CAJ | 학술논문

目的探讨外源性瘦素(leptin)对重症急性胰腺炎(SAP)大鼠胰腺组织NF-κB活性及血清炎症因子的影响.方法 Wister大鼠36只,分为假手术组、SAP动物模型组、瘦素治疗组,各12只.采用5%牛磺胆酸钠胰胆管顺行注射胰胆管制模,治疗组行外源性瘦素腹腔注射,6h后采血、取胰腺标本,检测各组动物血淀粉酶、瘦素、肿瘤坏死因子α、白细胞介素1β的含量,采用免疫组织化学法测定NF-κB活性,并对大鼠胰腺组织进行病理学评分.结果制模6 h后血淀粉酶、leptin、TNF-α、IL-1β水平均升高,胰腺组织NF-κB活性增高,胰腺组织出血坏死明显,外源性瘦素干预组可显著降低血淀粉酶、TNF-α及IL-1β水平,NF-κB活性降低,胰腺组织出血坏死程度减轻,NF-κB活性与炎症因子水平呈正相关.结论外源性瘦素可能通过通过抑制NF-κB活性,降低促炎性因子TNF-α、IL-1β的产生,从而达到对SAP大鼠的保护作用.
목적 탐토외원성수소(leptin)대중증급성이선염(SAP)대서이선조직NF-κB활성급혈청염증인자적영향.방법 Wister대서36지,분위가수술조、SAP동물모형조、수소치료조,각12지.채용5%우광담산납이담관순행주사이담관제모,치료조행외원성수소복강주사,6h후채혈、취이선표본,검측각조동물혈정분매、수소、종류배사인자α、백세포개소1β적함량,채용면역조직화학법측정NF-κB활성,병대대서이선조직진행병이학평분.결과 제모6 h후혈정분매、leptin、TNF-α、IL-1β수평균승고,이선조직NF-κB활성증고,이선조직출혈배사명현,외원성수소간예조가현저강저혈정분매、TNF-α급IL-1β수평,NF-κB활성강저,이선조직출혈배사정도감경,NF-κB활성여염증인자수평정정상관.결론 외원성수소가능통과통과억제NF-κB활성,강저촉염성인자TNF-α、IL-1β적산생,종이체도대SAP대서적보호작용.
Objective To investigate the effect of leptin on transcription factor nuclear-κB (NF-κB) activity of pancreatic tissue and blood inflammatory cytokines (TNF-α,IL-1β) in severe acute pancreatitis. Methods Thirty-six rats were randomly divided into three groups, including sham group (group A, n = 12), AP model group(group B, n = 12) and Leptin treatment group (group C, n = 12). SAP was induced by intraductal injection of 5% sodium taurocholate into the pancreatic duct. Exogenous leptin was injected I. P. Fifteen minutes later. The concentration of serum amylase, leptin, TNF-α, IL-1βwere measured by radioimmunoassay 6 hours later. NF-κB activity of the pancreatic tissue were measured by immunohistochemistry. The changes of pathology of the pancreas were observed. Results The levels of serum amylase, cytokine TNF-αand IL-1βwere significantly reduced in group C, and the levels of serum leptin were significantly increased in group C. NF-κB activity in the pancreatic tissue in group B were significantly higher than that in group A. However, NF-κB activity of the pancreatic tissue in group C were significantly lower than that in group B. Furthermore, the extent of necrosis of the pancreatic tissue was re-lieved. Conclusion Exogenous leptin protected the rats pancreas against damage by sodium taurocholate. The protective effects of exoge-nous leptin were attributive to the reduction in cytokines TNF-α, IL-1β. The possible protective mechanism was that leptin decreased NF-κB activity.