Nie X.-H.,Tianjin Medical University |
Han T.,Tianjin Third Central Hospital |
Ha F.-U.,Tianjin Medical University |
Liang N.,Tianjin Medical University |
And 3 more authors.
European Review for Medical and Pharmacological Sciences | Year: 2014
OBJECTIVE: To compare the effects of the pretreatment and treatment with recombinant human interleukin-11 (rhIL-11) on acute liver failure induced by D-galactosamine (D-GalN). METHODS: The Sprague Dawley (SD) male rats were randomly divided into five groups: control, model, pretreatment, treatment and repeated treatment groups. The acute liver failure model was established by intraperitoneal injections with D-GalN (1400 mg/kg). The pretreatment, treatment and repeated treatment groups were injected subcutaneously with rhIL-11 (500 μg/kg). The rats were killed 24, 48, or 72 h after the D-GalN injection. The symptoms and survival rate of the rats were analysed. Liver injury was assessed by serum ALT and AST levels and by histological analysis. The percentage of Proliferating Cell Nuclear Antigen (PCNA+) cells in the liver tissue was evaluated by immunohistochemistry. RESULTS: Compared with the model group, the survival rate of the pretreatment group improved markedly, and these rats were protected from severe hepatic injury, as shown by the decreased serum ALT and AST levels and improved histological results. In the pretreatment group, the percentage of PCNA+ cells was significantly increased in the late stage. In contrast, the treatment and repeated treatment groups did not show improved survival rates or the prevention of severe hepatic injury, as shown by the absence of any decrease in the serum ALT and AST levels and the lack of any improvement in the histological results. The treatment and repeated treatment groups also have a significant increase in the percentage of PCNA+ cells in the late stage. CONCLUSIONS: The pretreatment with rhIL-11 can reduce acute liver failure and protect the liver. In contrast, the treatment with rhIL-11 cannot reduce acute liver failure or protect the liver.
Zhang X.,China Institute of Medical Equipment |
Li J.,China Institute of Medical Equipment |
Li J.,College of Logistics |
Wan Z.,China Institute of Medical Equipment |
And 8 more authors.
Annals of Biomedical Engineering | Year: 2013
Bone remodeling is strictly mediated by the coupled activities of osteoblasts and osteoclasts, which are responsible for bone formation and resorption, respectively. Although many papers have been published on the mechanical responses of osteoblasts and osteoclasts, little is known about their communication during mechanical loading. In this study, a novel co-culture system was first established using Transwell culture inserts; MC3T3-E1 cells were embedded in the lower compartment of the inserts, and RAW264.7 cells were co-cultured in the upper compartment. The MC3T3-E1 cells were subjected to a mechanical strain of 2500 με at 0.5 Hz to investigate the effect of strain-loaded osteoblasts on co-cultured osteoclasts. The results showed that osteoblast-like cells were activated with an increase of alkaline phosphatase (ALP) activities. The strain-conditioned medium caused decreased activity of tartrate-resistant acid phosphatase and reduced the number of mature multinucleated osteoclasts, which subsequently resulted in the suppressed formation of resorption pits. The expression levels of cathepsin-K and matrix metalloproteinase-9 were also depressed by the strain-conditioned medium. In addition, we found that the expression ratio between osteoprotegerin (OPG) and receptor activator of NF-kB ligand in osteoblasts was significantly up-regulated due to the enhanced levels of OPG. In summary, we conclude that the strain-stimulated osteoblasts inhibited the differentiation and bone resorption of osteoclasts and that the mechanism was associated with the increased secretion of OPG in osteoblasts. © 2013 Biomedical Engineering Society.
Mi Y.,Tianjin Medical University |
Gao Y.-T.,Key Laboratory of Artificial Cell |
Jiao X.-L.,Tianjin Medical University |
Du Z.,Key Laboratory of Artificial Cell
World Chinese Journal of Digestology | Year: 2013
AIM: To study the association between interleukin-28B (IL-28B) single nucleotide polymorphism (SNP) rs8099917 and susceptibility to hepatitis C virus (HCV) infection in Chinese patients. METHODS: The IL-28B rs8099917 locus was genotyped in 263 patients infected with HCV and 244 healthy controls using TaqMan SNP genotyping assay. The differences in rs8099917 genotypes and allele frequencies between the two groups were analyzed by statistics. RESULTS: Among 263 patients with chronic HCV, 223 (84.8%) had the TT genotype, 39 (14.8%) had the TG genotype, and 1 (0.40%) carried GG genotype. The frequency of T allele was 0.922. Of 244 healthy controls, the numbers of people who carried TT, TG and GG genotypes were 222 (91.0%), 21 (8.6%) and 1 (0.4%), respectively. T allele frequency was 0.953. TG/GG genotype frequencies differed significantly between patients with chronic HCV and healthy controls (OR = 1.810, 95% CI: 1.042-3.145; P = 0.033). Patients with HCV infection had a higher G allele frequency than healthy controls (OR = 1.709, 95% CI: 1.010-2.893; P = 0.044). CONCLUSION: The IL-28B rs8099917 gene polymorphism correlates with susceptibility to HCV infection in Chinese patient. G allele is associated with a higher risk of HCV infection. © 2013 Baishideng. All rights reserved.
Mi Y.,Key Laboratory of Artificial Cell |
Mi Y.,Zhengzhou University |
Gao Y.T.,Key Laboratory of Artificial Cell |
Jiao X.L.,Key Laboratory of Artificial Cell |
And 5 more authors.
Hepatitis Monthly | Year: 2014
Background: Interleukin-28B (IL28B) single nucleotide polymorphism (SNP) rs8099917 has been described to be associated with response to treatment with pegylated interferon and ribavirin (PEG-IFN/RBV) in patients with chronic hepatitis C from the North America, Europe, Asia countries like Japan and Taiwan. Whether this holds true for Chinese patients remains unknown. Objectives: We aimed to study the effects of IL28B rs8099917 on antiviral therapy responses in Chinese patients with hepatitis C. Patients and Methods: IL28B rs8099917 was genotyped in 263 patients with hepatitis C virus (HCV) infection and 244 healthy controls in Tianjin, China using TaqMan SNP genotyping method. The roles of rs8099917 and clinical characteristics in antiviral treatment were analyzed by logistic regression. Results: Among 263 patients with chronic HCV infection, 223 had a TT genotype (84.8%). Frequencies of TG/GG genotypes in patients with hepatitis C were significantly different from those of healthy controls (15.2% vs. 9.0%; P = 0.033). Patients with HCV infection had a higher G allele frequency than healthy controls (7.8% vs. 4.7%; P = 0.044). Univariate analysis revealed no significant association between rs8099917 and sustained virological response (SVR) (P = 0.612). However, it was found that HCV genotypes 2a/3a, age, prothrombin time (PT), albumin (ALB) and cholesterol (CHO) were associated with SVR. In multivariate analysis, only ALB was significantly an independent predictor of SVR (OR = 1.223; 95%CI: 1.046-1.430; P = 0.011). Conclusions: In contrast with T, rs8099917 G is a susceptible allele to HCV in China. ALB can independently predict SVR. Rs8099917 may play a quiet role to predict treatment response of patients with hepatitis C who received PEG-IFN/RBV therapy in China. © 2014, Kowsar Corp.; Published by Kowsar Corp.
Zhang S.-G.,Nankai University |
Song W.-Q.,Nankai University |
Gao Y.-T.,Key Laboratory of Artificial Cell |
Yang B.,Key Laboratory of Artificial Cell |
Du Z.,Key Laboratory of Artificial Cell
Molecular Biology Reports | Year: 2010
Genome copy number variation (CNV) is one of the mechanisms to regulate the expression level of genes which contributes to the development and progression of cancer. In order to investigate the regions of high-level amplification and potential target genes within these amplicons in hepatocellular carcinoma (HCC), we analyzed HCC cell line (TJ3ZX-01) for CNV regions at the whole genome level using GeneChip Human Mapping 500K array, and also examined the relative copy number and expression levels of the related genes at candidate amplicons in 41 HCC tissues via real-time fluorescence quantitative PCR methods. Through analysis of sequence tag site (STS) markers by quantitative PCR, The two candidate amplicons at 1q found by SNP array were shown to occur in 56.1% (23/41) HCC samples at 1q21 and 80.5% (33/41) at 1q22-23.1. Wilcoxon signed rank test showed expression of CD1d, which located at amplicon of 1q22-23.1 increased significantly within tumor tissues compared with paired nontumor tissues. Our study provides evidences that a novel, high-level amplicon at 1q22-23.1 occurs in both HCC cell line and tissues. CD1d is a potential target for this amplicon in HCC. The up-regulation of CD1d may be used as a novel molecular signature for diagnosis and prognosis of HCC. © 2009 Springer Science+Business Media B.V.