乳酸杆菌CL22菌株治疗Balb/c小鼠Hp感染性胃炎模型的有效性研究

目的: 观察乳酸杆菌对Balb/c小鼠Hp感染性胃炎的治疗作用,探讨一种非抗生素治疗Hp的可能方式. 方法:通过接种Hp,建立Balb/c小鼠Hp感染胃炎动物模型,将造模成功的32只Balb/c小鼠随机分为4组,每组8只:第1组(PPI三联干预治疗组)、第2组(乳酸杆菌CL22处理组)、第3组(乳酸杆菌CL24处理组)、第4组(生理盐水对照组),用相应干扰剂分别连续灌胃治疗10 d.另8只正常小鼠为第5组(空白对照组).最后一次灌胃4周后处死小鼠,HE染色判断小鼠胃黏膜组织学损伤,并用快速尿素酶试验、Giemsa染色和细菌培养进行Hp的检测.结果: 5组间胃窦黏膜病理组织学评分比较有统计学差异(F＝7.932,P＝0.000),其中第1组、第2组、第3组、第5组的胃窦黏膜病理组织学评分均低于第4组(P＜0.05),第1组、第2组、第5组两两比较差异无统计学意义(P＞0.05),第3组与第5组比较差异有显著性(P＜0.05);胃体黏膜病理组织学评分5组比较有统计学差异(F=6.241,P＝0.001),其中第1组、第2组、第3组、第5组的胃体黏膜病理组织学评分均低于第4组(P＜0.05),第1组、第2组、第3组、第5组两两比较差异无统计学意义(P＞0.05).胃窦部Hp根除率5组间比较有统计学差异(χ2=16.923,P=0.002),其中第1组、第2组明显高于第4组(P＜0.05),第3组与第4组比较,无统计学差异(P＞0.05);胃体部Hp根除率5组间比较有统计学差异(χ2=14.295,P=0.006),其中第1组、第2组明显高于第4组(P＜0.05),第3组与第4组比较,无统计学差异(P＞0.05).结论:乳酸杆菌CL22菌株可有效抑杀Balb/c小鼠Hp感染性胃炎模型体内Hp,疗效与PPI 抗生素相当,可以成为非抗生素治疗Hp的又一选择.

Effect of Bacillus acidi lactici CL22 strain on Helicobacter Pyloriinfectious gastritis in Balb/c mouse model

OBJECTIVE: To observe the therapeutic effect of Bacillus acidi lactici on Helicobacter Pylori (Hp) infectious gastritis in Balb/c mouse model so as to explore a possible non-antibiotic treatment for Hp. METHODS: To establish a Balb/c mouse model with Hp infectious gastritis through inoculation of mankind Hp,32 Balb/c mice infected by Hp were randomly divided into 4 groups:Group 1(PPI trigeminy treatment group),Group 2 (Bacillus acidi lactici CL22 treatment group),Group 3 (Bacillus acidi lactici CL24 treatment group),and Group 4 (normal saline control group). Intragastric administration was given continuously for 10 days.Another 8 normal mice were chosen as Group 5(blank control group).All mice were killed after 4 weeks since last intragastric administration. Hp was detected by rapid urease test,Giemsa dying, and bacterial culture,and histopathologic changes in the gastric mucosa of mice were determined by H-E staining. RESULTS: There were significant differences in pathohistologic scores in sinus ventriculi among the 5 groups (F = 7.932, P = 0.000). The scores in Group 1, Group 2, Group 3, and Group 5 were obviously lower than those in Group 4 (P < 0.05), but there were not significant differences among Group 1, 2, and 5 (P>0.05). The pathohistologic score in Group 3 was obviously higher than that in Group 5 (P <0.05). There were significant differences in pathohistologic scores in corpus ventriculi among the 5 groups (F = 6.241, P = 0.001). The scores in Group 1,Group 2,Group 3,and Group 5 were obviously lower than those in Group 4(P <0.05), but there were not significant differences among Group 1, 2, 3,and 5 (P>0.05).There was significant difference in Hp eradication rates in sinus ventriculi among the 5 groups (chi2 = 16.923, P=0.002). The Hp eradication rates in Group 1 and 2 were obviously lower than those in Group 4 (P <0.05), but there was not significant difference between Group 1 and Group 2, Group 3 and Group 4 (P>0.05). There also were significant differences in Hp eradication rate in corpus ventriculi among the 5 groups (chi2 = 14.295, P=0.006). Of them, Group 1 and Group 2 were higher than Group 4 (P <0.05), but there were not obviously differences between Group 1 and 2,Group 3 and 4 (P>0.05). CONCLUSION: Bacillus acidi lactici strain CL22 can effectively inhibit and eradicate Hp in Balb/c mouse model with Hp infectious gastritis in vivo. The therapeutic effect of Bacillus acidi lactici strain CL22 is equal to PPI + antibiotics and could be another choice of nonjantibiotic treatment for Hp.