论文部分内容阅读
目的:观察解毒化瘀生津方对干燥综合征小鼠颌下腺IL-1(interleukin-1,)、IL-6(interleukin-6)含量表达的影响,探讨其作用机制。方法:采用免疫诱导法建立干燥综合征小鼠动物模型,以解毒化瘀生津方灌胃治疗,并以硫酸羟氯喹片(Hydroxychloroquine Sulfate,HCQ)灌胃作为对照,采用酶联免疫吸附法检测小鼠颌下腺IL-1、IL-6含量表达,并对小鼠颌下腺IL-1、IL-6进行免疫组织化学法检测及免疫荧光染色观察。结果:酶联免疫吸附法检测发现,模型组颌下腺IL-1、IL-6的含量高于正常组(P<0.01),中药高剂量组和硫酸羟氯喹组IL-1、IL-6蛋白含量低于中药低剂量组(P<0.05,P<0.01)。免疫组化方法检测小鼠颌下腺IL-1、IL-6的平均吸光度,模型组与正常组比较,差异有统计学意义(P<0.05,P<0.01),中药高剂量组和硫酸羟氯喹组吸光度低于中药低剂量组(P<0.05),接近于正常组。免疫荧光技术观察,模型组荧光染色最强,正常组染色最弱。结论:解毒化瘀生津方能够降低小鼠颌下腺IL-1、IL-6水平,抑制了细胞因子的促炎效应,这可能是该药能够治疗干燥综合征的疗效机制之一。
Objective: To observe the effect of Jiedu Huayu Shengjin Fang on expression of interleukin-1 (IL-1) and interleukin-6 (IL-6) in the submandibular gland of mice with Sjogren’s syndrome and to explore its mechanism. Methods: The animal model of Sjogren’s syndrome was established by immune induction method. The mice were treated with detoxification, blood stasis and sore throat, and the control group was given intragastric administration of Hydroxychloroquine Sulfate (HCQ). The enzyme-linked immunosorbent assay The expressions of IL-1 and IL-6 in rat submandibular gland were detected by immunohistochemistry and immunofluorescence staining. Results: The levels of IL-1 and IL-6 in the submandibular gland of the model group were significantly higher than those in the normal group (P <0.01) by ELISA. The contents of IL-1 and IL-6 in high dose group and hydroxychloroquine group Lower than the traditional Chinese medicine low dose group (P <0.05, P <0.01). The mean absorbance of IL-1 and IL-6 in the submandibular gland of mice was detected by immunohistochemistry. The difference between the model group and the normal group was statistically significant (P <0.05, P <0.01) Absorbance was lower than the low dose group (P <0.05), close to the normal group. Immunofluorescence staining showed that the model group had the strongest staining and the normal group had the weakest staining. Conclusion: Jiedu Huayu Recipe can reduce the levels of IL-1 and IL-6 in the submandibular gland of mice and inhibit the proinflammatory effects of cytokines, which may be one of the therapeutic mechanisms for the treatment of Sjogren’s syndrome.