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Shijiazhuang, China

Hebei Medical University is a university in Shijiazhuang, Hebei, People's Republic of China,under the provincial government.... a capital city of Hebei Province which is 4 hours away from Beijing by car and 1 and a half hours by train, Hebei Medical University Established in 1894, it is one of the oldest and AAA graded medical schools in China. Wikipedia.

Aims: Chemerin is a novel adipokine that is closely associated with cardiovascular diseases and glucose homeostasis. This study aimed to investigate the effects of chemerin on insulin resistance in rat cardiomyocytes. Methods: Rat cardiomyocytes were treated with high concentrations of glucose and tumor necrosis factor-alpha (TNF-α), and chemerin and chemokine-like receptor 1 (CMKLR1) were measured by Western blot analysis. Then, the cardiomyocytes were treated with chemerin and insulin. Glucose uptake was evaluated using a fluorescence microplate reader. Western blot analysis was used to evaluate the phosphorylation of Akt, insulin receptor substrate-1, p38 mitogen-activated protein kinase (MAPK), as well as extracellular signal-regulated kinase (ERK)1/2. Results: Chemerin and CMKLR1 were found to be expressed in rat cardiomyocytes. Pretreatment with chemerin caused decreases in glucose uptake and phosphorylation of Akt in insulin-stimulated cardiomyocytes. Furthermore, chemerin activated the phosphorylation of p38 MAPK and ERK1/2 in insulin-stimulated cardiomyocytes. Inhibition of ERK partially rescued chemerin-induced insulin resistance. Conclusion: Chemerin is a novel adipokine that induces insulin resistance in rat cardiomyocytes in part through the ERK1/2 pathway. © 2014 S. Karger AG, Basel Copyright © 2014, S. Karger AG. All rights reserved.

Ma Y.,Hebei Medical University
American Journal of Therapeutics | Year: 2014

Overwhelming clinical and epidemiological studies have identified elevated plasma total homocysteine (Hcy) as new important risk factor for atherosclerotic vascular disease. But the relationship between outcome and hyperhomocysteinemia in patients with acute myocardial infarction (AMI) has been rarely reported. This study aimed to evaluate the association between hyperhomocysteinemia and short-term outcomes of patients with AMI. Eight hundred five patients were divided into high Hcy level group (group H: N = 457) and low Hcy level group (group L: N = 348) according to the plasma Hcy levels of 15 mmol/L. The comparisons were made between 2 groups in the following aspects: sex, hypertension, diabetes, hyperlipidemia, the time for symptom from onset to percutaneous coronary intervention, homoccyteine, creatine phosphokinase isoenzyme (creatine kinase myocardial band), and the incidence of 30-day adverse events. The incidences of heart failure, cardiac rupture, death, and the total adverse cardiovascular events were statistically significantly higher in group H than in group L. But the incidence of postoperative angina pectoris and reinfarction was similar between groups. The results of logistic regression showed that the incidence of 30-day adverse events was closely related to the age and the level of Hcy. An elevated plasma total Hcy level in patients with AMI experienced pemutaneous coronary intervention may be related to the short-term outcomes. An elevated high plasma Hcy level also seems to be an independent predictor of 30-day cardiovascular events in patients with AMI. © 2014 by Lippincott Williams & Wilkins.

Jia J.,Hebei Medical University
Investigative ophthalmology & visual science | Year: 2013

To explore the regulation of inducible nitric oxide synthase (iNOS) expression by nuclear factor kappa B (NF-κB) in human lens epithelial cells (LECs) treated with high levels of glucose, and to elucidate the impact of this in the pathogenesis of cataracts associated with diabetes. LECs (SRA01/04) were cultured in vitro. NF-κB nuclear translocation and iNOS expression were measured at different glucose concentrations and at various time points, and the optimal concentration for detecting changes in the patterns of NF-κB nuclear translocation and iNOS expression was chosen. As a specific NF-κB inhibitor, pyrrolidine dithiocarbamate (PDTC) was used to assess the effect of inhibiting NF-κB. Western blotting and inverted fluorescence microscopy were used to monitor the nuclear translocation of NF-κB. PCR and Western blotting were used to measure iNOS expression. Using the University of California, Santa Cruz database and the TFSEARCH program, we searched the DNA sequence upstream of iNOS for the core binding sequence for NF-κB. Chromatin immunoprecipitation (ChIP) was used to measure the binding of NF-κB. The nuclear translocation of NF-κB was measured upon glucose treatment, and the concentration of NF-κB in the nucleus was found to peak at 25 to 30 minutes of treatment with 25 mM glucose. iNOS mRNA and protein levels also increased significantly in a time- and concentration-dependent manner and iNOS mRNA and protein reached their peak values after 8 hours of treatment with 25 mM glucose. The binding of NF-κB to the promoter of the iNOS gene was enhanced in the 25 mM glucose group compared with the 5.5 mM glucose group or the 25 mM glucose + 100 μL PDTC group, and this difference was statistically significant (P < 0.05). NF-κB regulates iNOS expression in a time- and concentration-dependent manner. Under high glucose conditions, NF-κB is activated and rapidly translocates to the nucleus, leading to increased binding to the iNOS promoter and a consequent increase in iNOS expression. The findings of this study provide important experimental evidence that clarifies the pathogenesis of cataracts associated with diabetes and contributes to the search for therapeutic targets of these cataracts.

Liu C.,Hebei Medical University
Cochrane database of systematic reviews (Online) | Year: 2013

Pulmonary arterial hypertension is a devastating disease, which leads to right heart failure and premature death. Recent evidence suggests that endothelin receptor antagonists may be promising drugs in the treatment of pulmonary arterial hypertension. To evaluate the efficacy of endothelin receptor antagonists in pulmonary arterial hypertension. We searched CENTRAL (Cochrane Central Register of Controlled Trials), MEDLINE, EMBASE, and the reference section of retrieved articles. Searches are current as of January 2012. We included randomised trials (RCTs) and quasi-randomised trials involving patients with pulmonary arterial hypertension. Five review authors independently selected studies, assessed study quality and extracted data. We included 12 randomised controlled trials involving 1471 patients. All the trials were of relatively short duration (12 weeks to six months). After treatment, patients treated with endothelin receptor antagonists could walk on average 33.71 metres (95% confidence interval (CI) 24.90 to 42.52 metres) further than those treated with placebo in a six-minute walk test. Endothelin receptor antagonists improved more patients' World Health Organization/New York Heart Association (WHO/NYHA) functional class status than placebo (odds ratio (OR) 1.60; 95% CI 1.20 to 2.14), and reduced the odds of functional class deterioration compared with placebo (OR 0.26; 95% CI 0.16 to 0.42). There was a reduction in mortality that did not reach statistical significance on endothelin receptor antagonists (OR 0.57; 95% CI 0.26 to 1.24), and limited data suggest that endothelin receptor antagonists improve the Borg dyspnoea score and cardiopulmonary haemodynamics in symptomatic patients. Hepatic toxicity was not common, and endothelin receptor antagonists were well tolerated in this population. However, several cases of irreversible liver failure caused by sitaxsentan have been reported that led to license holder for sitaxsentan to withdraw the product from all markets worldwide. Endothelin receptor antagonists can increase exercise capacity, improve WHO/NYHA functional class, prevent WHO/NYHA functional class deterioration, reduce dyspnoea and improve cardiopulmonary haemodynamic variables in patients with pulmonary arterial hypertension with WHO/NYHA functional class II and III. However, there was only a trend towards endothelin receptor antagonists reducing mortality in patients with pulmonary arterial hypertension. Efficacy data are strongest in those with idiopathic pulmonary hypertension. The irreversible liver failure caused by sitaxsentan and its withdrawal from global markets emphasise the importance of hepatic monitoring in patients treated with endothelin receptor antagonists.

Previous reports indicate a potential role for calcitonin (CT) in the treatment of osteoarthritis (OA). To evaluate this potential therapeutic role, we investigated the effect of CT pretreatment on the activation of mitogen-activated protein kinase (MAPK) signaling and the expression of matrix metalloproteinase-13 (MMP-13) in interleukin-1β (IL-1β)-induced chondrocytes, and further assessed its protective effect in a rat model of anterior cruciate ligament transection (ACLT), using sham-operated and saline-treated controls. Using western blotting in vitro, we found that CT pretreatment inhibited the IL-1β-induced phosphorylation of 38,000-dalton protein (p38) and extracellular regulated protein 1/2 (ERK1/2) and reduced the expression of MMP-13 protein. For the in vivo experiment, 30 male rats were randomly divided into three groups of 10, subjected to bilateral ACLT or sham surgery, and then treated for 12 weeks with subcutaneous injections of CT or normal saline. Histological observations showed that CT treatment reduced the severity of the cartilage lesions stemming from the ACLT surgery and provided a lower Mankin score when compared with that determined for rats in the saline-treated ACLT group. Immunohistochemical staining revealed that CT treatment increased type II collagen expression and decreased MMP-3 and a disintegrin and metalloproteinase with thrombospondin motifs-4 (ADAMTS-4) expression when compared with the saline-treated group. Subchondral bone analysis indicated that CT treatment inhibited the reduction in bone mineral density observed in the saline-treated ACLT group and reduced the ACLT-induced destruction to the subchondral trabecular microstructure. Our data demonstrate that CT induces its protective effects by reducing the chondrocyte response to inflammatory stimuli, cartilage extracellular matrix degradation, and subchondral trabecular microstructure damages brought on by OA.

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