Publications by authors named "Zhaobo Zhang"

10 Publications

  • Page 1 of 1

Comparative analysis of ketone body metabolism in BALB/c mice infected with Trypanosoma evansi and Toxoplasma gondii.

Res Vet Sci 2021 Dec 20;143:134-141. Epub 2021 Dec 20.

Key Laboratory of Livestock Infectious Diseases, Ministry of Education, China; College of Animal Science and Veterinary Medicine, Shenyang Agricultural University, Shenyang 110866, China. Electronic address:

KBs (ketone bodies), i.e., acetoacetate, acetone, and (R)-3-Hydroxybutanoate, constitute the intermediate products of the incomplete oxidative degradation of fatty acids. These KBs are used as a source of energy in the hosts' brain, skeletal muscles, and heart. Additionally, they regulate inflammation and oxidative stress of the host by acting as signaling mediators. Parasitic infection is known to result in abnormal physiological and biochemical metabolism, ketoacidosis, and other damage to the host. In this study, we investigated the effects of Trypanosoma evansi and Toxoplasma gondii on ketone body metabolism in mice, as well as the KB levels in the brain, liver, and peripheral blood. T. gondii was found to significantly increase the KB levels, resulting in ketonemia; T. evansi was found to stabilize KB levels in mice. Further investigations showed that T. evansi downregulated the expression of genes encoding enzymes involved in KBs synthesizing pathway and enhanced KBs synthesizing to eliminate ketonemia. Conversely, T. gondii significantly increased the expression of genes encoding enzymes involved in KBs synthesizing pathway and decreased KBs metabolism pathway ones and resulting in increased KBs levels in peripheral blood, culminating in ketonemia. These findings elucidate the differences in the KBs metabolism resulting from infection with T. evansi and T. gondii.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.rvsc.2021.12.016DOI Listing
December 2021

Role of microRNA and long non-coding RNA in Marek's disease tumorigenesis in chicken.

Res Vet Sci 2021 Mar 8;135:134-142. Epub 2021 Jan 8.

Department of Bioscience, Changchun Normal University, Changchun 130032, China. Electronic address:

Marek's disease virus (MDV), the causative agent of Marek's disease (MD), results in highly infectious phymatosis, lymphatic tissue hyperplasia, and neoplasia. MD is associated with high morbidity and mortality rate. Non-coding RNAs (ncRNAs) entails long non-coding RNA (lncRNA) and microRNA (miRNA). Numerous studies have reported that specific miRNAs and lncRNAs participate in multiple cellular processes, such as proliferation, migration, and tumor cell invasion. Specialized miRNAs and lncRNAs militate a similar role in MD tumor oncogenesis. Despite its growing popularity, only a few reviews are available on ncRNA in MDV tumor oncogenes. Herein, we summarized the role of the miRNAs and lncRNAs in MD tumorigenesis. Altogether, we brought forth the research issues, such as MD prevention, screening, regulatory network formation, novel miRNAs, and lncRNAs analysis in MD that needs to be explored further. This review provides a theoretical platform for the further analysis of miRNAs and lncRNAs functions and the prevention and control of MD and malignancies in domestic animals.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.rvsc.2021.01.007DOI Listing
March 2021

The Nature and Oxidative Reactivity of Urban Magnetic Nanoparticle Dust Provide New Insights into Potential Neurotoxicity Studies.

Environ Sci Technol 2020 09 19;54(17):10599-10609. Epub 2020 Aug 19.

Nanosystems Engineering Research Center for Nanotechnology-Enabled Water Treatment, School of Sustainable Engineering and the Built Environment, Arizona State University, Tempe, Arizona 85287-3005, United States.

The recent discovery of magnetic nanoparticles (NPs) in human brain tissue has raised concerns regarding their source and neurotoxicity. As previous studies have suggested that magnetite in urban dust may be the source, we collected urban magnetic dust and thoroughly characterized the nature of ambient urban magnetic dust particles prior to investigating their neurotoxic potential. In addition to magnetite, magnetic dust contained an abundance (∼40%) of elemental iron (Fe). The coexistence of magnetite and elemental iron was found in magnetic dust particles of inhalable (<10 μm) and nanoscale (<200 nm) size ranges with these particles small enough to enter the human brain via the respiratory tract and olfactory bulbs. The magnetic dust also contained nonferrous water-soluble metals (particularly Cu) that can induce formation of reactive oxygen species (ROS). Previous studies used engineered pure-magnetite for ROS studies. However, while magnetite was present in all magnetic dust particles collected, engineered pure-magnetite was relatively unreactive and contributed minimally to the generation of ROS. We fill a critical knowledge gap between exposure to heterogeneous ambient iron-particles and experiments with engineered versus ambient, incidental iron-bearing nanoscale minerals. Our work points to the need to further investigate the presence and properties of magnetic NPs in respirable dust with respect to their potential role in neurodegeneration.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1021/acs.est.0c01962DOI Listing
September 2020

Eugenol promotes functional recovery and alleviates inflammation, oxidative stress, and neural apoptosis in a rat model of spinal cord injury.

Restor Neurol Neurosci 2018 ;36(5):659-668

Department of Physical Medicine and Rehabilitation, The Second Hospital of Shandong University, Shandong University, Jinan, Shandong, PR China.

Background: Eugenol, a natural phenolic compound found in essential oils, shows a variety of remedial properties, while its effect on spinal cord injury (SCI) is still unknown.

Objective: To study the effects of Eugenol on SCI-related impairments in rats.

Methods: Rats received SCI or sham surgery were administered by oral gavage with Eugenol or physiological saline 6 hours following SCI and once a day for seven consecutive weeks. Basso, Beattie, Bresnahan (BBB) score and inclined plane test were used to assess locomotion function, while mechanical allodynia and thermal hyperalgesia were used to evaluate the withdrawal response to painful stimuli. Spinal cord water content was counted and permeability of the blood-spinal cord barrier was assessed by Evans blue extravasation. Serum tumor necrosis factor (TNF)-α, interleukin (IL)-1β, interleukin (IL)-6, nuclear factor (NF)-κB p65, superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), and glutathione peroxidase (GSH-Px) were determined by ELISA (enzyme-linked immunosorbent assay), while NF-κB p65, p38 mitogen-activated protein kinase (MAPK), inducible nitric oxide synthase (iNOS), and Caspase-3 in the spinal cord were detected by Western blot.

Results: Eugenol markedly improved locomotor function and alleviated neuropathic pain, accompanied by decreased inflammation, oxidative stress, and neural apoptosis-associated molecules in the serum and injured spinal cord. Downregulated pathway molecules NF-κB and p38 MAPK were also found in the spinal cord.

Conclusions: These findings suggest that down-regulating NF-κB and MAPK signaling pathway may support the neuroprotective effect of Eugenol against traumatic SCI.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.3233/RNN-180826DOI Listing
November 2018

High expression levels of Cyr61 and VEGF are associated with poor prognosis in osteosarcoma.

Pathol Res Pract 2017 Aug 6;213(8):895-899. Epub 2017 Jun 6.

Department of Rehabilitation, The Second Hospital of Shandong University, Shandong University, Jinan, Shandong 250033, PR China. Electronic address:

Cysteine Rich Angiogenic Inducer 61 (Cyr61) and Vascular Endothelial Growth Factor (VEGF) are signaling proteins involved in the regulation of tumor angiogenesis and progression. The purpose of this study was to investigate the clinicopathological and prognostic significance of Cyr61 and VEGF expressions in osteosarcoma. Immunohistochemical staining was performed to evaluate the expression of both the proteins in 84 osteosarcoma samples. Correlation between Cyr61/VEGF expressions and clinicopathological parameters was determined using Rank sum test and Spearman's rank correlation coefficient. Prognostic factors were identified using univariate and multivariate Cox regression analysis. The expressions of Cyr61 and VEGF were weak in 26.2% and 17.9%, moderate in 26.2% and 23.8%, and strong in 47.6% and 58.3% of osteosarcoma samples, respectively. Cyr61 and VEGF expressions moderately correlated with each other in osteosarcoma, and exhibited significant association with Enneking stage and distant metastasis. In addition, the high expression of both proteins significantly correlated with short overall survival time in these patients. The key finding in this study was that both Cyr61 and VEGF expressions were independent prognostic indicators of overall survival. In summary, our results indicate that expression of Cyr61 and VEGF may serve as important prognostic predictors in patients with osteosarcoma.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.prp.2017.06.004DOI Listing
August 2017

Meta-analysis of the association between COL9A2 genetic polymorphisms and lumbar disc disease susceptibility.

Spine (Phila Pa 1976) 2014 Sep;39(20):1699-706

From the Department of Orthopedics, Taizhou Central Hospital, Taizhou, Zhejiang Province, China.

Study Design: Meta-analysis to collect all the relevant studies to date to further investigate whether or not the COL9A2 gene rs12077871, rs12722877, and rs7533552 polymorphism are associated with susceptibility to lumbar disc disease (LDD).

Objective: The aim of this study was to assess the association between the COL9A2 gene rs12077871, rs12722877, and rs7533552 and LDD.

Summary Of Background Data: LDD is a common musculoskeletal disease with strong genetic determinants. COL9A2 encodes the α2 (IX) chain of type IX collagen, which is the major collagen component of the hyaline cartilage. Growing numbers of studies have revealed the association between COL9A2 polymorphisms and susceptibility to LDD. However, those studies have yielded contradictory results.

Methods: Data were collected from the following electronic databases: PubMed, Web of Knowledge, and China National Knowledge Infrastructure, with the last report up to November 30, 2013. The odds ratio (OR) and 95% confidence interval (CI) were used to assess the strength of association under the allelic genetic model. We summarized the data on the association between COL9A2 rs12077871, rs12722877, and rs7533552 polymorphism and LDD in the overall studies.

Results: Nine case-control studies, including 1522 LDD cases and 1646 controls, were identified. The results indicated that the rs12077871, rs12722877, and rs7533552 variants in COL9A2 were not associated with LDD (rs12077871: C vs. T, OR = 0.541, 95% CI = 0.256-1.147, P = 0.109; rs12722877: C vs. G, OR = 1.199, 95% CI = 0.992-1.448, P = 0.06; rs7533552: A vs. G, OR = 0.993, 95% CI = 0.815-1.069, P = 0.320). Furthermore, the Egger test and the Begg funnel plot did not show any evidence of publication bias.

Conclusion: Our results suggest that the COL9A2 rs12077871, rs12722877, and rs7533552 polymorphisms may not be associated with LDD. More studies based on larger sample sizes and homogeneous samples of patients with LDD are needed to confirm these findings.

Level Of Evidence: 2.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1097/BRS.0000000000000497DOI Listing
September 2014

MicroRNA-149 negatively regulates TLR-triggered inflammatory response in macrophages by targeting MyD88.

J Cell Biochem 2014 May;115(5):919-27

General Hospital of Ningxia Medical University, Yinchuan, 750004, China; School of Laboratory Medicine, Ningxia Medical University, Yinchuan, 750004, China; Huashan Hospital, Fudan University, Shanghai, 200400, China.

MicroRNAs (miRNAs) have been shown to be important regulators of TLR signaling pathway at the post-transcriptional level. In this study, the potential role of miR-149 was explored in murine alveolar macrophage RAW264.7 cells. Our results demonstrated a dynamic change of the expressions of miR-149 expression and MyD88 in macrophage RAW264.7 upon Mycobacterium bovis Bacillus Calmette-Guerlin (BCG) infection or lipopolysaccharide (LPS) stimulation. The presence of BCG or LPS dynamically reduced the miR-149 expression, along with a substantially striking increase of MyD88 expression in these cells. More importantly, overexpression of miR-149 in RAW264.7 cells was associated with a significant decrease of MyD88 protein expression, as well as a reduced production of inflammatory mediator NF-κB 1, TNF-α and IL-6 in response to BCG infection or LPS stimulation. Further studies using immunoblotting assay against anti-MyD88 antibody and microRNA targeting luciferase reporter assay revealed that miR-149 was able to directly target the 3'-UTR of MyD88 mRNA and post-transcriptionally regulated MyD88 protein expression. These data suggested that miR-149 might be a key player of immune modulator for TLR/MyD88 signaling pathway in macrophages, which may through a mechanism of negatively regulating MyD88-dependent Toll-like receptors signaling pathway.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1002/jcb.24734DOI Listing
May 2014

MicroRNA-21 promotes hepatocellular carcinoma HepG2 cell proliferation through repression of mitogen-activated protein kinase-kinase 3.

BMC Cancer 2013 Oct 10;13:469. Epub 2013 Oct 10.

General Hospital of Ningxia Medical University, Yinchuan 750004, China.

Background: microRNA 21 (miR-21) has been demonstrated to be significantly elevated in many types of cancers, including the hepatocellular carcinoma (HCC). In the present study, we investigated the role of miR-21 in HCC by identifying its novel targets, as well as its underlying molecular mechanism.

Methods: The expression of mitogen-activated protein kinase-kinase 3 (MAP2K3) in human HCC tumor tissues and adjacent non-tumor tissues was determined by immunohistochemistry staining (IHC) analysis. The 3'-untranslated region (3'-UTR) of MAP2K3 combined with miR-21 was experimentally verified by a miRNA luciferase reporter approach. Moreover, the role of miR-21 in regulating HCC cell proliferation was analyzed by an MTT assay infected with miR-21mimics/sponge inhibitor Adenoviral viral vectors.

Results: By immunohistochemistry staining analysis, we found that mitogen-activated protein kinase-kinase 3 (MAP2K3) was strikingly repressed in the human HCC tumor tissues, in comparison with the adjacent non-tumor tissues in clinical settings. More importantly, the repression of MAP2K3 was inversely correlated with the expression of miR-21 in HCC. Further study demonstrated that the MAP2K3 was a novel direct target of miR-21, which was experimentally validated by a miRNA luciferase reporter approach. In HepG2 cells, inhibition of miR-21 expression with an adenoviral miR-21 sponge vector profoundly suppressed cell proliferation by up-regulating MAP2K3 expression at both mRNA and protein levels.

Conclusions: These results provide a clinical evidence that MAP2K3 may be a tumor repressor gene, and it is a direct target of miR-21 in HCC, indicating an underlying mechanism by which miR-21 is able to directly target MAP2K3 and inhibit its expression during the carcinogenesis of HCC, at both transcriptional and post-translational levels. This study also suggests that targeting miR-21-MAP2K3 pathway may be a promising strategy in the prevention and treatment of HCC.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1186/1471-2407-13-469DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3852118PMC
October 2013

microR-142-3p down-regulates IRAK-1 in response to Mycobacterium bovis BCG infection in macrophages.

Tuberculosis (Edinb) 2013 Nov 20;93(6):606-11. Epub 2013 Aug 20.

General Hospital of Ningxia Medical University, Yinchuan 750004, China; School of Laboratory Medicine, Ningxia Medical University, Yinchuan 750004, China. Electronic address:

MicroRNAs (miRNAs) have been demonstrated to play a pivotal role in the regulation of target gene expression at the post-transcriptional level. In order to better understand the role of miRNA in the immunological regulation of macrophages against Mycobacterium bovis BCG infection, we explored the alteration of immune-related miRNA profile in macrophage RAW264.7 cells in response to BCG infection in this study. Our results demonstrated that miR-142-3p was a potential to negatively regulate the production of pro-inflammatory mediators NF-κB (NF-κB1), TNF-α and IL-6 in the macrophages in part through a mechanism of targeting IRAK-1 gene and post-transcriptionally down-regulating IRAK-1 protein expression.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.tube.2013.08.006DOI Listing
November 2013

MyD88 as a target of microRNA-203 in regulation of lipopolysaccharide or Bacille Calmette-Guerin induced inflammatory response of macrophage RAW264.7 cells.

Mol Immunol 2013 Oct 21;55(3-4):303-9. Epub 2013 Mar 21.

General Hospital of Ningxia Medical University, Yinchuan 750004, China.

MicroRNAs (miRNAs) have been demonstrated to play a pivotal role in the regulation of target gene expression at the post-transcriptional level. In order to better understand the role of microRNA-203 (miR-203) in the immunological regulation, the function of miR-203 was explored in the macrophage RAW264.7 cells against lipopolysaccharide (LPS) or Bacille Calmette-Guerin (BCG) stimulation. The results evidenced that myeloid differentiation factor 88 (MyD88) was a novel target of miR-203, miR-203 was capable of directly targeting the 3' untranslated region (3'UTR) of MyD88 and post-transcriptionally down-regulating the expression of protein. In addition, an overexpression of miR-203 in RAW264.7 cells was correlated with repressions of MyD88, as well as its downstream signaling of NF-κB (NF-κB1), TNF-α and IL-6. These results suggest that miR-203 may be an important regulator in macrophages against LPS or mycobacteria infection, which may through a mechanism of negatively regulating MyD88-dependent Toll-like receptors signaling pathway.
View Article and Find Full Text PDF

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.molimm.2013.03.004DOI Listing
October 2013
-->