三七总皂苷预处理对炎性内脏痛大鼠磷酸化细胞外信号调节激酸表达的影响

Panax notoginseng saponins pretreatment affects the p-ERK expression in rats with inflammatory visceral pain

目的：研究三七总皂苷（PNS）预处理对磷酸化细胞外信号调节激酶（p-ERK）在炎性内脏痛大鼠脊髓及背根节的表达影响,探讨PNS对炎性内脏痛影响的可能机制.方法：SD大鼠随机分为正常对照组、PNS预处理组、生理盐水（NS）预处理组,处理后15 d行乙酸腹腔注射造模,每15min记录内脏痛指数;取小肠组织进行H-E染色,光镜下计数粒细胞数目;应用免疫组织化学检测脊髓及背根节p-ERK的表达.结果：乙酸腹腔注射后,小肠炎性反应明显增强,小肠黏膜下层增厚,但各时间点与对照组比较,实验组粒细胞数无差异;120 min时PNS预处理组内脏痛指数明显低于NS预处理组;两预处理组脊髓后角p-ERK表达较正常组明显增高,30、60 min时PNS预处理组脊髓后角及相应背根节p-ERK表达明显高于NS预处理组.结论：PNS预处理缓解乙酸致炎性内脏痛可能是通过调节中枢神经系统起作用的,且可能与抑制p-ERK表达有关.

Objective： To explore the effect of panax notoginseng saponins （PNS） pretreatment on the expression of phospho- extracellular signal-regulated kinase （p-ERK） in the spinal dorsal horn and dorsal root ganglion （DRG） of rats with inflammatory visceral pain. Methods： SD rats were randomly divided into a normal group, a PNS pretreatment group, and a normal saline （NS） pretreatment group. Fifteen days later, the model of inflammatory visceral pain was made by intraperitoneal injection of 1% acetic acid. The visceral pain index of experimental rats were recorded every 15 minutes. The section of the small intestine was stained with hematoxylin-eosin （H-E） method to count the granulocyte. Expression of p- ERK in the spinal cord and DRG was examined with immunochemistry method. Results： Compared with the normal group, the small intestine tissues of the two experimental groups showed significant inflammatory response with thick submucosa, but there was no significant difference between the two experimental groups in the number of the granulocytes in the small intestine submucosa tissues; the score result of the NS pretreatment group was significantly higher than that of the PNS pretreatment group Compared with the normal group, the p-ERK expression of the two experimental groups was reduced apparently, but in PNS pretreatment group, p-ERK expression was significantly lower than that in the NS pretreatment group. Conclusion： PNS pretreatment may affect the acid-induced inflammatory visceral pain by promoting the expression of p-ERK in the primary visceral sensory neurons.