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Shijiazhuang, China

Yaping Z.,Hebei Medical University | Ying W.,Hebei Provincial Peoples Hospital | Luqin D.,Hebei Medical University | Ning T.,Hebei Medical University | And 2 more authors.
APMIS | Year: 2014

Hepatic stellate cells (HSCs) are the major producers of collagen in the liver. Their conversion from resting cells to proliferative, contractile, and activated cells is a critical step leading to liver fibrosis that is characterized by the deposition of excessive extracellular matrix. Interleukin-1 (IL-1) may play a role in maintaining HSC in a proliferative state that is responsible for hepatic fibrogenesis. The aim of this study was to study the roles of the IL-1 type I receptor (IL-1R1), c-Jun N-terminal kinase (JNK), and activation protein-1 (AP-1) in IL-1β-mediated proliferation in rat HSCs. We showed that IL-1β can upregulate proliferation in rat HSCs; however, inhibition of the JNK pathway could inhibit HSCs proliferation. Furthermore, IL-1β activated IL-1R1 expression, the JNK signaling pathway, and AP-1 activity in a time-dependent manner in rat HSCs. These data demonstrate that IL-1β could promote the proliferation of rat HSCs and that the IL-1R1, JNK, and AP-1 pathways were involved in this process. In summary, IL-1β-induced proliferation is possibly mediated by the IL-1R1, JNK, and AP-1 pathways in rat HSCs. Therefore, drugs that block these pathways may inhibit the proliferation of HSCs and suppress liver fibrosis. © 2013 APMIS. Source


Zhang W.,Central China Normal University | Shen Y.,University of Toronto | Jiao R.,Hebei Provincial Peoples Hospital | Liu Y.,Central China Normal University | And 2 more authors.
Biochemical and Biophysical Research Communications | Year: 2012

Rab proteins are the largest family of ras-related GTPases in eukaryotic cells. They act as directional molecular switches at membrane trafficking, including vesicle budding, cargo sorting, transport, tethering, and fusion. Here, we generated and crystallized the Rab3B:GDP complex. The structure of the complex was solved to 1.9. å resolution and the structural base comparison with other Rab3 members provides a structural basis for the GDP/GTP switch in controlling the activity of small GTPase. The comparison of charge distribution among the members of Rab3 also indicates their different roles in vesicular trafficking. © 2012 Elsevier Inc. Source


Tang N.,Hebei Medical University | Zhang Y.-P.,Hebei Medical University | Ying W.,Hebei Provincial Peoples Hospital | Yao X.-X.,Hebei Medical University
Molecular Medicine Reports | Year: 2013

Matrix metalloproteinase-13 (MMP-13) is crucial in the cleavage and remodeling of the extracellular matrix (ECM), and its expression levels are decreased following the induction of liver fibrosis. The aim of the present study was to investigate the role of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) in interleukin (IL)-1β-mediated MMP-13 gene expression in rat hepatic stellate cells (HSCs). In the present study, we demonstrated that IL-1β is capable of activating JNK and p38 in a time-dependent manner and the inhibition of the JNK pathway is able to increase MMP-13 mRNA expression; however, the inhibition of the p38 MAPK pathway is capable of inhibiting MMP-13 gene expression. These data demonstrate that IL-1β is able to promote MMP-13 mRNA expression in rat HSCs and the JNK and p38 MAPK pathways were involved in this process. In summary, IL-1β-induced MMP-13 mRNA expression is possibly mediated by cytoplasmic JNK and p38 MAPK pathways, and they play a distinct role in this process. Thus, the JNK and p38 MAPK pathway co-operatively mediate MMP-13 mRNA expression in rat HSCs. Source


Zhou J.,Hebei Provincial Peoples Hospital
Zhongguo shi yan xue ye xue za zhi / Zhongguo bing li sheng li xue hui = Journal of experimental hematology / Chinese Association of Pathophysiology | Year: 2013

This study was aimed to explore the killing effect of PBMNC induced by IL-23 alone or combined with IL-2 on K562 cells and its mechanism. The PBMNC were induced in vitro by IL-23 (50 ng/ml) alone or IL-23 combined with IL-2 (100 U/ml) for 72 h, and then were co-cultured with leukemia cell line K562. The CCK-8 method was used to detect the effect of PBMNC induced at different times on K562 cells, the ELISA was performed for detecting IFN-γ level in culture supernatant, and the perforin and granzymes B were detected by RQ-PCR. The results showed that the killing effect of PBMNC induced by IL-23 alone or IL-23 combined with IL-2 on K562 cells was observed, and obviously enhanced with prolonging of time, moreover, there was statistical difference among different time points (P < 0.05). The IFN-γ level in supernatant of PBMNC cultured with cytokines significantly increased, and the IFN-γ levels in group of IL-23 combined with IL-2 were higher than that in other groups (P < 0.05). The mRNA expressions level of perforin and granzymes B of the expanded PBMNC in groups cultured with cytokines were higher than that in control group (P < 0.05), and the mRNA expressions of perforin and granzymes B in group of IL-23 combined with IL-2 were significantly higher than that in others (P < 0.05). It is concluded that IL-23 can promote the killing effect of PBMNC on K562 cells. The combination of IL-2 with IL-23 displays synergic effect and a time-dependent manner. IL-23 also enhances the expression of IFN-γ, perforin and granzyme B in PBMNC. Its combination with IL-2 displays synergistic effect, suggesting that the anti-leukemic activity of IL-23 may be realized through inducing PBMNC to express IFN-γ, perforin and granzyme B. Source


Li S.R.,Hebei Provincial Peoples Hospital
Zhongguo Zhong xi yi jie he za zhi Zhongguo Zhongxiyi jiehe zazhi = Chinese journal of integrated traditional and Western medicine / Zhongguo Zhong xi yi jie he xue hui, Zhongguo Zhong yi yan jiu yuan zhu ban | Year: 2012

To study the effects of Naoxintong Capsule (NC) on the inflammation and long-term prognosis in the borderline lesion coronary heart disease patients. A total of 240 coronary heart disease patients with angina symptoms and accompanied with borderline lesion coronary heart disease (with the diameter stenosis in critical 50% -70%) by means of coronary angiography or multislice computed tomography coronary angiography were recruited. These patients were randomly assigned to the conventional treatment group (including nitrate, beta blockers, anti-platelet, anticoagulation, angiotensin converting enzyme inhibitors, and so on) and the NC treatment group (treated the same way as those for the conventional treatment group and NC). All patients were treated for 12 months. The occurrence of cardiovascular events was observed after treatment. The inflammatory factors in serum [interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and high sensitive C reaction protein (hs-CRP)], matrix metalloproteinases-9 (MMP-9), blood lipids and blood sugar, liver and kidney functions were measured before and after treatment. After 12 months of treatment, the incidence of angina pectoris patients (6.67% vs 15.83%, P < 0.05) and hospitalization due to acute coronary syndrome (ACS) attacks (4.17% vs 10.83%) was significantly lower in the NC treatment group than in the conventional treatment group. There was no statistical difference in the serum levels of IL-6, TNF-alpha, hs-CRP, and MMP-9 between the two groups before treatment (P > 0.05). After 12 months of treatment, serum levels of IL-6, TNF-alpha, hs-CRP, and MMP-9 were significantly lower when compared with before treatment in the same group (P < 0.05). Besides, the serum levels of IL-6, TNF-alpha, hs-CRP, and MMP-9 were significantly lower in the NC group than in the conventional treatment group (P < 0.05). By means of Logistic regression analysis we found that the post-treatment MMP-9 level and IL-6 level were independent risk factors influencing the recurrence of angina pectoris. NC could alleviate the inflammation. Long-term administration of NC could reduce the recurrence of angina pectoris and decrease the incidence of ACS attack in borderline lesion coronary heart disease patients. The post-treatment MMP-9 level and IL-6 level were independent risk factors influencing the recurrence of angina pectoris. Source

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