ABSTRACT
Objective:To investigate the neuroprotective effect of minocycline on the secondary injury after acute closed spinal cord injury in rats. Methods:A total of 24 Sprague-Dawley male rats were randomly divided into saline group (n = 8), magnesium chloride group (n = 8) and minocycline group (n = 8). The closed spinal cord injury model was prepared with balloon compression in the dorsal spinal cord of rat, which was evaluated with magnetic resonance imaging. All rats were successively administered their own drugs for seven days after injury, respectively. They were assessed with BBB score two to 31 days after operation. Their motor-evoked potential and sensory-evoked potential were detected 31 days after operation, and then Luxol Fast Blue was used to observe the area of secondary injury. Results:Animal magnetic resonance imaging showed hypointense in T2 images in T10 spinal cord. BBB score was more in the minocycline group than in the saline group since 17 days after operation (P < 0.05). The amplitude of motor-evoked potential was higher in the minocycline group than in the saline group (P < 0.05), while the area of secondary injury was less (P < 0.05). Conclusion:Minocycline may protect the nerves from secondary injury after acute spinal cord injury.
ABSTRACT
<p><b>BACKGROUND</b>Decoy receptor 3 (DcR3) is a protein with anti-apoptotic effect that belongs to the tumor necrosis factor receptor superfamily. DcR3 is highly expressed in a variety of malignant tumors including cholangiocarcinoma and its expression was found to be related to the clinical stage, the invasion, and the metastasis of the tumor. This in vitro study aimed to investigate the effect of downregulated expression of DcR3 on cell viability, cell apoptosis, and cell cycle in cholangiocarcinoma cell line TFK-1.</p><p><b>METHODS</b>Three different cell lines were cultured: human cholangiocarcinoma TFK-1, human biliary epithelial carcinoma HuCCT-1, and human cholangiocarcinoma RBE. The cholangiocarcinoma cell line with the highest expression of DcR3 was selected for further investigation. The expression of DcR3 was silenced/knocked down by transfection with DcR3-siRNA in the selected cell line. Various biological phenotype parameters such as cell viability, apoptosis, and cell cycle were observed.</p><p><b>RESULTS</b>The mRNA and protein levels of DcR3 were measured in the three cell lines, and TFK-1 was selected. After the treatment with DcR3-siRNA for 48 h, DcR3 mRNA and protein expression in the treatment group were 38.45% (P < 0.01) and 48.03% (P < 0.05) of that of the control, respectively. It was found that the cell viability decreased to 61.87% of the control group (P < 0.01) after the downregulation of DcR3 in cholangiocarcinoma cell line TFK-1 by transfection with DcR3-siRNA, while the percentage of apoptotic cells was 2.98 times as compared with the control group (P < 0.05). Compared with the control group the ratio of G0/G1increased, and the ratio of G2/M decreased in the treatment group. However, the differences were not statistically significant.</p><p><b>CONCLUSIONS</b>The effect of DcR3 on the growth and apoptosis of cholangiocarcinoma has been demonstrated. DcR3 is not only a predictive marker for malignant tumor but it is also likely to be a potential target for cancer gene therapy. Further studies should focus on exploring the binding ligand of DcR3, the signaling pathway involved, and the molecular mechanism for the regulation of DcR3 expression in cholangiocarcinoma.</p>