Xiaomei Li1, Bei Xu2, Yiping Wang3, Li Wei4. 1. Department of Rheumatology and Immunology, Anhui Medical University Affiliated Provincial Hospital Hefei, Anhui Province, P.R. China. 2. Department of Rheumatology and Immunology, The Third Affiliated Hospital of Anhui Medical University and The First People's Hospital of Hefei Hefei, Anhui Province, P.R. China. 3. Centre for Transplant and Renal Research, Westmead Millennium Institute, University of Sydney Sydney, New South Wales, Australia. 4. Medicines Monitoring Unit, Division of Medical Sciences, University of Dundee UK DD1 9SY.
Abstract
OBJECTIVE: To investigate the anti-inflammatory effect of peroxisome proliferator-activated receptor-γ (PPAR-γ) on non-obese diabetic mice (NOD mice) with Sjogren's syndrome. METHODS: 22 eight-week-old female NOD mice were randomly divided into 2 groups. Rosiglitazone and normal saline were administered in the PPAR-γ group and the control group respectively. At the age of 9, 12 and 15 weeks, one mouse in each group was sacrificed respectively, and the remaining mice were sacrificed at the age of 18 weeks. Blood were obtained by cardiac puncture, and salivary glands were resected. The degree of salivary gland damage and infiltration of lymphocytes were examined by H&E staining. The level of IL-1β, IL-4, IL-6 and TNF-α in serum were measured by ELISA. The mRNA expression level of IL-1β, IL-4, IL-6 and TNF-α in MSG were detected by Real-time PCR. Expression of PPAR-γ in the salivary glands was detected by Immunohistochemistry. RESULTS: Compared with the control group, mice in the PPAR-γ group showed that (1) histopathologic changes in the salivary glands were significantly ameliorated; (2) at the age of 18 weeks, IL-6 [(25.86 ± 7.32) vs (37.41 ± 11.34)] and TNF-α [(56.88 ± 22.19) vs (78.61 ± 20.76)] were expressed significantly lower and IL-4 [(25.76 ± 12.65) vs (12.11 ± 3.70)] was expressed significantly higher in serum (P < 0.05); (3) the expression of TNF-α was significantly decreased and the expression of IL-4 was significantly increased in MSG (P < 0.05). CONCLUSION: PPAR-γ ameliorates Sjogren's syndrome on NOD mice effectively. The mechanism may be related to the reduction of Th1 cytokines and change of T helper cell balance from Th1 to Th2.
OBJECTIVE: To investigate the anti-inflammatory effect of peroxisome proliferator-activated receptor-γ (PPAR-γ) on non-obese diabeticmice (NOD mice) with Sjogren's syndrome. METHODS: 22 eight-week-old female NOD mice were randomly divided into 2 groups. Rosiglitazone and normal saline were administered in the PPAR-γ group and the control group respectively. At the age of 9, 12 and 15 weeks, one mouse in each group was sacrificed respectively, and the remaining mice were sacrificed at the age of 18 weeks. Blood were obtained by cardiac puncture, and salivary glands were resected. The degree of salivary gland damage and infiltration of lymphocytes were examined by H&E staining. The level of IL-1β, IL-4, IL-6 and TNF-α in serum were measured by ELISA. The mRNA expression level of IL-1β, IL-4, IL-6 and TNF-α in MSG were detected by Real-time PCR. Expression of PPAR-γ in the salivary glands was detected by Immunohistochemistry. RESULTS: Compared with the control group, mice in the PPAR-γ group showed that (1) histopathologic changes in the salivary glands were significantly ameliorated; (2) at the age of 18 weeks, IL-6 [(25.86 ± 7.32) vs (37.41 ± 11.34)] and TNF-α [(56.88 ± 22.19) vs (78.61 ± 20.76)] were expressed significantly lower and IL-4 [(25.76 ± 12.65) vs (12.11 ± 3.70)] was expressed significantly higher in serum (P < 0.05); (3) the expression of TNF-α was significantly decreased and the expression of IL-4 was significantly increased in MSG (P < 0.05). CONCLUSION: PPAR-γ ameliorates Sjogren's syndrome on NOD mice effectively. The mechanism may be related to the reduction of Th1 cytokines and change of T helper cell balance from Th1 to Th2.
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