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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.


Lin Y.,Ningde Municipal Hospital | Lai X.,Fujian Medical University | Chen B.,Fujian Medical University | Xu Y.,Fujian Medical University | And 8 more authors.
Atherosclerosis | Year: 2011

Objectives: Two large-scale genome-wide association studies (GWAs) have identified multiple variants associated with blood pressure (BP) or hypertension. The present study was to investigate whether some variations were associated with BP traits and hypertension or even prehypertension in adult She ethnic minority of China. Methods: The population of the present study comprised 4460 (1979 males and 2481 females, respectively) unrelated she ethnic minority based on a cross-sectional study from Ningde City in Fujian province of China. There were 1692 hypertensives, 1600 prehypertensives and 1168 normotensive controls, respectively. We genotyped 7 variants in CYP17A1, PLEKHA7, CACNB2, ATP2B1, TBX3-TBX5, CSK-ULK3 and SH2B3 reported by the previous GWAs on Europeans. All analyses were performed in an additive genetic model. Results: As the minor allele of rs653178 in/near SH2B3 was very rare with the frequency of 0.018, we excluded this single nucleotide polymorphism (SNP) in the further analyses. Of the other 6 loci, linear regression analyses revealed that rs11191548 in CYP17A1 and rs11014166 in CACNB2 were significantly associated with systolic BP (β= -1.17, P= 0.002 and β= -0.50, P= 0.006, respectively), while only SNP rs11191548 was significantly associated with diastolic BP (β= -0.56, P= 0.002) after adjusted by age, sex and BMI. Two variants in CACNB2 and PLEKHA7 were found to be significantly related to hypertension (odds ratios [OR] and (95% confidence interval [CI]): 0.79 (0.65-0.97) and 1.19 (1.01-1.41), respectively) in logistic regression analyses after adjusted by age, sex and BMI. In addition, we found that combined risk alleles of the 6 SNPs increased risk of hypertension in a stepwise fashion (P for trend < 0.001). However, none of the 6 SNPs was significantly associated with BMI or prehypertension status. While logistic analysis showed that subjects with cumulative risk alleles more than 9 had significantly higher risk for prehypertension (adjusted OR: 3.10, P< 0.001) compared with those with risk alleles less than 4. Conclusions: We replicated that variations in CYP17A1, CACNB2 and PLEKHA7 were related to BP traits and/or hypertension in She population. In addition, although we failed to observe single gene associated with prehypertension, we first found that conjoint effect of multiple risk alleles on BP might increase the risk of progressing to prehypertension. © 2011 Elsevier Ireland Ltd.


Zheng X.,Xiamen University | Xia C.,Xiamen University | Chen Z.,Xiamen University | Chen Z.,Second Hospital of Xiamen | And 5 more authors.
Biochemical and Biophysical Research Communications | Year: 2012

Chondrocyte apoptosis is mainly responsible for the progressive degeneration of cartilage in osteoarthritis (OA). Interleukin-1beta (IL-1β) was widely used as a modulating and chondrocyte apoptosis-inducing agent. Nicotine is able to confer resistance to apoptosis and promote cell survival in some cell lines, but its regulatory mechanism is ambiguous. We aimed to investigate the effect of nicotine on IL-1β-induced chondrocyte apoptosis and the mechanism underlying how nicotine antagonizes IL-1β-induced apoptosis of rat chondrocytes. Chondrocytes isolated from newborn rat joints were exposed to IL-1β. The cell viability was analyzed by the MTT (3-(4,5-dimethylthiazol-2yl)-2,5-diphenyl tetrazolium bromide) assay, and the apoptotic cells were counted with DAPI staining. The levels of Akt, phosphorylated-Akt (p-Akt) and downstream protein targets of Akt were detected by western blotting. The results showed that nicotine neutralized the effect of IL-1β on chondrocytes by activating PI3K/Akt signaling pathways, including the PI3K/Akt/Bcl-2 pathway, to block IL-1β-induced cell apoptosis and the PI3K/Akt/p70S6K (p70S6 kinase)/S6 pathway for promoting protein synthesis, modulating its downstream effectors such as TIMP-1 and MMP-13. Activation of the PI3K/Akt pathway is, in part, required for the effect of nicotine on IL-1β-induced chondrocyte apoptosis in a rat model of osteoarthritis. © 2012 Elsevier Inc.


Lin Y.,Ningde Municipal Hospital | Lai X.,Fujian Medical University | Chen G.,Fujian Medical University | Xu Y.,Fujian Medical University | And 6 more authors.
Kidney and Blood Pressure Research | Year: 2012

Background: Little is known about the prevalence and cardiovascular risk factors for prehypertension and hypertension in the She ethnic minority population of Fujian province in China. Methods and Results: Between April 2009 and September 2009, 5,523 participants of She nationality aged between 20 and 80 years participated in this survey and 5,357 were eventually enrolled in analyses. The survey was carried out to assess blood pressure and cardiovascular risk factors. The prevalence of prehypertension and hypertension was 35.87 and 38.42%, respectively, in all participants. Only 26.63% of the subjects with hypertension were aware of their diagnosis. Multivariate logistic regression showed that age, gender, overweight/obesity, dyslipidemia and alcohol use were risk factors for prehypertension, and age, overweight/obesity, dyslipidemia, alcohol use, family history of hypertension and hyperuricemia were risk factors for hypertension. The clustering of 2 and ≥3 risk factors was in higher proportion for subjects with hypertension and prehypertension when compared with those with prehypertension and normotension, respectively. After adjusting for other confounding factors, multivariable logistic regression showed that the greater the number of clustering cardiovascular risk factors, the greater the odds ratios for prehypertension and hypertension are. Conclusion: Hypertension and prehypertension were common in the She population of Fujian province. Cardiovascular risk factors cluster during prehypertension and awareness of hypertension was minimal. Early lifestyle modifications could be advocated to prevent the transition from prehypertension to hypertension and cardiovascular disease. Copyright © 2012 S. Karger AG.


Zhu L.-X.,Ningde Municipal Hospital | Zhang H.-H.,Harbin Medical University | Mei Y.-F.,Harbin Medical University | Zhao Y.-P.,Harbin Medical University | Zhang Z.-Y.,Harbin Medical University
Chinese Medical Journal | Year: 2012

Tumor necrosis factor (TNF)-like weak inducer of apoptosis (TWEAK) is a member of the TNF superfamily of structurally related cytokines and is known to induce proliferation, migration, differentiation, apoptotic cell death, inflammation, and angiogenesis. These physiological processes are induced by the binding of TWEAK to fibroblast growth factor-inducible 14 (Fn14), a highly inducible cell-surface receptor that is linked to several intracellular signaling pathways, including the nuclear factor-κB (NF-κB) pathway. This review discusses the role of the TWEAK-Fn14 axis in several rheumatic diseases and the potential therapeutic benefits of modulation of the TWEAK-Fn14 pathway.


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 | Huang J.G.,Ningde Municipal Hospital | Xia C.,Xiamen University | Zheng X.P.,Xiamen University | And 4 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.


Liu M.,Southern Medical University | Liu M.,Ningde Municipal Hospital | Wu W.,Nanjing University | Li H.,Nanjing University | And 7 more authors.
Journal of Spinal Cord Medicine | Year: 2015

Background: Necroptosis is an emerging programmed necrosis other than traditional necrosis and apoptosis. Until recently, there have not been studies that have investigated a relationship between necroptosis and pathogenesis of cell death after spinal cord injury (SCI). Objective: To investigate whether necroptosis takes part in the early pathophysiological processes of traumatic SCI in mice. Methods: Female ICR mice were randomized equally into three groups: the sham, the vehicle-treated + SCI group, and the Nec-1-treated + SCI group. To induce SCI, the mice were subjected to a laminectomy at T9 and compression with a vascular clip. After mice were sacrificed 24 hours post-SCI, propidium iodide (PI)- positive cells were detected using in vivo PI labeling. Morphological analyses were performed by hematoxylin and eosin staining and Nissl staining. The samples were evaluated for apoptosis by the in situ TUNEL assay. The expression of caspase-3 was assessed by western blot. Locomotor behavior of hindlimb was evaluated by BMS (Basso mouse scale) score at 1, 3, 5, 7, and 14 days post-injury. Results: Compared with dimethyl sulfoxide -treated mice, necrostatin-1-treated mice showed decreased PIpositive cells (P < 0.05), alleviated tissue damage, more surviving neuron at 24 hours after SCI (P < 0.05), and improved functional recovery from days 7 to 14 (P < 0.05). Necrostatin-1 did not reduce the expression of caspase-3 and the number of TUNEL-positive cells at 24 hours after SCI (P > 0.05). Conclusions: Necroptosis contributes to necroptotic cell death and influences functional outcome after SCI in adult mice. The inhibition of necroptosis by necrostatin-1 may have therapeutic potential for patients with SCI. © 2015 The Academy of Spinal Cord Injury Professionals, Inc.


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.

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