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第43卷第11期                           南京医科大学学报(自然科学版)
                 2023年11月                   Journal of Nanjing Medical University(Natural Sciences)     ·1509 ·


               ·基础研究·

                白芍总苷抑制NLRP3活化治疗干燥综合征小鼠的实验研究



                江婷婷 ,郭俊巧 ,王         越 ,吴浩林 ,查       洁 ,姚根宏     1*
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                南京中医药大学鼓楼临床医学院风湿免疫科,江苏                    南京    210008;南京医科大学鼓楼临床医学院风湿免疫科,江苏                  南
                1                                                     2
                京 210008
               [摘   要] 目的:探讨白芍总苷(total glucosides of paeony,TGP)治疗干燥综合征的效果及与抑制核苷酸结合寡聚化结构域
               (nucleotide binding oligomerization domain,NOD)样受体热蛋白结构域相关蛋白 3(NOD⁃like receptor pyrin domain containing 3,
                NLRP3)炎症体活化的关系,旨在阐明TGP治疗干燥综合征的新机制。方法:选取雌性非肥胖性糖尿病小鼠为干燥综合征模
                型。400 mg/kg TGP灌胃1个月后,测量小鼠唾液流量,观察颌下腺组织淋巴细胞浸润情况,检测脾脏细胞NLRP3炎症体活化
                状态。体外刺激脾脏细胞NLRP3炎症体活化,并用100 μg/mL TGP处理,RT⁃qPCR和Western blot法检测脾脏细胞NLRP3炎症
                体活化状态。结果:与对照组相比,TGP灌胃组小鼠唾液流量显著增加(P<0.05),颌下腺组织淋巴细胞浸润显著减少,脾脏细
                胞的NLRP3炎症体表达水平显著下降(P<0.05);体外实验也表明,TGP抑制脾脏细胞的炎症体活化(P<0.05)。结论:TGP改
                善干燥综合征小鼠症状,其机制与抑制 NLRP3 炎症体活化相关,揭示了 TGP 治疗干燥综合征的新机制,为进一步推广应用
                TGP治疗干燥综合征提供了新的证据。
               [关键词] 白芍总苷;干燥综合征;炎症体
               [中图分类号] R392.32                   [文献标志码] A                     [文章编号] 1007⁃4368(2023)11⁃1509⁃06
                doi:10.7655/NYDXBNS20231105



                Total glucosides of paeony inhibited NLRP3 activation for treatment of mice with Sjögren’s
                syndrome
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                JIANG Tingting ,GUO Junqiao ,WANG Yue ,WU Haolin ,ZHA Jie ,YAO Genhong 1*
                1 Department of Rheumatology and Immunology,Nanjing Drum Tower Hospital Clinical College of Nanjing University
                of Chinese Medicine,Nanjing 210008;Department of Rheumatology and Immunology,Nanjing Drum Tower
                                                   2
                Hospital Clinical College of Nanjing Medical University,Nanjing 210008,China
               [Abstract] Objective:The efficacy of total glucosides of paeony(TGP)in the treatment of Sjögren’s syndrome(SS)and its
                relationship with inhibition of nucleotide binding oligomerization domain(NOD)⁃like receptor pyrin domain containing 3(NLRP3)
                inflammasome activation were investigated,so as to clarify the novel mechanisms of TGP on treatment of SS. Methods:Female non⁃obese
                diabetic mice were selected as the model of SS. The non⁃obese diabetic mice were intragastric administrated with TGP(400 mg/kg)for
                1 month. The saliva flow rates of mice were measured. The lymphocyte infiltration in submandibular gland was determined. The NLRP3
                inflammasome activation of spleen was detected. In vitro,the NLRP3 inflammasome was activated in cultured splenocytes with 100 μg/mL
                TGP treatment. Then,the NLRP3 inflammasome activation was determined by RT⁃qPCR and Western blot. Results:Compared with
                the mice of control group,the saliva flow rates were significantly increased(P<0.05)and the lymphocyte infiltration in submandibular
                gland was significantly reduced in non⁃obese diabetic mice of TGP treatment group. The NLRP3 inflammasome of spleen was inhibited
                in non ⁃ obese diabetic mice with TGP treatment(P<0.05). In vitro,the NLRP3 inflammasome activation of splenocytes was also
                suppressed by TGP(P<0.05). Conclusion:TGP alleviates SS⁃like symptoms in non⁃obese diabetic mice,and these beneficial effects
                are related to the inhibition of NLRP3 inflammasome activation. These findings not only uncover the novel mechanisms of therapeutic
                effects of TGP in SS,but also provide new evidences for application of TGP in treatment of SS patients.
               [Key words] total glucosides of paeony;Sjögren’s syndrome;inflammasome
                                                                            [J Nanjing Med Univ,2023,43(11):1509⁃1514]

               [基金项目] 国家自然科学基金(81970062);南京市医学科技发展项目(ZKX21027)
                ∗
                通信作者(Corresponding author),E⁃mail:yaogenhong@nju.edu.cn
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