摘要
目的探讨胰岛素强化治疗(IIT)对重度颅脑损伤(sTBI)应激性高血糖患者高迁移率族蛋白B1/核转录因子-κB(HMGB1/NF-κB)相关炎症信号的影响。方法选取2015年7月至2017年10月南京医科大学附属淮安第一医院重症加强治疗病房(ICU)收治的61例sTBI应激性高血糖患者〔格拉斯哥昏迷评分(GCS)≤8分,3次随机血糖均>11.1 mmoI/L,糖化血红蛋白(HbA1c)<0.065〕,按随机数字表法将患者分为IIT组(29例,使血糖保持在4.4~7.8 mmol/L)和传统治疗组(CGT组,32例,使血糖保持在7.8~12.2 mmo/L)。分别于治疗前及治疗1、7、14 d采用酶联免疫吸附试验(ELISA)检测血浆HMGB1、肿瘤坏死因子-α(TNF-α)水平,用全自动生化仪测定C?-反应蛋白(CRP)水平,用实时定量聚合酶链反应(PCR)检测外周血单核细胞NF-κB p65基因表达。结果9例患者因连续4次血糖监测未达目标值、合并重症感染或脑损伤严重放弃治疗而退出观察,最终纳入52例患者,其中CGT组28例,IIT组24例。两组治疗1 d血浆HMGB1、TNF-α、CRP水平及单核细胞NF-κB基因表达均较治疗前明显升高,并达峰值,之后逐渐下降,治疗7 d起即显著低于治疗1 d时。IIT组治疗7 d血浆CRP、TNF-α水平即显著低于CGT组〔CRP(mg/L):36.7±4.4比45.1±6.1,TNF-α(ng/L):42.4±9.7比53.2±9.1,均P<0.05〕,治疗14 d血浆HMGB1水平及单核细胞NF-κB p65基因表达即较CGT组显著下降〔HMGB1(μg/L):60.1±8.7比80.5±9.1,NF-κB p65(ΔCt):35.8±8.5比53.5±7.3,均P<0.05〕。结论IIT通过HMGB1/NF-κB通路抑制sTBI应激性高血糖患者的炎症反应。
Objective To explore the effect of intensive insulin therapy(IIT)on high mobility group box-1/nuclear factor-κB(HMGB1/NF-κB)signaling pathway in severe traumatic brain injury(sTBI)patient with stress hyperglycemia.Methods Sixty-one sTBI patients with stress hyperglycemia[Glasgow coma scale(GCS)≤8,three times of random blood glucose levels>11.1 mmoL/L,glycosylated hemoglobin(HbA1c)<0.065]admitted to the Affiliated Huaian No.1 People's Hospital of Nanjing Medical University from July 2015 to October 2017 were enrolled.Patients were divided into IIT group(29 cases,keeping blood glucose at 4.4-7.8 mmol/L)and conventional glycemic therapy(CGT)group(32 cases,keeping blood glucose at 7.8-12.2 mmo/L)according to the random number table method.Before treatment and 1,7 and 14 days after treatment,the levels of plasma HMGB1 and tumor necrosis factor-α(TNF-α)were measured by enzyme linked immunosorbent assay(ELISA);C-reactive protein(CRP)was determined by automatic biochemical analyzer,and NF-κB p65 gene expression in peripheral blood mononuclear cells was detected by real-time quantitative polymerase chain reaction(PCR).Results Nine patients were withdrawn from the observation because the 4 consecutive blood glucose monitoring did not reach the target value,combined with severe infection,or abandoned the treatment with serious brain damage.Finally,52 patients were enrolled in the analysis,including 28 in CGT group and 24 in IIT group.The levels of plasma HMGB1,TNF-α,CRP and the expression of NF-κB gene in monocytes of the two groups at 1 day after treatment were significantly higher than those before treatment,and reached the peak value,then gradually decreased.After 7 days of treatment,they were significantly lower than 1 day.The levels of plasma CRP and TNF-αin the IIT group were significantly lower than those in the CGT group[CRP(mg/L):36.7±4.4 vs.45.1±6.1,TNF-α(ng/L):42.4±9.7 vs.53.2±9.1,both P<0.05],the level of HMGB1 in plasma and the expression of NF-κB p65 in monocytes were significantly lower than t
作者
朱星星
张红
尚福泰
臧奎
章向成
Zhu Xingxing;Zhang Hong;Shang Futai;Zang Kui;Zhang Xiangcheng(Department of ICU,the Affiliated Huaian No.1 People's Hospital of Nanjing Medical University,Huaian 223300,Jiangsu,China;Department of Endocrinology,the Affiliated Huaian No.1 People's Hospital of Nanjing Medical University,Huaian 223300,Jiangsu,China)
出处
《中华危重病急救医学》
CAS
CSCD
北大核心
2019年第8期949-952,共4页
Chinese Critical Care Medicine
基金
国家自然科学基金(81400807).
