Lin D.,Ningde Municipal Hospital |
Wu X.,Wenzhou Medical College |
Ji X.,Wenzhou Medical College |
Zhang Q.,Wenzhou Medical College |
And 7 more authors.
Cell Biochemistry and Biophysics | Year: 2012
Current large animal models that could closely resemble the typical features of cirrhotic portal hypertension in human have not been well established. Thus, we aimed to develop and describe a reliable and reproducible canine cirrhosis model of portal hypertension. A total of 30 mongrel dogs were randomly divided into four groups: 1 (control; n = 5), 2 (portal vein stenosis [PVS]; n = 5], 3 (thioacetamide [TAA]; n = 5), and 4 (PVS plus TAA; n = 15). After 4-months modeling period, liver and spleen CT perfusion, abdominal CT scans, portal hemodynamics, gastroscopy, hepatic function, blood routine, the bone marrow, liver, and spleen histology were studied. The animals in group 2 (PVS) developed extrahepatic portosystemic collateral circulation, particularly esophageal varices, without hepatic cirrhosis and portal hypertension. Animals from group 3 (TAA) presented mild cirrhosis and portal hypertension without significant symptoms of esophageal varices and hypersplenism. In contrast, animals from group 4 (PVS + TAA) showed well-developed micronodular and macronodular cirrhosis, associated with significant portal hypertension and hypersplenism. The combination of PVS and TAA represents a novel, reliable, and reproducible canine cirrhosis model of portal hypertension, which is associated with the typical characteristics of portal hypertension, including hypersplenism. © 2011 Springer Science+Business Media, LLC.
Huang L.-T.,Southern Medical University |
Li H.,Nanjing University |
Sun Q.,Soochow University of China |
Liu M.,Ningde Municipal Hospital |
And 5 more authors.
Cellular and Molecular Neurobiology | Year: 2015
Subarachnoid hemorrhage (SAH) is a pervasive and devastating condition in which inflammatory and apoptotic pathways contribute to poor outcome. Interleukin-33 (IL-33) plays a crucial role in the inflammatory and apoptotic pathways through binding of the transmembrane ST2 receptor. This study investigated the expression and cellular localization of IL-33 in the cerebral cortex after SAH in order to clarify the role of IL-33 after SAH. Sprague–Dawley rats were randomly divided into sham and SAH groups and evaluated 2, 6, and 12 h and 1, 2, 3, and 5 days after the surgery, with SAH animals subjected to prechiasmatic cistern SAH. IL-33 expression was measured by western blot analysis, real-time PCR, immunohistochemistry, and immunofluorescence. The mRNA levels of tumor necrosis factor (TNF)-α and IL-1β were also assessed. The expression of IL-33, IL-1β, and TNF-α was markedly elevated in the SAH as compared to the sham group; IL-33 was mainly localized in neurons and astrocytes and not microglia after SAH. Moreover, a significant positive association was observed between IL-33 and IL-1β expression. These findings indicate that IL-33 might play an important role in the inflammatory response following SAH. © 2014, Springer Science+Business Media New York.
Huang J.G.,Xiamen University |
Xia C.,Xiamen University |
Zheng X.P.,Xiamen University |
Yi T.T.,Xiamen University |
And 3 more authors.
Cellular and Molecular Biology Letters | Year: 2011
Osteoarthritis (OA) is the most common cause of musculoskeletal pain and disability. The importance of chondrocytes in the pathogenesis of OA is unequivocal. 17β-estradiol (E2) has a potential protective effect against OA. However, the mechanism of E2 in OA chondrocytes remains unclear. In this study, we investigated the regulative effect of E2 on cell growth and the relationship between E2 and the PI3K/Akt pathway in rat OA model chondrocytes (pretreated with interleukin-1β). We found that E2 induced chondrocyte proliferation, and increased the expression level of Akt simultaneously, especially the expression level of P-Akt. Furthermore, the inhibition of P-Akt could block chondrocyte proliferation induced by E2. These results suggest that PI3K/Akt activation induced by E2 may be an important factor in the mechanism of E2 in cell proliferation in rat OA model chondrocytes, and help further understanding the role of E2 in OA progression. © 2011 © Versita Warsaw and Springer-Verlag Wien.
Yang Y.-Q.,Nanjing University |
Li H.,Nanjing University |
Zhang X.,Shanghai University |
Wang C.-X.,Nanjing University |
And 8 more authors.
Cellular and Molecular Neurobiology | Year: 2015
Subarachnoid hemorrhage (SAH) is one of the life-threatening diseases with high morbidity and mortality rates. Small ubiquitin-like modifier (SUMO)-specific proteases 3 (SENP3), a member of the SUMO-specific protease family, was identified as an isopeptidase that deconjugates SUMOylation (The covalent modification by SUMO) of modified protein substrates. It is reported that SUMO-2/3 conjugation, a member of SUMOylation, presented neuroprotection. The study aimed to evaluate the expression of SENP3 and to explore its role potential role in SAH. A total of 95 Sprague–Dawley rats were randomly divided into sham group and SAH groups at 6, 12, 24, 48 h, day 3, day 5, and day 7. SAH groups suffered experimental SAH by injection with 0.3 ml nonheparinized autoblood into the prechiasmatic cistern. SENP3 expression is surveyed by western blot analysis, real-time polymerase chain reaction, immunohistochemistry, and immunofluorescence. The levels of cleavage caspase-3 were determined by western blot and immunohistochemistry. SENP3 protein expression was significantly up-regulated after SAH which peaked at 24 h; however, the mRNA expression of SENP3 remained unchanged. Meanwhile, the level of cleaved caspase-3 was also increased after SAH. There is a highly positive correlation between cleavage caspase-3 and SENP3 in protein level. Immunofluorescent results showed that the expression of SENP3 was increased in neurons, rather than astrocytes nor microglia. Our findings indicated a possible role of SENP3 in the pathogenesis of early brain injury mediated by apoptosis following SAH. © 2014, Springer Science+Business Media New York.
Chen G.,Fujian Medical University |
Wu J.,Fujian Medical University |
Lin Y.,Ningde Municipal Hospital |
Huang B.,Ningde Municipal Hospital |
And 4 more authors.
European Journal of Endocrinology | Year: 2010
Objective: To investigate the associations between cardiovascular risk, insulin resistance (IR), β-cell function and thyroid dysfunction in She ethnic minority group in China. Methods: We enrolled 5080 participants of She ethnicity in this analysis eventually. We measured serum TSH and thyroid peroxidase antibody (TPOAb) concentrations, blood glucose and insulin levels in both fasting and 2-h postprandial states, serum lipid levels, blood pressure (BP), brachial-ankle pulse wave velocity (baPWV), electrophysiological parameters, including Tpeak-Tend interval (T p-e), QT interval and height of the R wave in lead aVL (RaVL), and anthropometric parameters. Results: The total prevalence of thyroid dysfunction in this population is 12.1%. Hyperthyroid subjects had shorter Tp-e interval and QT interval in electrocardiogram (ECG), while hypothyroid subjects had shorter Tp-e interval and longer QT interval in ECG than euthyroid subjects. Neither hyperthyroid nor hypothyroid subjects showed significant difference in BP, pulse pressure, and baPWV compared with euthyroid subjects. RaVL was slightly higher in hyperthyroid subjects, though the difference did not reach statistical significance (P = 0.08). Subjects with TSH < 0.3 mIU/l had higher blood glucose, insulin, homeostasis model assessment of insulin resistance (HOMA-IR), and β-cell function (HOMA-β), whereas subjects with TSH > 10 mIU/l had lower insulin, HOMA-IR, and HOMA-β than the reference group. There was a significant negative correlation, albeit weak, between TSH and HOMA-IR, HOMA-β after adjustment for confounding factors. Conclusions: Hypothyroid subjects may carry higher cardiovascular risk than euthyroid subjects. Moreover, IR and β-cell function are inversely correlated with TSH, which may be explained by the decreasing insulin-antagonistic effects of thyroid hormones along with increasing TSH. © 2010 European Society of Endocrinology.