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Handan, China

Zhu T.,Southern Medical University | Zhang W.,Chengdu Medical College | Feng S.-J.,Handan Central Hospital | Yu H.-P.,Southern Medical University
International Immunopharmacology | Year: 2016

Inflammation is a defense and protective response to multiple harmful stimuli. Over and uncontrolled inflammation can lead to local tissues or even systemic damages and injuries. Actually, uncontrolled and self-amplified inflammation is the fundament of the pathogenesis of a variety of inflammatory diseases, including sepsis shock, acute lung injury and acute respiratory distress syndrome (ALI/ARDS). Our recent study showed that emodin, the main active component of Radix rhizoma Rhei, could significantly ameliorate LPS-induced ALI/ARDS in mice. However, its underlying signal pathway was not still very clear. Then, the aim of current study was to explore whether emodin could attenuate LPS-induced inflammation in RAW264.7 cells, and its involved potential mechanism. The mRNA and protein expression of ICAM-1, MCP-1 and PPARγ were measured by qRCR and western blotting, the production of TNF-α was evaluated by ELISA. Then, the phosphorylation of NF-κB p65 was also detected by western blotting. And NF-κB p65 DNA binding activity was analyzed by ELISA as well. Meanwhile, siRNA-PPARγ transfection was performed to knockdown PPARγ expression in cells. Our data revealed that LPS-induced the up-regulation of ICAM-1, MCP-1 and TNF-α, LPS-induced the down-regulation of PPARγ, and LPS-enhanced NF-κB p65 activation and DNA binding activity were substantially suppressed by emdoin in RAW264.7 cells. Furthermore, our data also figured out that these effects of emdoin were largely abrogated by siRNA-PPARγ transfection. Taken together, our results indicated that LPS-induced inflammation were potently compromised by emodin very likely through the PPARγ-dependent inactivation of NF-κB in RAW264.7 cells. © 2016 Elsevier B.V. All rights reserved. Source

Li X.,Capital Medical University | He X.,Capital Medical University | Tian W.,Handan Central Hospital | Wang J.,Chinese Peoples Armed Police forces Academy
Molecular Medicine Reports | Year: 2014

Notch signaling has been reported to be oncogenic or tumor suppressive, depending on the tissue context. To investigate the effects of Notch2 knockdown on U87 human glioma cell proliferation in vitro and in vivo, and the associated mechanisms, U87 cells were stably transfected with p green fluorescent protein (GFP)-V-RS Notch2 short hairpin (sh) RNA plasmid and pGFP-V-RS scramble-shRNA plasmid. The former was referred to as the Notch2-shRNA group and the latter as the negative-shRNA group. mRNA and protein expression, cell proliferation, cell cycle and apoptosis were measured by reverse transcription-polymerase chain reaction, western blot analysis, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide analysis and flow cytometry using propidium iodide, respectively. Tumor volume, tumor weight and cumulative survival rate were determined in a nude mouse xenograft tumor model. Notch2 mRNA and protein expression in the Notch2-shRNA group were reduced by 87.6 and 94.5% compared with the negative-shRNA group (P<0.001). Notch2 knockdown significantly inhibited U87 cell proliferation after three days of culture (P<0.05). Notch2 silencing induced cell cycle arrest at G0/G1 phase by upregulation of p21 protein expression and downregulation of mini chromosome maintenance complex 2 and cyclin-D1 protein expression. Furthermore, knockdown of Notch2 also induced U87 cell apoptosis. On day 50 after inoculation, tumor weight in the Notch2-shRNA group was significantly lower than that in the negative-shRNA group (0.55±0.10 vs. 1.23±0.52 g; P<0.01). The cumulative survival rate was significantly longer in the Notch2-shRNA group compared with the negative-shRNA group (log rank test P=0.01). In conclusion, Notch2 silencing inhibited U87 glioma cell proliferation by inducing cell cycle arrest and apoptosis in vitro and in vivo. Thus, Notch2 may be a key therapeutic target for the treatment of glioma. Source

Zhao J.-J.,Hebei Medical University | Zhao J.-J.,Hebei University of Engineering | Chen P.-J.,Handan Central Hospital | Duan R.-Q.,Hebei University of Engineering | And 3 more authors.
International Journal of Clinical and Experimental Pathology | Year: 2014

Introduction: MicroRNAs (miRNAs) are noncoding RNAs that regulate multiple cellular processes during cancer progression. MiR-630 has recently been identified to be involved in tumorigenesis of several cancers such as lung cancer and gastric cancer. However, the regulation of miR-630 in clear cell renal cell carcinoma (ccRCC) has not yet been reported before. Methods: Expression of miR-630 was evaluated by quantitative real-time PCR in tumour and their normal matched tissues in n = 92 ccRCC patients, and its association with overall survival of patients was analyzed by statistical analysis. Results: The expression level of miR-630 was significantly higher in renal cancer in comparison to normal matched tissue (P < 0.05). It is also proved that miR-630 expression was to be associated with renal cancer histologic grade, lymphnode metastasis, distant metastasis (P < 0.05). In addition, the Kaplan-Meier survival curves revealed that high miR-630 expression was associated with poor prognosis in ccRCC patients. miR-630 expression was an independent prognostic marker of overall ccRCC patient survival in a multivariate analysis. Conclusions: The study proves for the first time that miR-630 is upregulated in a majority of ccRCC patients. It also shows that miR-630 expression is an independent prognostic factor for patients with renal cancer, which might be a potential valuable biomarker for ccRCC. Source

Xiao J.,Hubei University of Arts and Science | Xiao J.,University of California at Davis | Yang R.,Handan Central Hospital | Yang L.,Hubei University of Arts and Science | And 4 more authors.
Scientific Reports | Year: 2015

Experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis (MS), is characterized by CNS demyelination mediated by autoreactive T cells. Kirenol, a biologically active substance isolated from Herba Siegesbeckiae, has potent anti-inflammatory activities. Here we investigated effects of kirenol on EAE. Kirenol treatment markedly delayed onset of disease and reduced clinical scores in EAE mice. Kirenol treatment reduced expression of IFN-γ and IL-17A in the serum and proportion of Th1 and Th17 cells in draining lymph nodes. Priming of lymphocytes was reduced and apoptosis of MOG-activated CD4+ T cells was increased in kirenol treated EAE mice. Kirenol treatment of healthy animals did not affect the lymphocytes in these non-immunized mice. Further in vitro studies showed that kirenol inhibited viability of MOG-specific lymphocytes and induced apoptosis of MOG-specific CD4+ T cells in a dose- and time-dependent manner. Kirenol treatment upregulated Bax,downregulated Bcl-2,and increased activation of caspase-3 and release of cytochrome c, indicating that a mitochondrial pathway was involved in kirenol induced apoptosis. Moreover, pretreatment with either a pan-caspase inhibitor z-VAD-fmk or a more specific caspase 3 inhibitor Ac-DEVD-CHO in lymphocytes reduced kirenol induced apoptosis. Our findings implicate kirenol as a useful agent for the treatment of MS. © 2015, Nature Publishing Group. All rights reserved. Source

Tan Z.-X.,Handan Central Hospital | Liu H.-J.,Hebei Medical University | Hou B.,Handan Central Hospital
International Journal of Clinical and Experimental Pathology | Year: 2016

Purpose: This study intended to determine the expression of AT rich interactive domain 1A (SWI-like) (ARID1A) in serum of glioma patients and explore the relevance between ARID1A expression and the prognosis of glioma patients. Methods: The expression of ARID1A in serum of glioma patients and healthy controls were measured by high performance liquid chromatography (HPLC). Chi-square test was applied to evaluate the statistical difference between ARID1A expression and the clinicopathologic characteristics. Kaplan-Meier analysis combing with log-rank test was used to compare the overall survival of glioma patients with different ARID1A expression. Cox regression analysis was performed to evaluate the relationship between ARID1A expression and the prognosis of glioma patients. Results: The ARID1A expression was significantly lower in serum of glioma patients than in the healthy controls (P < 0.001). Moreover, the ARID1A expression was closely related to pathological grading, age and KPS score (P < 0.05), while no relationship was found between ARID1A expression and gender, preoperative epilepsy, or tumor range (P > 0.05). Besides, the overall survival time of patients with high ARID1A expression was significantly longer than those with low ARID1A expression according to Kaplan-Meier analysis (P = 0.005). Cox regression analysis illustrated that ARID1A expression was a potential factor for prognosis of glioma patients and it might be an independent biomarker (P = 0.002, HR = 4.992, 95% CI = 1.831-13.611). Conclusion: In a word, our study indicated that down-regulation of ARID1A was a promising biomarker for the prognosis of glioma patients. Source

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