川芎嗪诱导急性胰腺炎胰腺细胞凋亡及其机制的初步研究

目的研究川芎嗪（tetramethylpyrazine，TMP）对大鼠急性胰腺炎（acutepancreatitis，AP）的治疗作用，并探讨川TMP治疗AP的机理。方法采用腹腔内注射蛙皮素制备急性水肿型胰腺炎（acuteedematouspancreatitis，AEP）模型，腹腔内注射TMP，端口标记法（triphosphate-biotinnick-endlabeling，TUNEL）检测胰腺腺泡细胞凋亡，免疫组化法检测Bax基因表达，同时观察IL-6、TNF-α、CRP、AMY等变化，并进行胰腺组织形态学检查。结果采用蛙皮素腹腔注射造成AEP，发现AEP胰腺存在明显细胞凋亡。TMP可以抑制IL-6、TNF-α、CRP等表达，上调促凋亡基因Bax的表达，诱导AEP胰腺细胞凋亡。结论TMP对AEP有明显疗效，其机制与降低IL-6、TNF-α含量，抑制CRP等表达，上调促凋亡基因Bax表达，促进胰腺细胞凋亡有关。

Study of tetramethylpyrazine treatment on rats with acute pancreatitis and its mechanism

Objective To study the influence of tetramethylpyrazine(TMP) on experimental acute pancreatitis model(AP) and investigate the acting machanism of TMP on AP.Methods Acute edematous pancreatitis(AEP) were induced by bombesin(ip,40 μg/kg),pancreatic acinar cell apoptosis and expression of Bax gene were tested respectively by means of triphosphate-biotin nick-end labeling(TUNEL) and immunohistochemical method.Meanwhile,levels of serum IL-6,TNF-α,CRP,AMY and pancreatic histomorphology were observed.Results TMP could markedly inhibit experession of serum IL-6,TNF-α and CRP,regulate the expression of Bax gene up and induce AEP cell apoptosis.Conclusion TMP could treat AP,the acting mechanism is related to down-regulation of IL-6,TNF-α,CRP,up-regulation of Bax gene expression and promotion of pancreatic acinar cell apoptosis.