中华消化外科杂志
中華消化外科雜誌
중화소화외과잡지
CHINESE JOURNAL OF DIGESTIVE SURGERY
2008年
6期
419-421
,共3页
周一农%黄鹤光%李谮%陈先强%刘夏磊
週一農%黃鶴光%李譖%陳先彊%劉夏磊
주일농%황학광%리참%진선강%류하뢰
胰腺炎,急性%甲基强的松龙%凋亡%神经细胞
胰腺炎,急性%甲基彊的鬆龍%凋亡%神經細胞
이선염,급성%갑기강적송룡%조망%신경세포
Panereatitis,acute%Methylprednisolone%Apoptosis%Neurocyte
目的 探讨甲基强的松龙对重症急性胰腺炎大鼠脑组织神经细胞凋亡的影响.方法 将36只SD大鼠分为3组,假手术组、重症急性胰腺炎组、甲基强的松龙组,每组12只.逆行胰胆管注射5%牛磺脱氧胆酸钠建立重症急性胰腺炎模型.观察各组血清淀粉酶、IL-6、TNF-α水平、腹水量和胰腺组织的病理学改变.RT-PCR法分析脑组织Bcl-2、Bax mRNA的表达水平,TUNEL法检测神经细胞凋亡.结果 重症急性胰腺炎组血清IL-6、TNF-α升高,腩组织Bcl-2 mRNA表达减少,Bax mRNA表达上调,Bcl-2/Bax比值降低,脑组织神经细胞凋亡增加;甲基强的松龙组血清IL-6、TNF-α表达明显下降,脑组织Bcl-2 mRNA表达变化不明显,但Bax mRNA表达下调明显,Bcl-2/Bax比值升高,脑组织神经细胞凋亡显著减少.结论 重症急性胰腺炎时脑组织神经细胞凋亡可能是胰性脑病的发病机制之一;甲基强的松龙可抑制细胞因子的释放,促进脑组织Bcl-2和Bax基因表达的平衡,降低脑组织神经细胞凋亡指数,使脑组织损伤得以改善.
目的 探討甲基彊的鬆龍對重癥急性胰腺炎大鼠腦組織神經細胞凋亡的影響.方法 將36隻SD大鼠分為3組,假手術組、重癥急性胰腺炎組、甲基彊的鬆龍組,每組12隻.逆行胰膽管註射5%牛磺脫氧膽痠鈉建立重癥急性胰腺炎模型.觀察各組血清澱粉酶、IL-6、TNF-α水平、腹水量和胰腺組織的病理學改變.RT-PCR法分析腦組織Bcl-2、Bax mRNA的錶達水平,TUNEL法檢測神經細胞凋亡.結果 重癥急性胰腺炎組血清IL-6、TNF-α升高,腩組織Bcl-2 mRNA錶達減少,Bax mRNA錶達上調,Bcl-2/Bax比值降低,腦組織神經細胞凋亡增加;甲基彊的鬆龍組血清IL-6、TNF-α錶達明顯下降,腦組織Bcl-2 mRNA錶達變化不明顯,但Bax mRNA錶達下調明顯,Bcl-2/Bax比值升高,腦組織神經細胞凋亡顯著減少.結論 重癥急性胰腺炎時腦組織神經細胞凋亡可能是胰性腦病的髮病機製之一;甲基彊的鬆龍可抑製細胞因子的釋放,促進腦組織Bcl-2和Bax基因錶達的平衡,降低腦組織神經細胞凋亡指數,使腦組織損傷得以改善.
목적 탐토갑기강적송룡대중증급성이선염대서뇌조직신경세포조망적영향.방법 장36지SD대서분위3조,가수술조、중증급성이선염조、갑기강적송룡조,매조12지.역행이담관주사5%우광탈양담산납건립중증급성이선염모형.관찰각조혈청정분매、IL-6、TNF-α수평、복수량화이선조직적병이학개변.RT-PCR법분석뇌조직Bcl-2、Bax mRNA적표체수평,TUNEL법검측신경세포조망.결과 중증급성이선염조혈청IL-6、TNF-α승고,남조직Bcl-2 mRNA표체감소,Bax mRNA표체상조,Bcl-2/Bax비치강저,뇌조직신경세포조망증가;갑기강적송룡조혈청IL-6、TNF-α표체명현하강,뇌조직Bcl-2 mRNA표체변화불명현,단Bax mRNA표체하조명현,Bcl-2/Bax비치승고,뇌조직신경세포조망현저감소.결론 중증급성이선염시뇌조직신경세포조망가능시이성뇌병적발병궤제지일;갑기강적송룡가억제세포인자적석방,촉진뇌조직Bcl-2화Bax기인표체적평형,강저뇌조직신경세포조망지수,사뇌조직손상득이개선.
Objective To investigate the effects of methylprednisolone on neurocyte apoptosis in rats with severe acute pancreatitis(SAP).Methods Thirty-six SD rats were divided into sham operation group,SAP group and methylprednisolone group(12 rats in each group).SAP model was constructed by injecting 5%sodium taurodeoxycholate into biliary-pancreatic duct.Serum amylase,interleukin-6(IL-6),tumor necrosis factor α (TNF-α),volume of aseites and histopathological changes of pancreas were determined.The mRNA expressions of Bcl-2 and Bax in brain tissue were analyzed by RT-PCR.and neuroeyte apoptosis was detected by TUNEL method.Results The levels of serum IL-6 and TNF-α were significantly increased:the expression of Bcl-2 mRNA in brain tissue was down-regulated;the expression of Bax mRNA was up-regulated;the Bcl-2/Bax ratio Was decreased:the apoptosis of the neurocytes was increased in SAP group.Compared with SAP group,the levels of serum IL-6 and TNF-α were significantly decreased;the expression of Bcl-2 mRNA was unchanged but the expression of Bax mRNA was down-regulated in brain tissue,so the Bcl-2/Bax ratio was elevated significantly;the rate of the ueurocyte apoptosis in brain tissue were reduced in methylprednisolone group.Conclusions The apoptosis of neurocytes in brain tissue may be one of the factors causing pancreatic encephalopathy.Methylprednisoione can inhibit the release of IL-6 and TNF-α.improve the balance of Bcl-2 and Bax expression and decrease the apoptosis of neurocytes in brain tissue.