PPAR-γ and tollip are associated with toll-like receptors in colitis rats.

To elucidate the significance of Toll-like receptors and their negative regulating factors PPAR-γ and Tollip on the pathogenesis of colitis. Colitis model was induced by TNBS in rat. The expression of TLR2, TLR4, NF-κBp65, PPAR-γ and Tollip was examined by immunohistochemistry (IHC) and reverse-transcription polymerase chain reaction (RT-PCR). RT-PCR revealed a significant increased expression of TLR2, TLR4, and NF-κBp65 in the colitis group compared with the normal group (TLR2: 1.057 ± 0.092, 0.463 ± 0.101, t = 4.125, P = 0.001; TLR4: 0.376 ± 0.029, 0.215 ± 0.049, t = 2.731, P = 0.013; NF-κBp65: 0.746 ± 0.049, 0.206 ± 0.063, t = 6.055, P = 0.000). The expression was positively correlated with the generally damage score and the histological injury score correspondingly (TLR2: r = 0.573, r = 0.559; TLR4: r = 0.754, r = 0.866; NF-κBp65: r = 0.548, r = 0.919). The Tollip mRNA wasn't obviously diversity between the normal and colitis groups by RT-PCR (Tollip: 0.288 ± 0.050, 0.140 ± 0.046, t = 1.993, P = 0.061). While the Tollip protein was mainly assembled in the lamina propriaand higher in the colitis group compared with the normal group by IHC. The expression of PPAR-γ in the colitis group was obviously lower than that in the normal group (PPAR-γ: 0.255 ± 0.065, 0.568 ± 0.072, t = 2.882, P = 0.010). The expression of Tollip and PPAR-γ was negative correlated with the generally damage score and histological injury score correspondingly (Tollip: r = -0.497, r = -0.551; PPAR-γ: r = -0.683, r = -0.853). The disbalance between TLRs and their negative regulating factors PPAR-γ and Tollip was closely associated with the course of colitis.

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