中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2015年
5期
1066-1068
,共3页
急性胰腺炎%ω-3多不饱和脂肪酸%肿瘤坏死因子-α%白细胞介素-10
急性胰腺炎%ω-3多不飽和脂肪痠%腫瘤壞死因子-α%白細胞介素-10
급성이선염%ω-3다불포화지방산%종류배사인자-α%백세포개소-10
Acute pancreatitis%ω-polyunsaturated fatty acids%Tumor necrosis factor-α%Interleukin-10
目的 观察ω-3多不饱和脂肪酸(ω-PUFA)对大鼠急性胰腺炎炎性介质及其p38丝裂原活化蛋白激酶(p38MAPK)的影响.方法 150只SD大鼠,体质量220～ 260 g,注入3.5％牛磺胆酸(60 μl/min).建模成功后,随机分为重症急性胰腺炎(SAP)对照组(SAP组)、传统肠内营养组(EN组)和加入ω-3PUFA肠内营养组(ω-EN组)各50只.EN组采用能全力.ω-EN组加入ω-PUFA3 g/kg.各组大鼠能量摄入均为126 kJ/(kg·d).建模后24h内,各组均经颈内静脉以400 ml/(kg·d)输入平衡液,建模后24 h后,开始分别行肠内营养,输注速度控制在12 ml/(kg·h),应用14 d.EN和ω-EN组营养液第2天输入日需总量的1/3,第3天输入1/2,不足量由静脉营养补充,从第4天开始全量肠内营养支持.各组总液体量入量相等.基础治疗:自建模成功后,每组大鼠腹部皮下注射善宁6 μg/(kg·d)作为基础治疗,每日分3次给药.于实验第1、4、7、14天分别经分批处死大鼠:检测血淀粉酶、采用酶联免疫吸附试验(ELISA)检测细胞因子肿瘤坏死因子-α(TNF-α)和白细胞介素-10(IL-10),电镜下检测胰腺组织;免疫组织化学检测大鼠胰腺组织p38MAPK的表达,并计算大鼠14 d的生存率.结果 SAP组各时段血清TNF-α显著升高,IL-10降低,到4d时达峰值,TNF-α[(257.40±4.52) ng/L],IL-10[(3.40 ±4.52) ng/L],胰腺组织p38MAPK的表达显著升高;用药后,EN组及ω-EN组TNF-α显著降低,EN组[(207.40±0.65) ng/L],ω-EN组[(96.51±0.92) ng/L];IL-10升高,EN组[(9.40 ±0.61) ng/L],ω-EN组[(4.35±1.91) ng/L],与SAP组比较差异有统计学意义(P＜0.01),胰腺组织p38MAPK的表达也显著减少;SAP组大鼠到7d时,全部死亡,EN组及其ω-EN组全部成活.结论 ω-PUFA的治疗作用之一是可能抑制大鼠急性胰腺炎p38MAPK的表达,从而减少炎性介质的释放来实现.
目的 觀察ω-3多不飽和脂肪痠(ω-PUFA)對大鼠急性胰腺炎炎性介質及其p38絲裂原活化蛋白激酶(p38MAPK)的影響.方法 150隻SD大鼠,體質量220～ 260 g,註入3.5％牛磺膽痠(60 μl/min).建模成功後,隨機分為重癥急性胰腺炎(SAP)對照組(SAP組)、傳統腸內營養組(EN組)和加入ω-3PUFA腸內營養組(ω-EN組)各50隻.EN組採用能全力.ω-EN組加入ω-PUFA3 g/kg.各組大鼠能量攝入均為126 kJ/(kg·d).建模後24h內,各組均經頸內靜脈以400 ml/(kg·d)輸入平衡液,建模後24 h後,開始分彆行腸內營養,輸註速度控製在12 ml/(kg·h),應用14 d.EN和ω-EN組營養液第2天輸入日需總量的1/3,第3天輸入1/2,不足量由靜脈營養補充,從第4天開始全量腸內營養支持.各組總液體量入量相等.基礎治療:自建模成功後,每組大鼠腹部皮下註射善寧6 μg/(kg·d)作為基礎治療,每日分3次給藥.于實驗第1、4、7、14天分彆經分批處死大鼠:檢測血澱粉酶、採用酶聯免疫吸附試驗(ELISA)檢測細胞因子腫瘤壞死因子-α(TNF-α)和白細胞介素-10(IL-10),電鏡下檢測胰腺組織;免疫組織化學檢測大鼠胰腺組織p38MAPK的錶達,併計算大鼠14 d的生存率.結果 SAP組各時段血清TNF-α顯著升高,IL-10降低,到4d時達峰值,TNF-α[(257.40±4.52) ng/L],IL-10[(3.40 ±4.52) ng/L],胰腺組織p38MAPK的錶達顯著升高;用藥後,EN組及ω-EN組TNF-α顯著降低,EN組[(207.40±0.65) ng/L],ω-EN組[(96.51±0.92) ng/L];IL-10升高,EN組[(9.40 ±0.61) ng/L],ω-EN組[(4.35±1.91) ng/L],與SAP組比較差異有統計學意義(P＜0.01),胰腺組織p38MAPK的錶達也顯著減少;SAP組大鼠到7d時,全部死亡,EN組及其ω-EN組全部成活.結論 ω-PUFA的治療作用之一是可能抑製大鼠急性胰腺炎p38MAPK的錶達,從而減少炎性介質的釋放來實現.
목적 관찰ω-3다불포화지방산(ω-PUFA)대대서급성이선염염성개질급기p38사렬원활화단백격매(p38MAPK)적영향.방법 150지SD대서,체질량220～ 260 g,주입3.5％우광담산(60 μl/min).건모성공후,수궤분위중증급성이선염(SAP)대조조(SAP조)、전통장내영양조(EN조)화가입ω-3PUFA장내영양조(ω-EN조)각50지.EN조채용능전력.ω-EN조가입ω-PUFA3 g/kg.각조대서능량섭입균위126 kJ/(kg·d).건모후24h내,각조균경경내정맥이400 ml/(kg·d)수입평형액,건모후24 h후,개시분별행장내영양,수주속도공제재12 ml/(kg·h),응용14 d.EN화ω-EN조영양액제2천수입일수총량적1/3,제3천수입1/2,불족량유정맥영양보충,종제4천개시전량장내영양지지.각조총액체량입량상등.기출치료:자건모성공후,매조대서복부피하주사선저6 μg/(kg·d)작위기출치료,매일분3차급약.우실험제1、4、7、14천분별경분비처사대서:검측혈정분매、채용매련면역흡부시험(ELISA)검측세포인자종류배사인자-α(TNF-α)화백세포개소-10(IL-10),전경하검측이선조직;면역조직화학검측대서이선조직p38MAPK적표체,병계산대서14 d적생존솔.결과 SAP조각시단혈청TNF-α현저승고,IL-10강저,도4d시체봉치,TNF-α[(257.40±4.52) ng/L],IL-10[(3.40 ±4.52) ng/L],이선조직p38MAPK적표체현저승고;용약후,EN조급ω-EN조TNF-α현저강저,EN조[(207.40±0.65) ng/L],ω-EN조[(96.51±0.92) ng/L];IL-10승고,EN조[(9.40 ±0.61) ng/L],ω-EN조[(4.35±1.91) ng/L],여SAP조비교차이유통계학의의(P＜0.01),이선조직p38MAPK적표체야현저감소;SAP조대서도7d시,전부사망,EN조급기ω-EN조전부성활.결론 ω-PUFA적치료작용지일시가능억제대서급성이선염p38MAPK적표체,종이감소염성개질적석방래실현.
Objective To investigate the effects of ω-polyunsaturated fatty acids (ω-PUFA) on the inflammatory mediators and p38 mitogen-activated protein kinase (p38MAPK) in rats with severe acute pancreatitis (SAP).Methods 150 Sprague Dawley rats were randomized into SAP group,enteral nutrition (EN) group and ω-PUFA EN group.SAP model was induced by low pressure retrograde infusion of biliopancreastic duct with 3.5％ sodium taurocholate solution (0.1 ml/100 g).The rats were sacrificed at 1st,4th,7th and 14th day after operation.The serum amylase (AMY),tumor necrosis factor-α (TNF-α) and interleukin (IL)-10 were determined.The expression of p38MAPK in the pancreas was detected by immunohistochemistry.Pancreas tissue samples were stained with hematoxylin and eosin for histopathological evalution.Results The serum TNF-α was significantly increased,and IL-10 was significantly reduced in SAP group at all time points,and they reached the peak at 4th day after operation [for TNF-α,(257.40 ±4.52) ng/L;for IL-10,(3.40 ±4.52) ng/L],and the expression of p38MAPK the pancreatic tissue was significantly increased.After treatment,serum TNF-α was significantly reduced in EN group [(207.40±0.65) ng/L],and ω-PUFA EN group [(96.51 ±0.92) ng/L],and IL-10 increased in EN group [(9.40 ±0.61) ng/L],and ω-PUFA EN group [(4.35 ± 1.91) ng/L] as compared with SAP group (P ＜ 0.01 for all).The p38MAPK expression in pancreatic tissues was also significantly reduced in EN group andω-PUFA EN group.The animals in SAP group were died at 7th day after operation,and those in EN group and ω-PUFA EN group survived.Conclusion The activation and over-expression of p38MAPK in pancreas tissue may be one of the reasons for SAP,and ω-PUFA can be used to treat the SAP through downregulating the expression of p38MAPK in the pancreas tissue.
