(PHN)的临床疗效。方法选取2021年1月至2023年1月本院收治的208例顽固性PHN患者为对象,随机数表法分为联合组和对照组,每组各104例。对照组接受CT引导下脉冲射频治疗,联合组在对照组的基础上行连续硬膜外神经阻滞治疗。比较两组患者不同时间点疼痛情况、临床有效率、镇痛补救情况、睡眠质量,血清高迁移率族蛋白B1(HMGB1)、白细胞介素-1β(IL-1β)和白细胞介素-10(IL-10)水平。结果随访期间,4例患者失访。最终纳入联合组103例,对照组101例。联合组治疗总有效率为89.32%,明显高于对照组的78.22%(P<0.05)。患者疼痛视觉模拟量表(VAS)评分、阿森斯失眠量表(AIS)评分的时间、组间、时间与组间交互效应差异均具有统计学意义(P<0.05);治疗后1、2、4周联合组VAS、AIS评分均低于对照组(P<0.05);联合组镇痛补救次数低于对照组,曲马多使用剂量少于对照组(P<0.05);治疗后4周联合组血清HMGB1、IL-1β、IL-10水平均低于对照组(P<0.05)。结论CT引导下脉冲射频联合连续神经阻滞治疗顽固性PHN,能有效减轻神经炎性损伤,改善患者疼痛症状,提高睡眠质量,其镇痛效果及临床疗效优于单纯使用CT引导下脉冲射频疗法。

High mobility group box 1 protein： possible pathogenic link to atrial fibrillation

Atrial fibrillation （AF） is the most common sustained dysrhythmia in clinical practice. The bulk of evidence suggests that inflammatory processes, oxidative stress and matrix metalloproteinase are associated with development of AF. However, these agents may be involved in high mobility group box 1 protein （HMGB1）. We hypothesized that HMGB1 may be a possible pathogenic link to AF. A growing body of evidence supports these hypotheses. First, the level of serum HMGB1 is significantly increased in patients with AF including paroxysmal and persistent AF. Second, HMGB1 has been identified as a new pro-inflammatory cytokine in cardiovascular diseases, along with tumor necrosis factor （TNF）-a, interleukin （IL）-6, and C-reactive protein, and there is cross-talk between HMGB1 and inflammatory cytokines. Third, oxidative stress is involved in the release of the pro-inflammatory cytokine, HMGB1, indicating there is cross-talk between oxidative stress and inflammation, and oxidative stress may reinforce the effect of inflammation on the pathogenesis of AF and inflammation may play a more important role in the pathogenesis of AF. Fourth, HMGB1 can promote matrix metalloproteinase-9 upregulation and activation. Fifth, HMGB1 receptors （receptor for advanced glycation end products, Toll-like receptor-2,4） may mediate the atrial structural remodeling or be up-regulated in patients with non-valvular AF. These results suggest that HMGB1 may participate in the pathogenesis of AF and provide a potential target for pharmacoloclical interruption of AF.

下调人高迁移率族蛋白1对人前列腺癌细胞PC-3的影响

目的研究小干扰RNA(siRNA)抑制高迁移率族蛋白1(HMGB1)基因对PC-3侵袭和转移的影响。方法构建真核表达载体Pgenesil-1/HMGB1siRNA,转染PC-3细胞系,通过RT-PCR和Western blot检测HMGB1的mRNA及蛋白;通过细胞划痕、transwell和明胶酶谱分析检测PC-3体外侵袭能力。结果成功构建siRNA表达载体Pgene-sil-1/HMGB1siRNA,可使PC-3细胞HMGB1mRNA和蛋白表达水平显著降低(P<0.05),并能有效抑制PC-3体外侵袭和转移活性(P<0.05)。结论应用siRNA技术能有效的抑制基因的表达,同时也能有效抑制PC-3细胞的体外侵袭和转移,为肿瘤的生物学治疗提供了新思路。

高迁移率族蛋白B1对宫颈癌细胞化学治疗敏感性的影响及其机制

目的:探讨高迁移率族蛋白B1(high mobility group box-1,HMGB1)对宫颈癌细胞化学治疗敏感性的影响及其机制。方法:采用Western印迹法检测宫颈癌细胞HeLa和CaSki经不同药物浓度顺铂处理后LC3,Beclin1及P62的表达水平,检测使用自噬抑制剂和/或顺铂处理后宫颈癌细胞HeLa和CaSki中LC3,Beclin1及P62的表达水平;采用细胞计数试剂盒8(cell counting kit-8,CCK-8)检测细胞增殖水平。构建HeLa-sh HMGB1,CaSkish HMGB1,HeLa-CTR及CaSki-CTR的稳定细胞系。以CCK-8检测上述细胞系顺铂半数抑制浓度(half maximum inhibitory concentration,IC50)水平;Western印迹法检测上述细胞系中HMGB1,LC3,Beclin1及P62的表达水平。结果:在一定浓度范围内,随着顺铂药物浓度的增加,宫颈癌细胞HeLa和CaSki中LC3及Beclin1的表达增加,P62表达降低。与单用顺铂组相比,顺铂联合自噬抑制剂组细胞存活率更低(P<0.05)。在宫颈癌细胞中,HMGB1的表达与顺铂药物敏感性有关(P<0.05),与LC3,Beclin1表达呈正相关,与P62表达呈负相关。结论:HMGB1可能通过调控宫颈癌细胞内自噬的水平,影响其对顺铂的敏感性。铂类药物结合自噬抑制剂可能成为宫颈癌治疗的新策略。HMGB1可能成为预测化学治疗药物敏感性的分子标志物。

炎性细胞因子与重症急性胰腺炎肠屏障功能障碍

重症急性胰腺炎(severe acute pancreatitis,SAP)患者易发生肠屏障功能障碍(intestinal barrier dy sfunction,IBD),导致肠源性内毒素血症,诱发和加重全身炎症反应综合征(sys-temic inflammatory response syndrome,SIRS)和多器官功能障碍综合征(multiple organ dys-functions yndrome,MODS).SAP并发IBD的发病机制复杂,炎性细胞因子在其发生发展过程起了重要作用,核因子-κB和高迁移率族蛋白B1(HMGB1)作为重要的炎性细胞因子亦介导了SAP全身炎症反应和IBD的发生.

高迁移率族蛋白1对心力衰竭合并睡眠呼吸暂停综合征的影响

目的:评估心力衰竭(心衰)合并睡眠呼吸暂停综合征(SAS)患者血清高迁移率族蛋白1(HMGB1)水平。方法:检测62例心衰合并SAS、62例单纯心衰患者及41例对照者的血清HMGB1、高敏C反应蛋白(hsCRP)和N端脑钠肽前体(NTproBNP)水平,同时评估患者的左室结构和功能。多元回归分析心衰合并SAS发病的危险因素。结果:心衰患者血清HMGB1、hsCRP和NT-proBNP,左房径、左室收缩末和舒张末径较对照组增加,而射血分数比对照组明显减少。心衰合并SAS患者的血清HMGB1、hsCRP水平又高于单纯性心衰患者。心衰患者血清HMGB1水平与左室收缩末和舒张末内径、NT-proBNP和hsCRP水平呈正相关。多因素回归分析显示HMGB1是心衰合并SAS发病的独立危险因素。结论:心衰合并SAS时血清HMGB1升高显著,且HMGB1是心衰合并SAS发病的独立危险因素。

HMGB1与缺血性脑卒中关系的研究进展

高迁移率族蛋白B1(HMGB1)是在哺乳动物体内广泛表达的一种非组蛋白染色体结合蛋白,与糖基化终末产物受体、Toll样受体等相互作用,促进炎性因子分泌、肿瘤细胞生长和迁移等。HMGB1在缺血性脑卒中的发生、发展过程中起重要作用,可能通过促进动脉粥样硬化形成、激活血小板功能等促进卒中的发生。脑卒中发生后,HMGB1可能通过调节卒中后的炎症反应等促进卒中病情的进展。在脑卒中后期,HMGB1还可能参与脑组织的修复过程。未来,深入研究HMGB1与脑卒中发生发展的相关性可能为脑卒中的预防、诊断及治疗等提供新的思路。