中华胰腺病学杂志
中華胰腺病學雜誌
중화이선병학잡지
CHINESE JOURNAL OF PANCREATOLOGY
2008年
2期
115-118
,共4页
陈磊%邹晓平%田觅%顾超
陳磊%鄒曉平%田覓%顧超
진뢰%추효평%전멱%고초
胰腺炎,急性坏死性%肠道免疫微生态营养%内毒素类%细胞因子类%NF-κB
胰腺炎,急性壞死性%腸道免疫微生態營養%內毒素類%細胞因子類%NF-κB
이선염,급성배사성%장도면역미생태영양%내독소류%세포인자류%NF-κB
Pancreatitis,acute necrotizing%Ecoimmunonutrition enteral nutrition%Endotoxins%Cytokines%NF-κB
目的 探讨肠内免疫微生态营养对ANP猪全身炎症反应的影响.方法 胰管注射5%牛磺胆酸钠1ml/kg体重制备猪ANP模型.造模后24 h,18头猪按随机分组法分为胃肠外营养组(PN)、肠内要素营养组(EN)和肠内免疫微生态营养组(EIN),分别进行相应的营养支持8 d.造模前、造模后24 h、营养支持1 d、2 d、4 d、8 d分别检测外周血内毒素、TNF-α、IL-1β、IL-6、IL-10及单核细胞NF-κB活性.8 d时取胰腺行病理学检查.结果 胰腺病理改变符合ANP.造模后24 h,EIN组外周血内毒素、TNF-α、IL-1β、IL-6、IL-10和单核细胞NF-κB水平分别为(1.85±0.18)EU/L、(461.59±128.25)pg/ml、(185.49±58.81)pg/ml、(354.26±34.63)pg/ml、(110.32±25.18)pg/ml、(51.06 ±2.27)%,均较造模前明显增高(P＜0.01),但与其他两组无显著差异;营养支持8 d后,EIN组血浆上述各项分别为(1.48±0.16)EU/L、(30.11±9.12)pg/ml、(20.17±7.04)pg/ml、(36.42±7.24)pg/ml、(89.46±13.54)pg/ml、(9.06±0.17)%,均较EN组、PN组明显下降(P＜0.05),且IL-10/IL-6比值为2.51±0.42,与制模前的2.28±0.19接近.结论 早期肠内免疫微生态营养能有效减轻内毒素血症,降低NF-κB活性及细胞因子浓度,维持促抗炎反应平衡.
目的 探討腸內免疫微生態營養對ANP豬全身炎癥反應的影響.方法 胰管註射5%牛磺膽痠鈉1ml/kg體重製備豬ANP模型.造模後24 h,18頭豬按隨機分組法分為胃腸外營養組(PN)、腸內要素營養組(EN)和腸內免疫微生態營養組(EIN),分彆進行相應的營養支持8 d.造模前、造模後24 h、營養支持1 d、2 d、4 d、8 d分彆檢測外週血內毒素、TNF-α、IL-1β、IL-6、IL-10及單覈細胞NF-κB活性.8 d時取胰腺行病理學檢查.結果 胰腺病理改變符閤ANP.造模後24 h,EIN組外週血內毒素、TNF-α、IL-1β、IL-6、IL-10和單覈細胞NF-κB水平分彆為(1.85±0.18)EU/L、(461.59±128.25)pg/ml、(185.49±58.81)pg/ml、(354.26±34.63)pg/ml、(110.32±25.18)pg/ml、(51.06 ±2.27)%,均較造模前明顯增高(P＜0.01),但與其他兩組無顯著差異;營養支持8 d後,EIN組血漿上述各項分彆為(1.48±0.16)EU/L、(30.11±9.12)pg/ml、(20.17±7.04)pg/ml、(36.42±7.24)pg/ml、(89.46±13.54)pg/ml、(9.06±0.17)%,均較EN組、PN組明顯下降(P＜0.05),且IL-10/IL-6比值為2.51±0.42,與製模前的2.28±0.19接近.結論 早期腸內免疫微生態營養能有效減輕內毒素血癥,降低NF-κB活性及細胞因子濃度,維持促抗炎反應平衡.
목적 탐토장내면역미생태영양대ANP저전신염증반응적영향.방법 이관주사5%우광담산납1ml/kg체중제비저ANP모형.조모후24 h,18두저안수궤분조법분위위장외영양조(PN)、장내요소영양조(EN)화장내면역미생태영양조(EIN),분별진행상응적영양지지8 d.조모전、조모후24 h、영양지지1 d、2 d、4 d、8 d분별검측외주혈내독소、TNF-α、IL-1β、IL-6、IL-10급단핵세포NF-κB활성.8 d시취이선행병이학검사.결과 이선병리개변부합ANP.조모후24 h,EIN조외주혈내독소、TNF-α、IL-1β、IL-6、IL-10화단핵세포NF-κB수평분별위(1.85±0.18)EU/L、(461.59±128.25)pg/ml、(185.49±58.81)pg/ml、(354.26±34.63)pg/ml、(110.32±25.18)pg/ml、(51.06 ±2.27)%,균교조모전명현증고(P＜0.01),단여기타량조무현저차이;영양지지8 d후,EIN조혈장상술각항분별위(1.48±0.16)EU/L、(30.11±9.12)pg/ml、(20.17±7.04)pg/ml、(36.42±7.24)pg/ml、(89.46±13.54)pg/ml、(9.06±0.17)%,균교EN조、PN조명현하강(P＜0.05),차IL-10/IL-6비치위2.51±0.42,여제모전적2.28±0.19접근.결론 조기장내면역미생태영양능유효감경내독소혈증,강저NF-κB활성급세포인자농도,유지촉항염반응평형.
Objective To evaluate the effect of ecoimmunonutrition on systemic inflammatory response in swine with acute necrotizing pancreatitis (ANP). Methods Swine model of ANP was induced by retrograde injection of 5% sodium taurocholate and trypsin into the pancreatic duct. 24h after the ANP models were established, eighteen swine were randomly divided into total parenteral nutrition (PN) group (n = 6), enteral nutrition (EN) group (n = 6), and ecoimmunonutrition (E1N) group (n = 6). Each of the three nutrition formulas was given to each group respectively for eight days. The level of plasma endotoxin and serum concentrations of TNF-α, IL-1β, IL-6 and IL-10 were measured before, 24 h after the induction of ANP and 1,2, 4, 8 d after nutrition support. Results 24 hours after the ANP models were established, the serum level of plasma endotoxin, TNF-α, IL-1β, IL-6 and IL-10, NF-κB activities in EIN group were ( 1.85 ± 0.18) EU/L,(461.59 ± 128.25 ) pg/ml, ( 185.49 ± 58.81 ) pg/ml, ( 354.26 ± 34.63 ) pg/ml, ( 110.32 s 25. 18 ) pg/ml,(51.06 ± 2.27 )%, respectively, which all were significantly higher than those before the ANP models were established, but there were no difference among three groups. Eight days after nutrition support, those levels in EIN group were (1.48 ±0.16 )EU/L, (30.11 ±9.12)pg/ml, (20.17 ±7.04)pg/ml, (36.42 ±7.24) pg/ml and ( 89.46 ± 13.54 ) pg/ml, (9.06 ± 0. 17 ) %, respectively, which all were significantly lower than those of TPN and EEN group ( P ＜ 0. 05 ). The ration of IL-10/IL-6 was 2.51 ± 0.42 in EIN group, and 2.28 ± 0. 19 before the ANP models were established. Conclusions EIN could attenuate endotoxemia, decrease NF-κB activities and serum concentrations of cytokines and maintained the balance of pro- and anti-inflammation.
