CAJ | 학술논문

目的：观察荆花胃康胶丸对幽门螺杆菌(Hp)感染小鼠胃黏膜核因子κB(NF-κB)p65表达的影响,探讨其抗炎作用机制。方法将44只SPF级KM小鼠随机分为空白组、模型组、三联组、荆花胃康组。除空白组外,其他小鼠采用短期免疫抑制联合经口感染方法建立Hp感染模型,三联组予兰索拉唑、甲硝唑、克拉霉素1周,荆花胃康组予荆花胃康胶丸挥发油4周,模型组给予灭菌注射用水,空白组不予干预。所有小鼠均于给药4周后处死。通过实时荧光定量PCR、免疫组化法测定NF-κB p65的表达。结果 NF-κB p65 mRNA相对表达量为空白组3.27±0.53、模型组2.18±0.50、三联组4.19±1.21、荆花胃康组7.70±1.41(P＜0.001),与模型组比较,其他3组表达均增高(P＝0.004),三联组与荆花胃康组比较差异有统计学意义(P＜0.001)。免疫组化显示,NF-κB p65细胞核平均光密度值为空白组25.18±7.42、模型组31.17±2.98、三联组30.06±4.69、荆花胃康组26.94±5.19(χ2＝10.960,P＝0.012)；细胞浆平均光密度值各组差异无统计学意义(F＝1.922, P＝0.134)；核/浆比值为空白组0.23±0.06、模型组0.28±0.03、三联组0.26±0.04、荆花胃康组0.24±0.04(χ2＝14.527,P＝0.002),其中模型组较空白组明显增加(P＝0.002),三联组与模型组比较差异无统计学意义(P＝0.420),荆花胃康组较模型组明显降低(P＝0.022),且与空白组比较差异无统计学意义(P＝0.750)。结论荆花胃康胶丸通过降低Hp感染小鼠NF-κB p65表达水平达到抗炎作用。
목적：관찰형화위강효환대유문라간균(Hp)감염소서위점막핵인자κB(NF-κB)p65표체적영향,탐토기항염작용궤제。방법장44지SPF급KM소서수궤분위공백조、모형조、삼련조、형화위강조。제공백조외,기타소서채용단기면역억제연합경구감염방법건립Hp감염모형,삼련조여란색랍서、갑초서、극랍매소1주,형화위강조여형화위강효환휘발유4주,모형조급여멸균주사용수,공백조불여간예。소유소서균우급약4주후처사。통과실시형광정량PCR、면역조화법측정NF-κB p65적표체。결과 NF-κB p65 mRNA상대표체량위공백조3.27±0.53、모형조2.18±0.50、삼련조4.19±1.21、형화위강조7.70±1.41(P＜0.001),여모형조비교,기타3조표체균증고(P＝0.004),삼련조여형화위강조비교차이유통계학의의(P＜0.001)。면역조화현시,NF-κB p65세포핵평균광밀도치위공백조25.18±7.42、모형조31.17±2.98、삼련조30.06±4.69、형화위강조26.94±5.19(χ2＝10.960,P＝0.012)；세포장평균광밀도치각조차이무통계학의의(F＝1.922, P＝0.134)；핵/장비치위공백조0.23±0.06、모형조0.28±0.03、삼련조0.26±0.04、형화위강조0.24±0.04(χ2＝14.527,P＝0.002),기중모형조교공백조명현증가(P＝0.002),삼련조여모형조비교차이무통계학의의(P＝0.420),형화위강조교모형조명현강저(P＝0.022),차여공백조비교차이무통계학의의(P＝0.750)。결론형화위강효환통과강저Hp감염소서NF-κB p65표체수평체도항염작용。
Objective To observe the effects of Jinghua Weikang Capsule on NF-κB p65 expression in gastric mucosa of Helicobacter pylori (Hp) infected mice;To discuss its mechanism of action. Methods Totally 44 SPF KM mice were randomly divided into blank group, model group, triple therapy group and Jinghua Weikang group. Except for the blank group, Hp infected model was set up by short term immunosuppression combined with peroral infection. The treatment strategies were triple therapy group with lansoprazole, metronidazole and clarithromycin for 1 week, Jinghua Weikang group with Jinghua Weikang volatile oil for 4 weeks, model group with sterile water for 4 weeks, and blank group free of any treatments. All the subjects were sacrificed in the 4th week after the treatment. NF-κB p65 was detected through real-time PCR and immunohistochemical method. Results The relative quantitative expressions of NF-κB p65 mRNA were 3.27±0.53 in blank group, 2.18±0.50 in control group, 4.19±1.21 in triple therapy group, and 7.70±1.41 in Jinghua Weikang group (χ2=86.303, P<0.001). Compared with model group, the expressions of NF-κB p65 mRNA of other three groups increased statistically differently (P=0.004), and there was also statistical difference between triple therapy and Jinghua Weikang group. Through immunohistochemical tests, the values of NF-κB p65 mean optical density of nucleus were 25.18± 7.42 in blank group, 31.17±2.98 in model group, 30.06±4.69 in triple therapy group, and 26.94±5.19 in Jinghua Weikang group (χ2=10.960, P=0.012). The values of NF-κB p65 mean optical density of cytoplasm had no statistical difference (F=1.922, P=0.134), and the nucleus/cytoplasm values were 0.23±0.06 in blank group, 0.28±0.03 in model group, 0.26±0.04 in triple therapy group, and 0.24±0.04 in Jinghua Weikang group (χ2=14.527, P=0.002). The statistical analysis of the nucleus/cytoplasm values showed significance between blank and model group (P=0.002), while triple therapy group was still equal to model group (P=0.420). Jinghua Weikang group was lower than model group (P=0.022) and equal to blank group (P=0.750). Conclusion Jinghua Weikang Capsule can effectively reduce the expression of NF-κB p65 in protein level in Hp infected mice.