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Abstract Number: 1504

Anti-Inflammation Effect Of Peroxisome Proliferator-Activated Receptor-ã (PPAR-ã) In Non-Obese Diabetic Mice With Sjogren’s Syndrome

Bei Xu1 and Xiaomei Li2, 1Department of Rheumatology and Immunology, The third Affiliated Hospital of Anhui Medical University, The First Hospital of Hefei, Hefei, China, 2Department of Rheumatology and Immunology, Anhui Medical University Affiliated Provincial Hospital, Hefei, Anhui, China

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: PPAR-gamma, Sjogren's syndrome and cytokines

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Session Information

Title: Sjögren's Syndrome: Pathogenesis

Session Type: Abstract Submissions (ACR)

Background/Purpose: To investigate the anti-inflammation effect of peroxisome proliferator-activated receptor-γ (PPAR-γ) in non-obese diabetic mice (NOD mice) with sjogren`s syndrome.

Methods: Twenty 8-weeks-old female NOD mice were randomly divided into 2 groups. rosiglitazone and normal saline were administered in PPAR-γ group and control group respectively. At the age of 12 weeks and 15 weeks, we killed one mouse in PPAR-γ group and control group respectively, and the others were sacrificed at the age of 17 weeks. Blood were obtained by cardiac puncture, and salivary glands were resected. The histopathological change was examined by H&E staining. The level of IL-1β, IL-4, IL-6 and TNF-α in serum were measured by ELISA. Real-time PCR was used to evaluate the mRNA expression level of IL-1β, IL-4, IL-6 and TNF-α in MSG.

Results: Compared with the control group, the mice in PPAR-γ group showed that: ‡@histopathological change was significantly ameliorated; ‡Aat the age of 17 weeks, IL-6 [(25.86±7.32) pg/ml vs(37.41±11.34) pg/ml] and TNF-α [(56.88±22.19) pg/ml vs (78.61±20.76) pg/ml] were expressed significantly lower and IL-4 [(25.76±12.65) pg/ml vs (12.11±3.70) pg/ml] was expressed significantly higher in serum (P<0.05); ‡Bthe expression of TNF-α was significantly decreased and the expression of IL-4 was significantly increased in MSG (P<0.05).

Conclusion: PPAR-γ can ameliorate Sjogren’s syndrome on NOD mice effectively. The mechanism may be related to reduce Th1 cytokines, and promote the direction of Th1/Th2 balance into Th2.


Disclosure:

B. Xu,
None;

X. Li,
None.

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