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目的:观察慢性鼻-鼻窦炎(CRS)时,鼻渊舒口服液对鼻窦黏膜上皮分子伴侣HSP70及其辅助因子CHIP的影响,从分子伴侣系统角度探索鼻渊舒治疗CRS的机制。方法:140只雄性C57小鼠,每组20只,随机分为正常对照组、假手术组、模型组、克拉霉素阳性对照组及鼻渊舒口服液低、中、高剂量组,建立CRS模型,以相应药物治疗14 d。HE染色观察鼻窦黏膜组织病理学变化,实时定量PCR鼻窦黏膜HSP70、CHIP mRNA表达,Western Blot法检测鼻窦黏膜HSP70、CHIP蛋白表达及IKK活性。结果:模型组鼻窦黏膜上皮大片坏死脱落,慢性炎细胞浸润明显;HSP70及CHIP的mRNA及蛋白表达较正常对照组及假手术组显著降低(P<0.05或P<0.01),p-IKKα/β表达较正常对照组及假手术组显著增高(P<0.01)。与模型组比较,鼻渊舒中、高剂量组鼻窦黏膜上皮修复较好,排列较为整齐,慢性炎细胞浸润明显减轻;CHIP及HSP70 mRNA及蛋白表达显著增高(P<0.01),p-IKKα/β表达显著降低(P<0.01)。结论:鼻渊舒能促进CRS小鼠鼻窦黏膜上皮修复,其机制可能与其增加鼻窦黏膜上皮分子伴侣HSP70及其辅助分子CHIP表达,增强细胞内蛋白质损伤保护机制,抑制IKK活性及其下游的NF-κB炎症通路有关。
OBJECTIVE: To observe the effect of Biyuan Shu oral solution on choriocarcinoma molecular chaperone HSP70 and its cofactor CHIP in chronic rhinosinusitis (CRS) and explore the mechanism of nasosinusitis in treating CRS from molecular chaperone system. METHODS: One hundred and forty male C57 mice were randomly divided into normal control group, sham operation group, model group, clarithromycin positive control group and low, medium and high dose group of BHD Model, the corresponding drug treatment 14 d. The pathological changes of mucosa were observed by HE staining. The expressions of HSP70 and CHIP mRNA were measured by real-time quantitative PCR. The expression of HSP70 and CHIP protein and the activity of IKK in sinus mucosa were detected by Western Blot. Results: The large mucosal epithelium necrosis and chronic inflammatory cell infiltration were obvious in model group. The mRNA and protein expression of HSP70 and CHIP were significantly lower than those in normal control group and sham operation group (P <0.05 or P <0.01) Compared with normal control group and sham operation group, the expression was significantly increased (P <0.01). Compared with the model group, the nasal mucosa epithelium of nasopharyngeal and nasal mucosa were repaired well and arranged neatly, and the infiltration of chronic inflammatory cells was significantly reduced; the mRNA and protein expressions of CHIP and HSP70 were significantly increased (P <0.01); p-IKKα / β expression was significantly lower (P <0.01). Conclusions: BHD can promote the repair of mucosal epithelial cells in CRS mice, which may be related to the increase of CHIP expression in sinusoidal mucosal epithelial chaperones CHIP and CHIP, the protection of intracellular protein damage, the inhibition of IKK activity and downstream NF- κB inflammatory pathway related.