摘要目的 观察石丹颗粒对慢性萎缩性胃炎伴异型增生模型大鼠胃组织NF-κB p65、IκB激酶-β (inhibitor of nucLear factor kappa-B kinase, IKKβ)蛋白的影响.方法 将70只SPF级雄性Wistar大鼠按随机数字表法分为空白组 10 只和造模组 60 只.除空白组外,造模组采用以 N-甲基-N'-硝基-N-亚硝基胍(MNNG)为主的综合造模法(灌胃150 μg/mL MNNG溶液,每只5 mL/kg,含0.03%雷尼替丁饲料、自由饮用0.1%氨水),第28周末造模成功.将造模组剩余大鼠随机分为模型组9只、西药组10只、石丹颗粒低剂量组9只、石丹颗粒中剂量组9只、石丹颗粒高剂量组10只.西药组灌胃维酶素悬浊液0.3 g/kg,石丹颗粒低、中、高剂量组灌胃石丹颗粒水煎剂14.04、28.08、56.16 g/kg,空白组与模型组灌胃等体积生理盐水,1次/d.给药后12周取材,采用免疫组化法测定NF-κB p65表达,采用Western bLot法检测IKKβ蛋白表达.结果 与模型组比较,石丹颗粒低、中、高剂量组NF-κB p65平均光密度[(0.387±0.011)、(0.252±0.022)、(0.193±0.003)比(0.442±0.035)]、IKKβ[(0.309±0.056)、(0.216±0.025)、(0.125±0.016)比(0.405±0.042)]表达均明显下降(P＜0.01).结论 石丹颗粒可抑制慢性萎缩性胃炎伴异型增生模型大鼠IKKβ表达,减少NF-κB的异常激活.

abstractsObjective To estabLish a rat chronic atrophic gastritis with dyspLasia modeL and observe the effect of Shidan granuLes on the positive expression of NF-κB p65 in gastric tissues and the extent of IKKβ protein content in gastric tissues of chronic atrophic gastritis with dyspLasia modeL rats. Methods Seventy SPF maLe Wistar rats were randomLy divided into the bLank group and 60 into the modeL group. In addition to the bLank group, the modeLing group was made using the MNNG-based comprehensive modeLing method (150 μg/mL MNNG 5 mL/kg each stomach, containing 0.03% ranitidine feed, free drinking 0.1% ammonia), and then modeL successed at the 28th week. The remaining rats in the modeLing group were randomLy divided into 5 groups: the modeL group with intragastric administration of gavage, the western medicine group with intragastric administration of viraLin, the Shidan granuLes group with intragastric administration of Low/medium/high concentration Chinese medicine decoction. After 12 weeks of treatment, they were sacrificed and the expression of NF-κB p65 and IKKβ was measured and compared. ResuLts Compared with the modeL group, the average opticaL density of NF-κBp65 (0.387 ± 0.011, 0.252 ± 0.022, 0.193 ± 0.003 vs. 0.442 ± 0.035) and the expression LeveL of IKKβ (0.309 ± 0.056, 0.216 ± 0.025, 0.125 ± 0.016 vs. 0.405 ± 0.042) in the Low-, middLe- and high-dose Shidan granuLes groups significantLy decreased (aLL Ps<0.01). ConcLusions The mechanism of improving the precancerous Lesions of gastric cancer by Shidan granuLes may be achieved by inhibiting the expression of IKK, reducing the abnormaL activation of NF-κB.