2,4,6-三硝基苯磺酸致肠炎大鼠背根神经节神经元电生理特性

The electrophysiology characteristics of dorsal root ganglion neurons in rats with TNBS-induced colitis

目的研究2，4，6一三硝基苯磺酸（TNBS）致肠炎大鼠的背根神经节（DRG）神经元电生理特性，为更全面地了解炎症性肠病（IBD）提供借鉴。方法SD大鼠（雄性，体质量160～200g）随机分为实验组和对照组，实验组（n=5）给予30％TNBS溶液（剂量40mg／kg）灌肠，对照组（n=5）给予等效体积的生理盐水灌肠。在灌肠的第8天（炎症急性期）处死大鼠，对其结肠进行H—E染色，以确定造模是否成功；取其DRG神经元用全细胞膜片钳技术分析其电生理特性。结呆实验组大鼠体质量降低（P〈0．001），H—E染色示肠黏膜腺体结构严重破坏，炎性细胞浸润明显，表明造模成功。TNBS致肠炎后大鼠DRG神经元动作电位的阈电流降低（P〈0．05）。结论TNBS致肠炎后大鼠DRG神经元兴奋性增高。

Objective To investigate the electrophysiology characteristics of dorsal root ganglion （DRG） neurons in rats with 2, 4, 6-trinitrobenzenesulfonic acid （TNBS）-induced colitis, so as to provide reference for a better understanding of inflammatory bowel disease（IBD）. Methods SD rats（male, 160-200 g）were randomly divided into two groups. Experimental colitis was induced in colitis group （n= 5） by intracolonic administration of TNBS （40 mg/kg diluted in 70% ethanol）, and control rats （n=5） received normal saline in the same manner. Rats were sacrificed on the eighth day（acute inflammation phase） after administration of TNBS or normal saline, and the DRG neuroNS were obtained to investigate its electrophysiology characteristics by the whole-cell patch clamping. Results The body weight of rats in the experimental group was significantly decreased. H-E staining showed severe damage of the intestinal mucosa glands and inflammatory cell infiltration, indiating successful model creation. The action potential threshold of DRG neurons was significantly decreased in rats with TNBS-induced colitis （P〈0.05）. Conclusion The excitability of DRG neurons is increased in rat model of TNBS-induced colitis.