Affiliated Hospital of Guangdong Medical University

Zhanjiang, China

Affiliated Hospital of Guangdong Medical University

Zhanjiang, China
SEARCH FILTERS
Time filter
Source Type

Huang S.A.,Affiliated Hospital of Guangdong Medical University
Zhonghua yi xue za zhi | Year: 2016

OBJECTIVE: To investigate expression changes and role of Gα11 protein in the processes of muscularization of non-muscular pulmonary arterioles and effect of sildenafil intervention in rats with pulmonary arterial hypertension (PAH).METHODS: Thirty SD rats were randomly divided into three groups, including normal control group, monocrotaline (MCT) group and sildenafil group; PAH model was prepared with 50 mg/kg MCT treatment for 4 weeks in the MCT group, and these rats were treated by 25 mg/kg sildenafil for 2 weeks after PAH formation in the sildenafil group, and the normal control group were treated with the equal amounts of physiological saline instead of monocrotaline; pulmonary artery pressure was measured with jugular vein catheterization; hematoxylin and eosin (HE) staining method was used to detect the pulmonary arteriolar morphology and vascular tissue parameters; expression of the target Gα11 protein, vascular smooth muscle marker osteopontin (OPN) and proliferation marker proliferating cell nuclear antigen (PCNA) was detected by Western blot.RESULTS: Pulmonary artery mean pressure (mPAP), non-muscular pulmonary arterioles wall thickness index (TI) and area index (AI) of the MCT group were higher than those of the normal control group[(27.43±3.97) vs (11.93±1.52) mmHg (1 mmHg=0.133 kPa), 0.49±0.07 vs 0.31±0.09 and 0.74±0.05 vs 0.45±0.10](all P<0.05), and meanwhile the expression levels of Gα11 and the related proteins including OPN and PCNA were significantly enhanced. mPAP, TI and AI[(18.59±1.44) mmHg, 0.39±0.09 and 0.56±0.04]of the sildenafil group were all lower than those of the MCT group (all P<0.05), and furthermore, expressions of Gα11, OPN and PCNA also reduced in line with these changes.CONCLUSION: Gα11 protein plays a role in the development of PAH and pulmonary non-muscular arteriole muscularization, and sildenafil effectively suppresses PAH and pulmonary vascular remodeling by inhibiting Gα11 expression.


Guo M.,Harbin Medical University | Wang J.,Affiliated Hospital of Guangdong Medical University | Qi H.,Harbin Medical University | Liu F.,Harbin Medical University | And 3 more authors.
Neuroscience Letters | Year: 2016

Increasing evidence has demonstrated that inflammation plays an important role in epilepsy (EP). As a cell-surface molecule of the immunoglobulin superfamily, the receptor for advanced glycation end products (RAGE) is involved in inflammation-related disease. Functional polymorphisms in the regulatory elements and/or ligand-binding regions of RAGE may alter the expression and function of RAGE, thus affecting EP susceptibility. Here, we have identified a novel association between genetic variants in the RAGE G82S locus and EP (p = 0.033) using a case-control study in a Chinese population. Further analyses showed that the 82S+ genotype and S allele were more common in patients with drug-resistant epilepsy (DRE) than in those with drug-responsive EP compared with controls. The loci -374 T/A and -429 T/C did not demonstrate any association with EP, but the haplotype T-A-A exhibited significantly different frequencies between DRE patients and controls (OR = 1.696, 95% CI: 1.188-2.420, P = 0.003). Our study provides preliminary evidence that the G82S polymorphism in RAGE is associated with increased DRE risk and that the GS genotype of the G82S locus is a risk factor for DRE in the Chinese population. © 2016.


Liao Z.,Affiliated Hospital of Guangdong Medical University | Yang Z.,Affiliated Hospital of Guangdong Medical University | Piontek A.,Leibniz Institute for Molecular Pharmacology | Eichner M.,Charité - Medical University of Berlin | And 4 more authors.
Neuroscience | Year: 2016

The vertebrate blood-brain barrier (BBB) creates an obstacle for central nervous system-related drug delivery. Claudin-5 (Cldn5), expressed in large quantities in BBB, plays a vital role in restricting BBB permeability. The C-terminal domain of Clostridium perfringens enterotoxin (cCPE) has been verified as binding to a subset of claudins (Cldns). The Cldn5-binding cCPE194 - 319 variant cCPEY306W/S313H was applied in this study to investigate its ability to modulate the permeability of zebrafish larval BBB. In vitro results showed that cCPEY306W/S313H is able to bind specifically to Cldn5 in murine brain vascular endothelial (bEnd.3) cells, and is transported along with Cldn5 from the cell membrane to the cytoplasm, which in turn results in a reduction in transendothelial electrical resistance (TEER). Conversely, this effect can be reversed by removal of cCPEY306W/S313H. In an in vivo experiment, this study estimates the capability of cCPEY306W/S313H to modulate Cldn5 using a rhodamine B-Dextran dye diffusion assay in zebrafish larval BBB. The results show that cCPEY306W/S313H co-localized with Cldn5 in zebrafish cerebral vascular cells and modulated BBB permeability, resulting in dye leakage. Taken together, this study suggests that cCPEY306W/S313H has the capability - both in vitro and in vivo - to modulate BBB permeability temporarily by specific binding to Cldn5. © 2016 IBRO.


Ma C.-L.,Wuhan University | Ma X.-T.,Affiliated Hospital of Guangdong Medical University | Wang J.-J.,Wright State University | Liu H.,Wuhan University | And 2 more authors.
Behavioural Brain Research | Year: 2017

Accumulating evidence from animal and human research indicate that adult hippocampal neurogenesis plays a key role in cognition. Meanwhile, cognitive decline is well known to associate with ageing-related neurodegenerative diseases such as Alzheimer's disease (AD) and Parkinson's disease (PD). Therefore, prevention of hippocampal neurogenesis reduction should be critical for these diseases. Physical exercise, a potent enhancer of adult hippocampal neurogenesis, has emerged as a potential therapy or an adjunctive therapeutic strategy for cognitive decline. In this review, we discuss the recent findings on hippocampal neurogenesis and the incorporation of new born neurons into the neuronal network in humans and in rodents. By focusing on hippocampal neurogenesis, we illustrate the role and possible mechanisms of physical exercise in cognition preservation. © 2016 Elsevier B.V.


Chen J.-Y.,Affiliated Hospital of Guangdong Medical University
Chinese Journal of Tissue Engineering Research | Year: 2017

BACKGROUND: Extracellular vesicles (EVs) are a kind of subcellular component produced by paracine mechanism including exosomes, microparticles and microvesicles, which have become hotspots in recent years. OBJECTIVE: To review the research status and progress of EVs, especially in the studies about definition, secreting mechanism, isolation and identification, biological characteristics and functions in diseases as well as in biomedical research. METHODS: The first author retrieved PubMed and CNKI databases for relative articles published from July 2006 to August 2016. The keywords were “extracellular vesicles, exosome, microvesicle, microparticle” in English and Chinese, respectively. RESULTS AND CONCLUSION: A total of 44 eligible literatures are enrolled. Almost all cells can secrete EVs, which contain a variety of metrocyte-derived bioactive molecules, such as lipids, proteins, mRNAs, microRNA, lncRNA, cicrRNA, and non-coding RNA. These bioactive molecules are encapsulated in EVs or binding with the membrane. EVs are described to be involved in inflammation, immunity, signal transduction, cell survival and apoptosis, angiogenesis, thrombogenesis, and autophagy, which are of great significance to the maintenance of homeostasis and disease progression. Special EVs may be used as new biomarkers for the diagnosis and prognosis of many diseases and serve as novel tools in the fields of antitumor therapy, regenerative medicine, immunoregulation and vaccination and drug delivery. But the molecular mechanisms regulating the secretion of EVs and the specific pathways activated upon EVs interaction with the target cell are not fully understood. Based on miRNA, lncRNA and circRNA are attracting researchers’ attention. © 2017, Journal of Clinical Rehabilitative Tissue Engineering Research. All rights reserved.


Cai Z.,Chongqing General Hospital | Wan C.-Q.,Chongqing General Hospital | Liu Z.,Affiliated Hospital of Guangdong Medical University | Liu Z.,The Affiliated Hospital of Guangdong Medical University
Journal of Neurology | Year: 2017

The past several decades have given rise to more insights into the role of astrocytes in normal brain function and diseases. Astrocytes elicit an effect which may be neuroprotective or deleterious in the process of Alzheimer’s disease (AD). Impairments in astrocytes and their other functions, as well as physiological reactions of astrocytes to external injury, can trigger or exacerbate hyperphosphorylated tau and amyloid-beta (Aβ) pathologies, leading to the formation of both amyloid plaques and neurofibrillary tangles (NFTs), as well as neuronal dysfunction. This review addresses the involvement of astrocytes in the Aβ pathology, where the main mechanisms include the generation and clearance of Aβ, and the formation of NFTs. It is also discussed that metabolic dysfunction from astrocytes acts as an initiating factor in the pathogenesis of AD and a contributor to the onset and development of clinical presentation in AD. © 2017 Springer-Verlag GmbH Germany


Shian H.,Affiliated Hospital of Guangdong Medical University
National Medical Journal of China | Year: 2016

Objective To investigate expression changes and role of Gα11 protein in the processes of muscularization of non-muscular pulmonary7 arterioles and effect of sildenafil intervention in rats with pulmonary arterial hypertension (PAH). Methods Thirty SD rats were randomly divided into three groups, including normal control group, monocrotaline (MCT) group and sildenafil group; PAH model was prepared with 50 mg/kg MCT treatment for 4 weeks in the MCT group, and these rats were treated by 25 mg/kg sildenafil for 2 weeks after PAH formation in the sildenafil group, and the normal control group were treated with the equal amounts ot physiological saline instead of monocrotaline; pulmonary artery pressure was measured with jugular vein catheterization; hematoxylin and eosin (HE) staining method was used to detect the pulmonary arteriolar morphology and vascular tissue parameters; expression of the target Gall protein, vascular smooth muscle marker osteopontin (OPN) and proliferation marker proliferating cell nuclear antigen (PCNA) was detected by Western blot. Results Pulmonary artery mean pressure (mPAP), non-muscular pulmonary arterioles wall thickness index (TI) and area index (Al) of the MCT group were higher than those of the normal control group [ (27. 43 ± 3. 97) vs (11. 93 ± 1. 52) mmHg (1 mmHg =0. 133 kPa), 0. 49 ± 0. 07 vs 0. 31 ± 0. 09 and 0. 74 ± 0. 05 vs 0. 45 ± 0. 10 ] (all P < 0. 05), and meanwhile the expression levels of Gal 1 and the related proteins including OPN and PCNA were significantly enhanced. mPAP, TI and AI[ (18. 59 ± 1. 44) mmHg, 0. 39 ±0. 09 and 0. 56 ±0. 04] of the sildenafil group were all lower than those of the MCT group (all P <0. 05), and furthermore, expressions of Gal 1, OPN and PCNA also reduced in line with these changes. Conclusion Gal 1 protein plays a role in the development of PAH and pulmonary non-muscular arteriole muscularization, and sildenafil effectively suppresses PAH and pulmonary vascular remodeling by inhibiting Gαll expression.


PubMed | Affiliated Hospital of Guangdong Medical University
Type: | Journal: Mycopathologia | Year: 2017

To date, only one case of post-traumatic endophthalmitis caused by Scedosporium dehoogii has been reported, but its contamination or colonization might not be precluded due to the absence of pathogenic isolation and/or pathological examination. We report the first case to our knowledge of S. dehoogii-induced subcutaneous scedosporiosis in a psoriatic patient. A 58-year-old man with 5-year history of psoriasis vulgaris and immunosuppressant therapy developed pyrexia and multiple subcutaneous abscesses on both knees. Direct microscopy of the yellowish pus showed masses of bright green short spores. Skin biopsy revealed some branched septate hyphae within the granuloma. Two aspirated pus specimens collected at a 1-week interval produced white cottony colonies on Sabouraud dextrose agar. Bacterial cultures of one blood and two purulent samples were negative, and fungal culture of blood sample was not performed. The isolate was identified as S. dehoogii using -tubulin phylogeny and species-specific PCR with primer MSDE1/MSA2. Without addition of antifungal treatment, subcutaneous lesions disappeared spontaneously after immunosuppressant withdrawal and no relapse occurred during 64-month follow-up. The spontaneous recovery may result from immune reconstitution following immunosuppressant discontinuation.


PubMed | Guangdong Medical University and Affiliated Hospital of Guangdong Medical University
Type: Journal Article | Journal: Oncology letters | Year: 2017

Diosmetin (DIOS), a flavonoid compound, is abundant in Citrus limon. Emerging studies have shown that DIOS is an effective compound implicated in multiple types of cancer. However, whether DIOS serves a role in hepatocellular carcinoma (HCC) is still obscure. HepG2 cells were used in the present study, and it was observed that DIOS exhibited antitumor activity against liver cancer cells. Western blotting was performed to evaluate cell apoptosis and survival-associated proteins, and the results demonstrated that DIOS treatment resulted in the activation of the p53-dependent apoptosis pathway. Our results revealed that DIOS caused inhibition of the nuclear factor (NF)-B signaling pathway and downregulation of Notch3 receptor. Furthermore, by using small hairpin RNA-Notch3, it was confirmed that DIOS inhibited the NF-B signaling pathway by inactivation of Notch3. In conclusion, the present results demonstrated that DIOS triggered cell apoptosis by activation of the p53 signaling pathway and inhibited the NF-B cell survival pathway by downregulation of Notch3 receptor expression. DIOS is a potential agent for prevention of HCC.


PubMed | Affiliated Hospital of Guangdong Medical University
Type: Journal Article | Journal: Oncology letters | Year: 2017

Hepatocellular carcinoma (HCC), which is a type of malignant tumor, is the fifth most common cancer in men and ninth in women worldwide. The aim of the present study was to investigate the antitumor effect of diosmetin (DIOS) in hepatocellular carcinoma HepG2 cells. The proliferation, apoptosis and autophagy rates of HepG2 cells were measured following treatment with DIOS. The effects of DIOS treatment on HepG2 cell proliferation and apoptosis rates were analyzed using MTT assays and Annexin V staining, respectively. The effect of DIOS treatment on autophagy levels was assessed using transmission electron microscopy, green fluorescent protein (GFP)-microtubule-associated protein 1 light chain (LC3) transfection and LysoTracker Red staining. Furthermore, bafilomycin A1 (BA1), an autophagy inhibitor, was used to assess the association between DIOS and cell autophagy, proliferation and apoptosis. In addition, the expression of autophagy-related proteins [mammalian target of rapamycin (mTOR), phosphatidylinositol 3-kinase, P70S6K, phosphoinositide-dependent kinase-1, extracellular signal-regulated kinase, 5-AMP-activated protein kinase and Akt] and apoptosis-related proteins [B-cell lymphoma (Bcl)-2-associated X protein, Bak, p53, Bcl-2 and caspase-3] were analyzed by western blotting. The results revealed that DIOS significantly inhibited proliferation (P<0.01) and induced apoptosis (P<0.001) in HepG2 cells. It was also demonstrated that DIOS triggered autophagy by regulating the mTOR pathway in HepG2 cells. Notably, following treatment of HepG2 cells with the autophagy inhibitor, BA1, the expression of apoptosis-related proteins, including Bax, Bak and p53, were significantly decreased (P<0.05), and cell viability was recovered to a certain extent. In conclusion, DIOS inhibits cell proliferation and induces apoptosis in HepG2 cells via regulation of the mTOR pathway. Thus, the results of the current study indicate that DIOS may present a potential therapeutic agent for HCC treatment.

Loading Affiliated Hospital of Guangdong Medical University collaborators
Loading Affiliated Hospital of Guangdong Medical University collaborators