基于“脾开窍于口”探讨口周炎微环境与幽门螺杆菌相关性

Exploring the Correlation between Inflammatory Microenvironment of Perioral and Helicobacter pylori Based on “Spleen Opening at Mouth”

摘要: 目的：基于“脾开窍于口”探讨口周炎微环境与幽门螺杆菌(Helicobacter pylori, Hp)的相关性。方法：32只SPF级SD大鼠随机分为2组，空白组16只、模型组16只，模型组予以Hp菌液灌胃，造模4周。ELISA法检测Toll样受体4 (Toll-Like Receptor 4, TLR4)和NOD样受体蛋白3 (NOD-Like Receptor thermal Protein domain associated protein 3, NLRP3)在口周皮肤、口腔黏膜及胃组织中的表达水平，口周皮肤和口腔黏膜、胃组织中蛋白表达的相关性采用Pearson相关性分析。结果：与空白组相比，模型组小鼠口周皮肤、口腔黏膜、胃组织中TLR4和NLRP3表达水平均升高，差异有统计学意义(P < 0.001)。模型组口周皮肤TLR4和NLRP3表达水平与其在胃组织中含量呈正相关(r = 0.820，P < 0.001；r = 0.907，P < 0.001)，模型组口腔黏膜TLR4和NLRP3表达水平与其在胃组织中含量呈正相关(r = 0.546，P < 0.01；r = 0.641，P < 0.01)，差异均有统计学意义。结论：口周炎微环境与幽门螺杆菌有相关性，幽门螺杆菌感染会导致大鼠口周炎微环境改变。

Abstract: Objective: To explore the correlation between inflammatory microenvironment of perioral and Hel-icobacter pylori based on the theory of “spleen opening at mouth”. Method: 32 SPF grade SD rats were randomly divided into two groups: a normal group of 16 rats and a model group of 16 rats. The model group was given Hp bacterial solution by gavage for 4 weeks. ELISA was used to detect the expression levels of Toll like receptor 4 (Toll-Like Receptor 4, TLR4) and NOD like receptor protein 3 (NOD-like receptor thermal protein domain associated protein 3, NLRP3) in the perioral skin, oral mucosa, and gastric tissue. Pearson correlation analysis was used to investigate the correlation be-tween protein expression in the perioral skin, oral mucosa, and gastric tissue. Results: Compared with the normal group, the expression levels of TLR4 and NLRP3 in the perioral skin, oral mucosa, and gastric tissue of the model group mice increased, the difference was statistically significant (P < 0.001). The expression level of TLR4 and NLRP3 in the perioral skin of the model group was posi-tively correlated with its content in gastric tissue (r = 0.820, P < 0.001; r = 0.907, P < 0.001), and the expression level of TLR4 and in the oral mucosa of the model group were positively correlated with its content in gastric tissue (r = 0.546, P < 0.01; r = 0.641, P < 0.01), the differences were statistical-ly significant. Conclusion: Helicobacter pylori infection is associated with the microenvironment of perioral inflammation. Helicobacter pylori infection can lead to changes in the microenvironment of perioral inflammation in rats.