中华胰腺病杂志
中華胰腺病雜誌
중화이선병잡지
CHINESE JOURNAL OF PANCREATOLOGY
2009年
2期
105-108
,共4页
胰腺炎,急性坏死性%p38丝裂原活化蛋白激酶类%低钙血症%受体,甲状旁腺激素%肿瘤坏死因子
胰腺炎,急性壞死性%p38絲裂原活化蛋白激酶類%低鈣血癥%受體,甲狀徬腺激素%腫瘤壞死因子
이선염,급성배사성%p38사렬원활화단백격매류%저개혈증%수체,갑상방선격소%종류배사인자
Pancreatitis,acute neerotizing%p38 Mitogen-activated protein kinases%Hypocalcaemia%Receptors,parathyroid hormone%Tumor necrosis factor-alpha
目的 探讨p38丝裂原活化蛋白激酶(p38MAPK)信号转导通路对急性坏死性胰腺炎(ANP)大鼠低钙血症和甲状旁腺激素受体1(PTHR1)表达的影响.方法 将雄性SD大鼠72只按完全随机法分为ANP组、SB203580干预(SB)组和假手术(SO)组,每组分3、6、12 h 3个时间点,每个时间点8只.以5%牛磺脱氧胆酸钠逆行胰胆管注射建立ANP模型,SB组在造模前30 min腹腔注射p38MAPK特异抑制剂SB203580 10 mg/kg体重.观察各组血清钙浓度,蛋白质印迹法(Western blotting)分析骨组织磷酸化p38MAPK(P-p38 MAPK)和TNF-α变化,实时RT-PCR检测骨组织PTHR1 mRNA表达.结果 制模后6 h,SO组、ANP组和SB组血清钙浓度分别为(2.50±0.08)mmoL/L、(2.11±0.06)mmol/L和(2.35±0.10)mmol/L;骨组织P-p38 MAPK表达量分别为0.14±0.04、0.80±0.06和0.33±0.05;骨组织TNF-α表达量分别为0、0.91±0.04和0.44±0.03;骨组织PTHR1 mRNA表达量分别为1.00±0.12、0.23±0.04和0.44±0.06.SB组骨组织P-p38 MAPK及TNF-α表达较ANP组显著降低(P＜0.01);骨组织PTHR1 mRNA表达量及血清钙浓度较ANP组显著增加(P＜0.01).结论 p38MAPK信号转导通路可介导ANP低钙血症的发生,抑制该通路可改善ANP低钙血症.
目的 探討p38絲裂原活化蛋白激酶(p38MAPK)信號轉導通路對急性壞死性胰腺炎(ANP)大鼠低鈣血癥和甲狀徬腺激素受體1(PTHR1)錶達的影響.方法 將雄性SD大鼠72隻按完全隨機法分為ANP組、SB203580榦預(SB)組和假手術(SO)組,每組分3、6、12 h 3箇時間點,每箇時間點8隻.以5%牛磺脫氧膽痠鈉逆行胰膽管註射建立ANP模型,SB組在造模前30 min腹腔註射p38MAPK特異抑製劑SB203580 10 mg/kg體重.觀察各組血清鈣濃度,蛋白質印跡法(Western blotting)分析骨組織燐痠化p38MAPK(P-p38 MAPK)和TNF-α變化,實時RT-PCR檢測骨組織PTHR1 mRNA錶達.結果 製模後6 h,SO組、ANP組和SB組血清鈣濃度分彆為(2.50±0.08)mmoL/L、(2.11±0.06)mmol/L和(2.35±0.10)mmol/L;骨組織P-p38 MAPK錶達量分彆為0.14±0.04、0.80±0.06和0.33±0.05;骨組織TNF-α錶達量分彆為0、0.91±0.04和0.44±0.03;骨組織PTHR1 mRNA錶達量分彆為1.00±0.12、0.23±0.04和0.44±0.06.SB組骨組織P-p38 MAPK及TNF-α錶達較ANP組顯著降低(P＜0.01);骨組織PTHR1 mRNA錶達量及血清鈣濃度較ANP組顯著增加(P＜0.01).結論 p38MAPK信號轉導通路可介導ANP低鈣血癥的髮生,抑製該通路可改善ANP低鈣血癥.
목적 탐토p38사렬원활화단백격매(p38MAPK)신호전도통로대급성배사성이선염(ANP)대서저개혈증화갑상방선격소수체1(PTHR1)표체적영향.방법 장웅성SD대서72지안완전수궤법분위ANP조、SB203580간예(SB)조화가수술(SO)조,매조분3、6、12 h 3개시간점,매개시간점8지.이5%우광탈양담산납역행이담관주사건립ANP모형,SB조재조모전30 min복강주사p38MAPK특이억제제SB203580 10 mg/kg체중.관찰각조혈청개농도,단백질인적법(Western blotting)분석골조직린산화p38MAPK(P-p38 MAPK)화TNF-α변화,실시RT-PCR검측골조직PTHR1 mRNA표체.결과 제모후6 h,SO조、ANP조화SB조혈청개농도분별위(2.50±0.08)mmoL/L、(2.11±0.06)mmol/L화(2.35±0.10)mmol/L;골조직P-p38 MAPK표체량분별위0.14±0.04、0.80±0.06화0.33±0.05;골조직TNF-α표체량분별위0、0.91±0.04화0.44±0.03;골조직PTHR1 mRNA표체량분별위1.00±0.12、0.23±0.04화0.44±0.06.SB조골조직P-p38 MAPK급TNF-α표체교ANP조현저강저(P＜0.01);골조직PTHR1 mRNA표체량급혈청개농도교ANP조현저증가(P＜0.01).결론 p38MAPK신호전도통로가개도ANP저개혈증적발생,억제해통로가개선ANP저개혈증.
Objective To investigate the role of p38 mitogen-activated protein kinase (MAPK) signal transduction pathway in hypocaleaemia and parathyroid hormone receptor 1 ( PTHR1 ) of rats with acute necrotizing pancreatitis (ANP).Methods Seventy-two male health adult Spragne-Dawley rats were randomized into three groups:ANP group,ANP treated with SB203580 group (SB group),sham operation group (SO group).Every group was sub-divided into 3,6,12 h group with 8 rats in each one.ANP model was induced by retrograde infusion with 5% sodium taurocholate solution into the biliopancreatie duct.In the SB group,rats were treated with the specific p38MAPK inhibitor:SB203580 30 minutes before the induction of ANP model.The serum level of calcium was determined,the change of phosphorylated p38MAPK and TNFalpha were measured by western blot and the expression of PTHR1 mRNA was determined by quantitative real time RT-PCR.Results 6 h after ANP model induction,the serum levels of calcium in ANP,SB and SO group were (2.50±0.08 ) mmol/L,(2.11±0.06 ) mmol/L and (2.35±0.10 ) mmol/L,respectively;the expression levels of pbosphorylated p38MAPK in bone tissue were 0.14±0.04,0.80±0.06 and 0.33±0.05,respectively;the expression levels of p38MAPK TNF-alpha were 0,0.91±0.04 and 0.44±0.03,respectively;the expression levels of PTHR1 mRNA were 1.00±0.12,0.23±0.04 and 0.44±0.06,respectively.The expression levels of p38MAPK and TNF-α in SB group were significantly lower than those in the ANP group (P ＜ 0.01 );while the expression levels of PTHR1 mRNA and calcium were significantly higher than those in the ANP group (P ＜0.01 ).Conclusions P38MAPK signal transduction pathway may mediate the development of hypocaleaemia in the course of ANP,and hypoealcaemia could be improved by blocking this pathway.
