Expression and function of vascular endothelial growth factor and angiopoietins in rat brain after cerebral ischemia / 中华病理学杂志

<p><b>OBJECTIVE</b>To examine the temporal and spatial expression of vascular endothelial growth factor (VEGF) and angiopoietins (Ang) in rat brain after cerebral ischemia, and to elucidate the roles they played in angiogenesis and vascular permeability.</p><p><b>METHODS</b>Rats were subjected to either middle cerebral artery occlusion (MCAO) or sham operation. Reverse transcriptase-polymerase chain reaction, Western blotting, and immunohistochemistry were used to detect the expression of VEGF, Ang-1 and Ang-2 at different time points after ischemia. CD31 was used to label endothelial cells after MCAO. Vascular permeability was determined by Evans blue.</p><p><b>RESULTS</b>VEGF was markedly increased at 2 h, had an initial peak at 12 h (0.7249 ± 0.1933, P < 0.01), and a second peak at 7 days (0.5264 ± 0.1519, P < 0.01). Ang-2 mRNA and protein significantly increased after MCAO, both of them peaked at 12 h (0.6747 ± 0.2416, P < 0.01; 1.1197 ± 0.1780, P < 0.01). In contrast, Ang-1 mRNA and protein gradually decreased after MCAO, respectively reaching a minimum at 3 d (0.3220 ± 0.1427, P < 0.01) and 1 d (0.1298 ± 0.0293, P < 0.01). Changes in the expression of these factors correlated with the progress of angiogenesis and vascular permeability. Evans blue test revealed that the vascular permeability gradually increased, and peaked at day 1 after ischemia [(6.219 ± 0.887) µg/g, P < 0.01].</p><p><b>CONCLUSION</b>Dynamic temporal changes in VEGF, Ang-1 and Ang-2 expression stimulate the cerebral angiogenesis after focal cerebral ischemia.</p>

Expression of thrombin and its associated protein in cerebellum of human and rat after intracerebral hemorrhage / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Intracerebral hemorrhage (ICH) can cause brain damage through a number of pathways. The purpose of the study was to explore the effect of thrombin, protease nexin-1 (PN-1) and protease activated receptor-1 (PAR-1) in rat and human cerebellum after ICH.</p><p><b>METHODS</b>A model of ICH was produced in adult Sprague-Dawley rats by direct injection of autologous blood (50 microl) into caudate nucleus. Patients with injured hemorrhage were also enrolled in this study. Different expressions of thrombin, PAR-1, PN-1 were detected in rat and human cerebellum by immunohistochemistry and in situ hybridization.</p><p><b>RESULTS</b>In rat cerebellum, thrombin protein significantly increased at 6 hours and reached the maximum 2 days after ICH. The expression of PAR-1 protein reached the maximum at 24 - 48 hours, and then began to decrease. The expression of PN-1 protein reached the maximum at 3 hours, decreased somewhat after that and increased a little at 5 days after ICH. While in human cerebellum, the changing tendency of thrombin, PAR-1 and PN-1 was almost conform to the rat.</p><p><b>CONCLUSION</b>In cerebellum, thrombin can activate PAR-1 expression after ICH, and PN-1 appears quickly after ICH in order to control the deleterious effect of thrombin.</p>

Hyalinizing trabecular tumor and papillary carcinoma of the thyroid / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Hyalinizing trabecular tumor (HTT) is a rare thyroid neoplasm, which shares some histologic features with thyroid papillary carcinoma (TPC). Clinically, it is frequently misdiagnosed as papillary carcinoma, even for some experienced pathologists. The aim of this study was to investigate whether HTT is variant of TPC or HTT is an independent entity of thyroid neoplasm.</p><p><b>METHODS</b>The expression of CK19, galectin-3, HBME-1 and MIB-1 was detected by immunohistochemical staining in 12 cases of hyalinizing trabecular tumor and 20 cases of thyroid papillary carcinoma.</p><p><b>RESULTS</b>Two of the 12 HTT samples were positive or focally positive for CK19. Four of the 12 samples of HTT presented positive to galectin-3; 3 were stained strongly and the other one was focally positive. None of the 12 samples of HTT was positive for HBME-1. Five in 12 HTT samples were stained in nucleus for MIB-1. Almost all the 20 cases of thyroid papillary carcinoma were intensely stained for CK19, galectin-3 and HBME-1. Fifteen in 20 cases of thyroid papillary carcinoma showed nuclear staining for MIB-1.</p><p><b>CONCLUSIONS</b>HTT is an independent thyroid neoplasm, not a variant of TPC. This study could help in the differential diagnosis of HTT from TPC. CK19, galectin-3 and HBME-1 are adequate to identify HTT and TPC, but MIB-1 does not play an important role in discrimination between HTT and TPC.</p>

Effect of mtrine on Fas expression in C6 glioma in rats / 中华神经医学杂志

Objective To investigate the effect of matrine on Fas expression in C6 glima in a tumor-bearing rat model. Methods Cultured cerebral glioma C6 cells wgre injected stereotactically into the lef tcaudate nucleus of the rats.The ratswere randomized into untreated group,bomeol-treated group,low-dose matrine group,high-dose maaine group,low-dose matrine+bomeol group,and high-dose matrine+borneol group.The effect of matrine on the quality of life of the rats and the glioma volume was evaluated according to the survival state of the rats and by gross observation,magnetic resonance imaging(MRJ)and HE smining of the brain tissue.Immunohistochemistry was performed to detect Fas expression in the glioma cells. Results The survival state ofthe rats,gross observation of the brain specimen. and results of MRI and HE staining all showed that matrine significantly improved the quality oflife of the glioma-bearing rats and inhibited the glioma cell proliferation.Fas expression Was significantly higher in low-dose matrine+bomeol group(98.16±11.82) and high-dose matrine+bomeol group(112.80±12.12)than in untreated group(39.09±7.79),bomeol group(46.87±7.43),low-dose matrinc group(42.41±7.83),and high-dose matrine group(44.20±7.47)(P＜0.05).Fas expression Was obviously upregulated in the high-dose matrine+bomeol group aS compared with the low-dose matrine+bomeol group(P＜0.05).Conclusion Matrine Can significantly upregulate Fas expression in glioma and inhibit glioma cell proliferation in the glioma-bearing rat model.