Objective To investigate the effect of taurine on colonic fibrosis in rats with colitis induced by 2,4,6-trinitrobenzene sulphonic acid(TNBS). Methods Thirty-two SD rats were divided into normal control group, model group, low-dose (400 mg/kg) taurine group and high-dose (800 mg/kg) taurine group. Rats in normal group were administrated with 0.9% NaCl solution enema, and the other three groups received TNBS enema. The rats in low-dose and high-dose taurine groups were administrated with 400 mg/kg and 800 mg/kg of taurine daily, respectively, one week before TNBS enema. Morphology and disease activity index (DAI) were evaluated, and the colonic tissues were histologically examined. Colon length and weight of the rats were also measured. The concentrations of hydroxyproline, collagen type Ⅰ, transforming growth factor-betal(TGF-β1), and Smad3 protein and mRNA in colon tissues were tested. Results In comparison with control group, the body weight and colon length were decreased while DAI score and colon weight were increased obviously in model group (P`0.01). All above parameters were improved after intervention of taurine. The fibrotie score in model group (1.88±0.35) was significantly higher than that in control group (0.25±0.46), low-dose (1.25±0.71) and high-dose (0.75±0.47) taurine groups (all P values <0.05). High levels of hydroxyproline, collagen type Ⅰ, TGF-β1 and Smad3 were detected in model group compared with low-dose and high-dose taurine groups (all P values < 0.05). Conclusions Taurine is effective in prevention of colonic fibrosis induced by TNBS in rats, which is mediated by the down regulation of TGF-β1 and the inhibition of TGF-β/ Smad3 pathway. It may be beneficial in treatment of Crohn's disease with colonic fibrosis and strictures.

Objective Benign childhood epilepsy with centrotemporal spikes (BECT) is the most common partial epilepsy syndrome in children, and responds well to carbamazepine (CBZ), oxcarbazepine (OXC), and valproic acid (VPA). The aim of this study is to investigate the therapeutic effect of OXC on BECT. Methods We retrospectively discussed a case of partial epilepsy in a 6-year-old boy with no abnormality on neuroradiologic examination. Results The patient′s seizures were easily controlled by administration of OXC, but electroencephalography (EEG) identified deterioration of the EEG features following the introduction of OXC monotherapy. Then OXC was gradually decreased in dose and substituted with VPA. When VPA was increased to the dose of 0.5g/d, the boy had no more seizures and exhibited normal EEG in the conscious state. Conclusion OXC may induce new types of seizure and aggravate EEG features although it is considered to be the first-line anti-epileptic drug (AED) and much better tolerated than either phenytoin or CBZ.

Objective To estimate the effect and the intracellular signal transduction pathway of insulin-like growth factor I (IGF-I) on the expression of stem cell factor(SCF) in colonic smooth-muscle cells(SMC). Methods The SMCs isolated from colon of the SD rats by enzymolysis were cultured and identified by α-actin immunocytochemical method. Colonic SMCs were cultured either with 100 μg/L of IGF-I at different time points (0, 8, 16, 24 and 48 hours) or with different concentrations (0,5,10,50,100 and 150 μg/L) of IGF-I for 16 hours. The expressions of SCF in colonic SMCs pretreated with or without speicific phosphatidylinositol 3-kinase (PI 3-kinase) inhibitor LY-294002 or mitogen-activated protein (MAP) kinase (MEK1) inhibitor PD-98059 were examined by Western blotting and quantitative reverse transeription-polymerase chain reaction and immunofluorescence. Results Low expression of SCF was found in colonic SMCs cultured in the bovine serum free medium. There was no effect of 5 or 10 μg/L of IGF- I on the expression of SCF. However, the expressions of SCF mRNA and protein were increased when stimulated with high concentrations (50,100,150 μg/L) of IGF-I. The peak expression of SCF was showed at the 16th hour after stimulating with 100 μg/L of IGF- I that was considered as the most effective concentration in vitro. The expression of SCF was not influenced by LY-294002, but was partly blocked by PD-98059. Conclusions The expression of SCF in colon SMCs may be induced by IGF-Ⅰ through MAP kinase signaling pathway.