中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2010年
9期
543-546
,共4页
宫蓓蕾%张永%许启霞%陈余清
宮蓓蕾%張永%許啟霞%陳餘清
궁배뢰%장영%허계하%진여청
重症肺炎%核转录因子-κB%D-二聚体%血必净注射液
重癥肺炎%覈轉錄因子-κB%D-二聚體%血必淨註射液
중증폐염%핵전록인자-κB%D-이취체%혈필정주사액
Severe pneumonia%Nuclear factor-κB%D-dimer%Xuebijing injection
目的 探讨核转录因子-κB(NF-κB)在重症肺炎发病机制中的作用及血必净注射液的干预效应.方法 重症肺炎患者30例,按随机数字表法分为常规治疗组14例,血必净干预治疗组16例,后者在常规治疗基础上加血必净注射液100 ml静脉滴注,每日1次,连用7 d;两组于治疗前及治疗3 d、7 d测定外周血单核细胞NF-κB DNA结合活性、炎症介质及凝血指标水平,同时行急性生理学与慢性健康状况评分系统Ⅱ(APACHEⅡ)评分.并以10例健康体检者作为健康对照组.结果 两组重症肺炎患者NF-κB DNA结合活性及肿瘤坏死因子-α(TNF-α)、降钙素原(PCT)、C-反应蛋白(CRP)、纤维蛋白原(Fib)、D-二聚体含量均明显高于健康对照组,凝血酶原时间(PT)、凝血酶时间(TT)短于健康对照组(P<0.05或P<0.01).与常规治疗组比较,干预治疗组治疗7 d NF-κB DNA结合活性(灰度值)显著降低(66.60±36.23比79.90±39.11),TNF-α(ng/L,25.81±11.67比33.78±13.36)、PCT(μg/L,1.91±1.09比2.96±1.80)、CRP(mg/L,20.01±7.21比26.59±10.66)、Fib(g/L,4.02±1.26比5.09±1.43)、D-二聚体(mg/L,0.24±0.06比0.31±0.11)均明显下降,治疗3 d时TT(s)即明显延长(15.68±1.89比14.65±1.33),7 d时APACHEⅡ评分(分,15.81±3.47比17.93±3.05)明显下降(均P<0.05).治疗前及治疗3 d、7 d NF-κB DNA结合活性分别与TNF-α含量(r1=0.373,r2=0.362,r3=0.419)、PCT含量(r1=0.800,r2=0.716,r3=0.920)、CRP含量(r1=0.368,r2=0.441,r3=0.366)呈正相关(均P<0.05).结论 重症肺炎患者NF-κB活化,凝血功能紊乱,NF-κB参与调控炎症反应;血必净注射液可减轻重症肺炎的全身炎症反应,可能与其抑制NF-κB活化及抗凝机制有关.
目的 探討覈轉錄因子-κB(NF-κB)在重癥肺炎髮病機製中的作用及血必淨註射液的榦預效應.方法 重癥肺炎患者30例,按隨機數字錶法分為常規治療組14例,血必淨榦預治療組16例,後者在常規治療基礎上加血必淨註射液100 ml靜脈滴註,每日1次,連用7 d;兩組于治療前及治療3 d、7 d測定外週血單覈細胞NF-κB DNA結閤活性、炎癥介質及凝血指標水平,同時行急性生理學與慢性健康狀況評分繫統Ⅱ(APACHEⅡ)評分.併以10例健康體檢者作為健康對照組.結果 兩組重癥肺炎患者NF-κB DNA結閤活性及腫瘤壞死因子-α(TNF-α)、降鈣素原(PCT)、C-反應蛋白(CRP)、纖維蛋白原(Fib)、D-二聚體含量均明顯高于健康對照組,凝血酶原時間(PT)、凝血酶時間(TT)短于健康對照組(P<0.05或P<0.01).與常規治療組比較,榦預治療組治療7 d NF-κB DNA結閤活性(灰度值)顯著降低(66.60±36.23比79.90±39.11),TNF-α(ng/L,25.81±11.67比33.78±13.36)、PCT(μg/L,1.91±1.09比2.96±1.80)、CRP(mg/L,20.01±7.21比26.59±10.66)、Fib(g/L,4.02±1.26比5.09±1.43)、D-二聚體(mg/L,0.24±0.06比0.31±0.11)均明顯下降,治療3 d時TT(s)即明顯延長(15.68±1.89比14.65±1.33),7 d時APACHEⅡ評分(分,15.81±3.47比17.93±3.05)明顯下降(均P<0.05).治療前及治療3 d、7 d NF-κB DNA結閤活性分彆與TNF-α含量(r1=0.373,r2=0.362,r3=0.419)、PCT含量(r1=0.800,r2=0.716,r3=0.920)、CRP含量(r1=0.368,r2=0.441,r3=0.366)呈正相關(均P<0.05).結論 重癥肺炎患者NF-κB活化,凝血功能紊亂,NF-κB參與調控炎癥反應;血必淨註射液可減輕重癥肺炎的全身炎癥反應,可能與其抑製NF-κB活化及抗凝機製有關.
목적 탐토핵전록인자-κB(NF-κB)재중증폐염발병궤제중적작용급혈필정주사액적간예효응.방법 중증폐염환자30례,안수궤수자표법분위상규치료조14례,혈필정간예치료조16례,후자재상규치료기출상가혈필정주사액100 ml정맥적주,매일1차,련용7 d;량조우치료전급치료3 d、7 d측정외주혈단핵세포NF-κB DNA결합활성、염증개질급응혈지표수평,동시행급성생이학여만성건강상황평분계통Ⅱ(APACHEⅡ)평분.병이10례건강체검자작위건강대조조.결과 량조중증폐염환자NF-κB DNA결합활성급종류배사인자-α(TNF-α)、강개소원(PCT)、C-반응단백(CRP)、섬유단백원(Fib)、D-이취체함량균명현고우건강대조조,응혈매원시간(PT)、응혈매시간(TT)단우건강대조조(P<0.05혹P<0.01).여상규치료조비교,간예치료조치료7 d NF-κB DNA결합활성(회도치)현저강저(66.60±36.23비79.90±39.11),TNF-α(ng/L,25.81±11.67비33.78±13.36)、PCT(μg/L,1.91±1.09비2.96±1.80)、CRP(mg/L,20.01±7.21비26.59±10.66)、Fib(g/L,4.02±1.26비5.09±1.43)、D-이취체(mg/L,0.24±0.06비0.31±0.11)균명현하강,치료3 d시TT(s)즉명현연장(15.68±1.89비14.65±1.33),7 d시APACHEⅡ평분(분,15.81±3.47비17.93±3.05)명현하강(균P<0.05).치료전급치료3 d、7 d NF-κB DNA결합활성분별여TNF-α함량(r1=0.373,r2=0.362,r3=0.419)、PCT함량(r1=0.800,r2=0.716,r3=0.920)、CRP함량(r1=0.368,r2=0.441,r3=0.366)정정상관(균P<0.05).결론 중증폐염환자NF-κB활화,응혈공능문란,NF-κB삼여조공염증반응;혈필정주사액가감경중증폐염적전신염증반응,가능여기억제NF-κB활화급항응궤제유관.
Objective To investigate the role of nuclear factor-κB (NF-κB) in severe pneumonia and observe the effects of Xuebijing injection (血必净注射液) in its treatment. Methods Thirty hospitalized patients with severe pneumonia were divided into the routine therapy group (n=14) and Xuebijing therapy group (n=16) in whom with Xuebijing injection 100 ml was given once daily for 7 days besides routine therapies, according to the random numeral. The DNA binding activity of NF-κB in human monocytes was detected before and 3 days and 7 days after administration, the contents of tumor necrosis factor-α (TNF-α), procalcitonin (PCT) and C-reactive protein (CRP) were determined, and the changes in coagulatory and fibrinolytic parameters were assayed at the same time. Acute physiology and chronic health evaluationⅡ (APACHEⅡ) score was also recorded. Ten healthy volunteers served as the healthy control group. Results The DNA binding activities of NF-κB, the contents of TNF-α, PCT, CRP, fibrinogen (Fib), D-dimer in hospitalized subjects with severe pneumonia were higher before treatment than those in healthy control group, while the prothrombin time (PT), thrombin time (TT) were significantly lower (P<0.05 or P<0.01). Compared with the routine therapy group, the DNA binding activity of NF-κB (grey level) at the 7 days (66.60±36.23 vs. 79.90±39.11) was notably decreased in Xuebijing therapy group; the levels of TNF-α (ng/L, 25.81±11.67 vs. 33.78±13.36), PCT (μg/L, 1.91±1.09 vs. 2.96±1.80), CRP (mg/L, 20.01±7.21 vs. 26.59±10.66), Fib (g/L, 4.02±1.26 vs. 5.09±1.43), D-dimer (mg/L, 0.24±0.06 vs. 0.31±0.11) were significantly lower in Xuebijing therapy group, and APACHEⅡ score (15.81±3.47 vs. 17.93±3.05) was obviously lowered (all P<0.05). There was statistical difference of the TT (s) between two groups at 3 days (15.68±1.89 vs. 14.65±1.33, P<0.05). There was a significant positive correlation between NF-κB DNA binding activity and the levels of TNF-α (r1=0.373, r2=0.362, r3=0.419), PCT (r1=0.800, r2=0.716, r3=0.920) or CRP (r1=0.368, r2=0.441, r3=0.366, all P<0.05) before and 3 days and 7 days after the treatment. Conclusion NF-κB activation and coagulopathy were observed in patients with severe pneumonia, and NF-κB was involved in the process of inflammatory response. Inflammatory response was partly alleviated by Xuebijing injection. These effects of Xuebijing injection may be mediated by inhibition of the activation of NF-κB and its anticoagulation property.
