title: [Effect of Banxia Qinlian Decoction on Th17/IL-17 Immune Inflammatory Way of Sjögren's Syndrome NOD Model Mice].
abstract: OBJECTIVE
  To explore the molecular mechanism of exocrine immune inflammatory injury of Sjögren's Syndrome and the intervention of Banxia Qinlian Decoction (BQD).
  
  
  METHODS
  Totally 18 female NOD mice were randomly divided into the model group, the positive drug group, and the BQD group, 6 in each group. Six female BALB/c mice were recruited as a blank control group. Mice in the blank control group and the model group were gavaged with deionized water at the daily dose of 0.1 mL/10 g body weight. Tripterygium Tablet was administered by gastrogavage to mice in the positive group at the daily dose of 10 mg/kg. BQD was administered by gastrogavage to mice in the BQD group at the daily dose of 60 g crude drugs/kg. After 12 weeks of medication, mice were sacrificed. Their eyeballs were excised and blood collected. Tissues of bilateral parotids and submandibular glands were kept. mRNA transcriptional levels of IL-17, IL-6, type 3 muscarinic acetylcholine receptors (M3R), aquaporin protein-5 (AQP5) were detected by RT-PCR. Expression levels of M3R and AQP5 protein were detected by Western blot. Protein expression levels of IL-17 and IL-6 were detected by ELISA.
  
  
  RESULTS
  Compared with the normal group, mRNA transcriptional levels and protein expression levels of IL-17, IL-6, M3R, and AQP5 were significantly up-regulated in the model group (P < 0.01). Compared with the model group, mRNA transcriptional levels and protein expression levels of IL-17, IL-6, M3R, and AQP5 were significantly down-regulated in the positive drug group and the BQD group with statistical difference (P < 0.01, P < 0.05). Compared with the BQD group, mRNA-transcriptional levels of IL-17, IL-6, and M3R, as well as M3R and AQP5 protein expression levels were significantly down-regulated in the positive drug group (all P < 0.01).
  
  
  CONCLUSIONS
  The molecular mechanism of BQD in inhibiting SS exocrine neurotoxic injury might be possibly related to regulating Th17/IL-17 immune inflammatory way.
authors.forename: Yan
authors.initials: Y
authors.lastname: Lu
authors.forename: Yi
authors.initials: Y
authors.lastname: Chen
authors.forename: Ya-nan
authors.initials: YN
authors.lastname: Wang
authors.forename: Hui
authors.initials: H
authors.lastname: Liu
authors.forename: Ji-sheng
authors.initials: JS
authors.lastname: Zhang
authors.forename: Wei-guo
authors.initials: WG
authors.lastname: Ma
authors.forename: Zhi-ming
authors.initials: ZM
authors.lastname: Shen
authors.forename: Jie
authors.initials: J
authors.lastname: Wang
authors.forename: Kang
authors.initials: K
authors.lastname: Wang
authors.forename: Feng-xian
authors.initials: FX
authors.lastname: Meng
mesh_terms: D000818:Animals; D051402:Aquaporin 5 / Q000378:metabolism; D004195:Disease Models, Animal; D004365:Drugs, Chinese Herbal / Q000494:pharmacology* / Q000627:therapeutic use; D005260:Female; D020381:Interleukin-17 / Q000378:metabolism*; D015850:Interleukin-6 / Q000378:metabolism; D051379:Mice; D008807:Mice, Inbred BALB C; D016688:Mice, Inbred NOD; D012859:Sjogren's Syndrome / Q000188:drug therapy* / Q000276:immunology; D013363:Submandibular Gland; D058504:Th17 Cells; D015854:Up-Regulation
chemical_list: D051402:Aquaporin 5; D004365:Drugs, Chinese Herbal; C515934:Il17a protein, rat; D020381:Interleukin-17; D015850:Interleukin-6