Jiangxi Academy of Medical science

Nanchang, China

Jiangxi Academy of Medical science

Nanchang, China

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Wei-xu H.,Fudan University | Qin X.,Chinese Institute of Clinical Medical Sciences | Zhu W.,Jiangxi Academy of Medical Science | Yuan-yi C.,Chinese Institute of Clinical Medical Sciences | And 5 more authors.
Molecular Immunology | Year: 2014

Background: Interleukin-1 beta (IL-1β) plays pivotal roles in the progression of allergic airway inflammation. This study aims to determine whether the blockade of IL-1β can inhibit airway inflammation in guinea pigs with allergic asthma induced by the inhalation of aerosolized ovalbumin (OVA). Methods: Healthy guinea pigs treated with saline were used as normal controls (group C). The guinea pigs with allergic asthma induced by the inhalation of aerosolized OVA were randomly divided into three groups: (1) the M group containing negative control animals treated with saline; (2) the Z1 group containing animals treated by the inhalation of atomized 0.1% anti-IL-1β immunoglobulin yolk (IgY); and (3) the Z2 group containing positive control animals that were treated with budesonide. The inflammatory cells in the peripheral blood (PB) and bronchoalveolar lavage fluid (BALF) were evaluated using methylene blue and eosin staining. Cytokine concentrations were measured using an enzyme-linked immunosorbent assay. Pulmonary sections were examined using hematoxylin-eosin staining. Results: Allergic inflammation and damage to the pulmonary tissues were decreased in the Z1 group compared to the M group. Eosinophils and neutrophils in the PB and BALF were significantly decreased in the Z1 group compared to the M group (P<0.05). Treatment with anti-IL-1β IgY significantly reduced the levels of IL-1β, IL-4, IL-8, IL-13, TNF-α, TGF-β1 and IgE in the BALF (P<0.05). Conclusion: The inhalation of aerosolized anti-IL-1β IgY inhibits pathological responses in the pulmonary tissues of guinea pigs with allergic asthma. The inhibitory activity may be due to the decrease in the numbers of eosinophils and neutrophils and the reduced levels of inflammatory cytokines and IgE in the PB and BALF. © 2013 Elsevier Ltd.


Gao D.,Nanchang University | Xu Z.,Nanchang University | Zhang X.,Nanchang University | Zhu C.,Nanchang University | And 3 more authors.
Developmental and Comparative Immunology | Year: 2013

Caspase-8, the essential initiator caspase, is believed to play a pivotal role in death receptor-mediated apoptotic pathway. It also participates in mitochondria-mediated apoptosis via cleavage of proapoptotic Bid in mammals. However, its role in fish remains elusive in Cadmium-induced apoptotic pathway. In this study, we isolated the caspase-8 gene from common carp, one of the most important industrial aquatic animals in China using rapid amplification of cDNA ends (RACE). The deduced amino acid sequence of caspase-8 comprised 475 amino acids, which showed approximately 64.1% identity and 79.8% similarity to zebrafish (. Danio rerio) caspase-8, possessed two conserved death effector domains, a large subunit and a small subunit. Phylogenetic analysis demonstrated that caspase-8 formed a clade with zebrafish caspase-8. In kidney, cadmium (Cd) exposure triggered apoptosis and increased caspase-3 and -9 activities, whereas it did not affect caspase-8 activity. Real-time quantitative PCR analysis revealed that caspase-8 transcriptional level was not significantly increased in kidney after exposure to Cd. Using Western blot analysis, no caspase-8 cleaved fragment was detected and no significant alteration of procaspase-8 level was found with the same Cd-treated condition. Moreover, the immunopositive staining was predominantly limited to the cytoplasm of renal tubular epithelial cells and no remarkable changes of immunoreactivities were observed using immunohistochemical detection after Cd treatment. The results reveal that Cd can trigger apoptosis, while it cannot activate caspase-8 in purse red common carp. © 2013.


Gao D.,Nanchang University | Xu Z.,Nanchang University | Zhang X.,Nanchang University | Wang H.,Nanchang University | And 3 more authors.
Aquatic Toxicology | Year: 2013

Caspase-9, the essential initiator caspase is believed to play a central role in mitochondria-mediated apoptosis signaling. In this study, we isolated the caspase-9 gene from common carp, one of the most important industrial aquatic animals in China using rapid amplification of cDNA ends (RACE). The deduced amino acid sequence of caspase-9, composed of 436 amino acids, showed approximately 47.6% identity and 64.7% similarity to human caspase-9. It also possessed a conserved caspase-associated recruitment domain (CARD), a large subunit and a small subunit. Phylogenetic analysis clearly demonstrated that caspase-9 formed a clade with cyprinid fish caspase-9. Real-time quantitative PCR analysis revealed that caspase-9 transcripts were not significantly increased in kidney after exposure to cadmium (Cd). Whereas caspase-9 cleaved fragments were detected using Western blot analysis with the same Cd treatment condition. Furthermore, the result of immunohistochemical detection showed immunoreactivities were predominantly limited to the cytoplasm of renal tubular epithelial cells and no remarkable changes of immunopositive staining were observed after Cd treatment. Accordingly, the results signify that caspase-9 may play an essential role in Cd induced apoptosis. © 2013.


Ding J.-H.,Nanchang University | Yuan L.-Y.,Jiangxi Academy of Medical Science | Huang R.-B.,Nanchang University | Chen G.-A.,Nanchang University
European Journal of Haematology | Year: 2014

Objectives: Aspirin (ASA) has been frequently used for thromboprophylaxis in patients with multiple myeloma (MM) when treated with thalidomide or lenalidomide. Despite the well-recognized chemopreventive role of ASA in some solid tumors particularly for colon cancer, whether ASA displays the antimyeloma activity remains unclear. Methods: MM1.S and RPMI-8226 cell lines harboring K-Ras and N-Ras mutation, respectively, were treated with various concentrations of ASA for different hours. The cell proliferation and apoptosis were performed to explore the effects of ASA on myeloma. Then, the exact mechanisms governing ASA's antimyeloma were explored by qRT-PCR and Western blot. Also, the effect of ASA on tumor growth was observed in NOD/SCID mice bearing myeloma xenografts. Results: ASA of 0-10 mm concentration inhibits proliferation MM1.S and RPMI-8226 cells in time- and dose-dependent manner. The myeloma cells exposed to ASA treatment displayed concentration-dependent apoptosis, which was closely associated with activation of caspases, upregulation of Bax, and downregulation of Bcl-2 and VEGF. Study in vivo revealed that ASA administration retarded the tumor growth accompanying the survival time of mice bearing myeloma xenografts. Conclusions: ASA exerted antiproliferative and pro-apoptotic action in myeloma cells in vitro and delayed the growth of human myeloma cells in vivo. The underlying mechanisms were ascribed to regulation of Bcl-2 and Bax and suppression of VEGF. © 2014 John Wiley & Sons A/S.


PubMed | Jiangxi Academy of Medical Science and Nanchang University
Type: Journal Article | Journal: PloS one | Year: 2016

The host immune response plays an important role in the pathogenesis of Helicobacter pylori infection. The aim of this study was to clarify the immune pathogenic mechanism of Helicobacter pylori infection via TLR signaling and gastric mucosal Treg cells in mice. To discover the underlying mechanism, we selectively blocked the TLR signaling pathway and subpopulations of regulatory T cells in the gastric mucosa of mice, and examined the consequences on H. pylori infection and inflammatory response as measured by MyD88, NF-B p65, and Foxp3 protein expression levels and the levels of Th1, Th17 and Th2 cytokines in the gastric mucosa. We determined that blocking TLR4 signaling in H. pylori infected mice decreased the numbers of Th1 and Th17 Treg cells compared to controls (P < 0.001-0.05), depressed the immune response as measured by inflammatory grade (P < 0.05), and enhanced H. pylori colonization (P < 0.05). In contrast, blocking CD25 had the opposite effects, wherein the Th1 and Th17 cell numbers were increased (P < 0.001-0.05), immune response was enhanced (P < 0.05), and H. pylori colonization was inhibited (P < 0.05) compared to the non-blocked group. In both blocked groups, the Th2 cytokine IL-4 remained unchanged, although IL-10 in the CD25 blocked group was significantly decreased (P < 0.05). Furthermore, MyD88, NF-B p65, and Foxp3 in the non-blocked group were significantly lower than those in the TLR4 blocked group (P < 0.05), but significantly higher than those of the CD25 blocked group (P < 0.05). Together, these results suggest that there might be an interaction between TLR signaling and Treg cells that is important for limiting H. pylori colonization and suppressing the inflammatory response of infected mice.


PubMed | Jiangxi Academy of Medical Science and Nanchang University
Type: Journal Article | Journal: Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine | Year: 2016

Pentose phosphate pathway (PPP) is a metabolic pathway that generates NADPH and pentose. PPP genes have been reported to be primarily or secondarily upregulated in many cancers. We aimed to study the general alteration of PPP in acute myelogenous leukemia (AML). We performed data mining and analysis of the Cancer Genome Atlas (TCGA) AML dataset for genetic alteration of the PPP gene set. In vitro studies including proliferation, migration, and invasion assays, together with metabolite consumption and oxidation assays, were performed. PPP genes were upregulated in 61% of patients with AML. The majority of altered cases were expression changes measured by RNA sequencing. Expressions of critical PPP genes such as G6PD, PFKL, PFKP, and PGLS were consistently upregulated in all altered cases. Altered PPP is not associated with survival or disease relapse. PPP inhibition using 6-aminonicotinamide (6AN) increases glucose oxidative metabolism in AML. 6AN decreased the glucose oxidation and increased fatty acid oxidation. Here, we showed that PPP inhibition increased glucose oxidative metabolism in AML. PPP inhibition suppressed growth, migration, and invasion of AML, but not colony formation. PPP plays an important role in AML. Our results could contribute to the development of novel targeted treatment.


PubMed | Jiangxi Academy of Medical science and Nanchang University
Type: Journal Article | Journal: International journal of molecular sciences | Year: 2016

The engulfment and cell motility (ELMOs) family of proteins plays a crucial role in tumor cell migration and invasion. However, the function of ELMO3 is poorly defined. To elucidate its role in the development and progression of colorectal cancer (CRC), we examined the expression of ELMO3 in 45 cases of paired CRC tumor tissues and adjacent normal tissues. Furthermore, we assessed the effect of the knockdown of ELMO3 on cell proliferation, cell cycle, migration, invasion and F-actin polymerization in HCT116 cells. The result shows that the expression of ELMO3 in CRC tissues was significantly increased in comparison to the adjacent normal colorectal tissues. Moreover, this overexpression was associated with tumor size (


PubMed | Fudan University, Nanchang University, Chinese Institute of Clinical Medical Sciences, Hunan University and Jiangxi Academy of Medical Science
Type: Journal Article | Journal: Experimental and therapeutic medicine | Year: 2016

An increase in the morbidity of upper respiratory tract infections and the attack and exacerbation of autoimmune diseases has been observed to occur in the few days following sudden environmental temperature decreases, but the mechanisms for these phenomena are not well understood. To determine the effect of a sudden ambient temperature drop on the levels of stress hormones and T-lymphocyte cytokines in the plasma, the Toll-like receptor 4 (TLR4) expression of immunocompetent cells in rat spleens and the levels of regulatory T (Treg) cells in the peripheral blood, Sprague Dawley rats were divided into three groups of different ambient temperatures (20, 4 and -12C). In each group, there were four observation time-points (1, 12, 24 and 48 h). Each ambient temperature group was subdivided into non-stimulation, lipopolysaccharide-stimulation and concanavalin A-stimulation groups. The levels of adrenocorticotropin (ACTH), epinephrine (EPI), angiotensin-II (ANG-II), interleukin-2 (IL-2), interferon- (IFN-), IL-4 and IL-10 in the plasma were determined using ELISA. The cellular expression levels of TLR4 and the presence of cluster of differentiation (CD)4


PubMed | Jiangxi Academy of Medical Science, Hunan University, Chinese Institute of Clinical Medical Sciences and Shanghai Proton and Heavy Ion Center
Type: | Journal: Mediators of inflammation | Year: 2016

This study aims to determine whether the combined blockade of IL-1 and TNF- can alleviate the pathological allergic inflammatory reaction in the nasal mucosa and lung tissues in allergic rhinitis (AR) guinea pigs. Healthy guinea pigs treated with saline were used as the healthy controls. The AR guinea pigs were randomly divided into (1) the AR model group treated with intranasal saline; (2) the 0.1% nonspecific IgY treatment group; (3) the 0.1% anti-TNF- IgY treatment group; (4) the 0.1% anti-IL-1 IgY treatment group; (5) the 0.1% combined anti-IL-1 and TNF- IgY treatment group; and (6) the fluticasone propionate treatment group. The inflammatory cells were evaluated using Wrights staining. Histopathology was examined using hematoxylin-eosin staining. The results showed that the number of eosinophils was significantly decreased in the peripheral blood, nasal lavage fluid, and bronchoalveolar lavage fluid (P < 0.05), and eosinophil, neutrophil, and lymphocyte infiltration and edema were significantly reduced or absent in the nasal mucosa and lung tissues (P < 0.05) in the combined 0.1% anti-IL-1- and TNF- IgY-treated guinea pigs. The data suggest that topical blockade of IL-1 and TNF- could reduce pathological allergic inflammation in the nasal mucosa and lung tissues in AR guinea pigs.


PubMed | Jiangxi Academy of Medical Science and Nanchang University
Type: Journal Article | Journal: Biomedical reports | Year: 2016

The aim of the present study was to explore the mechanism underlying the effects of a selective liver nitric oxide (NO) donor, O

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