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Objective To examine the effectiveness of HGF in blocking TGF-β1 induced α-SMA and extracellular matrix production in fibroblasts of the flexor tendon sheath. Methods Seven adult male New Zealand white rabbits (3.75-4.00 kg) were used for this study. Both of their front feet were sterilised and the middle digit flexor digitorum profundus tendon equivalents were identified and isolated. These specimens were used to establish primary cell cultures. Sheath fibroblasts were obtained from rabbit flexor tendons. After the cells reached confluence, cells were detached with trypsin/ethylenediamine tetra-acetic acid. All experiments were performed using the cells at the third passage. At 70% confluence the medium was supplemented with 5 ng/ml of TGF-β1 along with increasing doses of HGF (10-40 ng/ml). After 72 hours incubation, the productions of α-SMA were assayed by Western-Blot. The productions of collagen Ⅰ and fibronectin in supernatants culture were examined using ELISA. Results Evaluation of protein expression revealed that TGF-β1 markedly induced α-SMA expression in cultured rabbit flexor tendon sheath fibroblasts. TGF-β1 treated fibroblasts expressed 1.8-fold more protein compared to non-treated fibroblasts (P ＜ 0.05). However, simultaneous incubation of HGF significantly abrogated TGF-β1 induced α-SMA expression in a dose-dependent manner (P＜ 0.05). Treatment with TGF-β1 significantly stimulated collagen Ⅰ and fibronectin production in flexor tendon sheath fibroblasts (P ＜ 0.01). Remarkably, the addition of HGF reduced productions of all components induced by TGF-β1 in a dose-dependent manner (P ＜ 0.05). Conclusion HGF antagonizes TGF-β1 induced α-SMA, collagen Ⅰ, and fibronectin production in flexor tendon sheath fibroblasts. The findings provide a cellular and molecular basis for HGF's acting as a therapeutic agent for adhesions in flexor tendons.
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Objective To explore clinical characteristics of the digestive tract obstruction due to annular pancreas. Methods We reviewed retrospectively clinical features, operative findings and the autopsy of 5 children with annular pancreas. Results Neonate patients usually present complete upper gastro intestinal obstruction because most of them were complicated with duodenal atresia. Infants present chronic incomplete intestinal obstruction duo to annular pancreas. 35.8% of duodenal constriction was caused by annular pancreas. Conclusions All the symptomatic patients with annular pancreas should undergo exploration to restore the consecution of the digestive tract and to detect if there is a concurrent malformation such as intestinal atresia.
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Objective To establish the animal model of periventricular leukomalacia (PVL) caused by lipopolysaccharide (LPS) and investigate the immune mechanisms in the pathogenesis of cerebral palsy due to intrauterine infection. Methods Twenty-six mature pregnant Wistar rats were divided into experiment(n= 15)and control groups(n =11). LPS(0. 3 mg/kg) and distilled water were injected on 15 days of gestation to two groups respectively intraperitoneally. One hundred and twenty-eight neonatal rats of experiment group and 105 in the control group were obtained till the gestation day of 21. The level of IL-2, TNF-? and histology changes in neonatal rats' brain were observed by HE staining and RIA, water content in brain tissues were compared. Results IL-2[(3. 56?0. 450) ng/g] and TNF-? concentrations [(8. 23?0. 47)ng/g] in neonatal rats' brain of the experiment group were significantly higher than those in the control group [(0. 78?0. 2)ng/g and (5. 23?0. 32)ng/g, P