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目的探讨绞股蓝总皂苷（ｇｙｐｅｎｏｓｉｄｅｓ，ＧＰ）对ＣａｇＡ（＋），ＶａｃＡ（＋）ＮＣＴＣ１１６３７株幽门螺杆菌（Ｈｅｌｉｃｏｂａｃｔｅｒｐｙｌｏｒｉ，ＨＰ）延缓动物实验性胃溃疡愈合的治疗作用及其机制。方法用醋酸诱发大鼠实验性胃溃疡，以溃疡面积、溃疡面积占腺胃部百分比、粘膜组织内白细胞介素８（ＩＬ８）、ＰＧＥ２、ＭＤＡ、ＳＯＤ、·ＯＨ及溃疡愈合时间为指标，观察ｉｇ给予冻干ＮＣＴＣ１１６３７ＨＰ的影响及给予ＨＰ１ｈ后ｉｇＧＰ的治疗作用。结果单给ＨＰ组，溃疡面积加大，愈合延迟，粘膜组织内ＩＬ８、ＭＤＡ升高，ＳＯＤ活性下降；·ＯＨ生成无明显变化；损伤粘膜组织内ＩＬ８升高，ＰＧＥ２亦同时升高。ＨＰ＋ＧＰ组溃疡面积、溃疡面积百分率明显减小；粘膜内ＭＤＡ、·ＯＨ生成抑制，ＩＬ８、ＰＧＥ２平行下降，ＳＯＤ活性提高。结论ＮＣＴＣ１１６３７株ＨＰ可明显延缓醋酸性大鼠胃溃疡的愈合；绞股蓝总皂苷通过抑制炎症反应过程中ＩＬ８、ＭＤＡ、·ＯＨ生成，并通过提高ＰＧＥ２和ＳＯＤ活性增强胃粘膜保护机制，对感染ＮＣＴＣ１１６３７株ＨＰ大鼠实验性胃溃疡产生显著治疗作用。
Objective To investigate the therapeutic effect of gypenosides (GP) on CagA (+) and VacA (+) NCTC11637 strains of Helicobacter pylori (HP) in delaying experimental gastric ulcer healing in rats and its mechanism. METHODS: Rat experimental gastric ulcer was induced by acetic acid. The ulcer area, the percentage of ulcer area in the gland and stomach, the interleukin-8 (IL-8), PGE2, MDA, SOD, OH in the mucosal tissue and the ulcer healing time were Indicators, observe the effect of ig giving freeze-dried NCTC11637HP and the therapeutic effect of igGP after giving HP for 1 h. Results In the HP group alone, ulcer area was increased, healing was delayed, IL-8 and MDA were increased in the mucosal tissue, and SOD activity was decreased; OH production was not significantly changed; IL-8 was increased in the injured mucosa, and PGE2 also increased. high. In the HP+GP group, the percentage of the ulcer area and the ulcer area decreased significantly; the production of MDA and OH in the mucosa was inhibited; the levels of IL-8 and PGE2 decreased in parallel, and the SOD activity increased. Conclusion NCTC11637 strain HP can significantly delay the healing of acetic acid-induced gastric ulcer in rats; Gynostemma total saponins can inhibit the production of IL8, MDA, and OH during inflammatory reaction, and increase the protective mechanism of gastric mucosa by increasing the activity of PGE2 and SOD. The NCTC11637 Strain had significant therapeutic effects on experimental gastric ulcers in HP rats.