Jiao Liu

Binzhou Medical University, Pei-chen, Shandong Sheng, China

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Publications (2)1.45 Total impact

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    ABSTRACT: 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.
    Journal of Immunoassay and Immunochemistry 07/2013; 34(3):219-31. · 0.73 Impact Factor
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    ABSTRACT: This study elucidates the significance of Toll-like receptor 4 (TLR4), CD14, and nuclear factor (NF)-κB on the pathogenesis of ulcerative colitis (UC). Colonic biopsy specimens were collected from active UC and controls. The expression of TLR4, CD14, and NF-κBp 65 was analyzed by immunohistochemistry (IHC) and reverse-transcription polymerase chain reaction (RT-PCR). In UC, disease activity index (DAI) and pathological grade were classified according to the Powell-Tuck grade system and Truelove-Richards system, respectively. Fifty-six UC cases and 56 controls entered the investigation. IHC and RT-PCR revealed a significant increase of TLR4, CD14, and NF-κBp 65 antigen expression in colonic mucosa of UC compared with colonic mucosa of controls (p < .001). In UC, TLR4, CD14, and NF-κBp 65 expression were positively related to DAI (r = .873, p < .001; r = .576, p < .001; r = .747, p < .001 receptively). NF-κBp65 significantly correlated with TLR4 and CD14 (r = .669, p < .001; r = .576, p < .001, receptively). TLR4, CD14, and NF-κBp65 were positively related to pathological classification in UC (p < .01). Thus, TLR4, CD14, and NF-κBp65 were upregulated significantly in UC, to an extent that reflects the degree of inflammation and thereby might contribute to the occurrence and development of UC.
    Journal of Immunoassay and Immunochemistry 01/2011; 32(1):47-56. · 0.73 Impact Factor