Publications by authors named "Guangyao Shi"

12 Publications

  • Page 1 of 1

Ginsenoside Rb1 attenuates age-associated vascular impairment by modulating the Gas6 pathway.

Pharm Biol 2021 Dec;59(1):1369-1377

Department of Cardiology, The Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou, China.

Context: Ginsenoside Rb1 (Rb1) exerts many beneficial effects and protects against cardiovascular disease.

Objective: To investigate whether Rb1 could attenuate age-related vascular impairment and identify the mechanism.

Materials And Methods: Female C57BL/6J mice aged 2 and 18 months, randomly assigned to Young, Young + 20 mg/kg Rb1, Old + vehicle, Old + 10 mg/kg Rb1 and Old + 20 mg/kg Rb1 groups, were daily intraperitoneal injected with vehicle or Rb1 for 3 months. The thoracic aorta segments were used to inspect the endothelium-dependent vasorelaxation. Left thoracic aorta tissues were collected for histological or molecular expression analyses, including ageing-related proteins, markers relevant to calcification and fibrosis, and expression of Gas6/Axl.

Results: We found that in Old + vehicle group, the expression of senescence proteins and cellular adhesion molecules were significantly increased, with worse endothelium-dependent thoracic aorta relaxation (58.35% ± 2.50%) than in Young group (88.84% ± 1.20%). However, Rb1 treatment significantly decreased the expression levels of these proteins and preserved endothelium-dependent relaxation in aged mice. Moreover, Rb1 treatment also reduced calcium deposition, collagen deposition, and the protein expression levels of collagen I and collagen III in aged mice. Furthermore, we found that the downregulation of Gas6 protein expression by 41.72% and mRNA expression by 52.73% in aged mice compared with young mice was abrogated by Rb1 treatment. But there was no significant difference on Axl expression among the groups.

Conclusions: Our study confirms that Rb1 could ameliorate vascular injury, suggesting that Rb1 might be a potential anti-ageing related vascular impairment agent.
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http://dx.doi.org/10.1080/13880209.2021.1986076DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8510614PMC
December 2021

Overlapping stent-assisted coil embolization for vertebrobasilar dissecting aneurysms: a single-center study.

Neurol Res 2021 Sep 18;43(9):701-707. Epub 2021 Jul 18.

Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, People's Republic of China.

Effective treatment strategies for vertebrobasilar dissecting aneurysms (VBDAs) remain controversial due to their high morbidity and mortality. The aim of the present study was to evaluate the efficacy of overlapping stent-assisted coil embolization (OSCE) in VBDA patients. A total of 42 patients with VBDA were retrospectively examined by OSCE from May 2015 to August 2019. Patients' clinical and radiological parameters were assessed at discharge and during interim follow-up. Safety, technical feasibility and follow-up clinical and imaging observations for therapy were also evaluated retrospectively. The average age of the 42 patients who underwent OSCE was 54 years (range 33 to 74 years). Overlapping stents were successfully implanted in all patients after coil embolism. Overall clinical results were effective (score on a modified Rankin scale from 0 to 2) in all patients. In the meantime, all patients had favorable outcomes when evaluating telephone calls or digital subtractive angiography (DSA) imaging. Among 42 patients, one patient died due to a perioperative rupture. All the remaining 41 patients had a good prognosis during the follow-up telephone call, with a median follow-up of 28 months (range, 2 to 55 months). The total number of DSA recurrences was 20. Subsequent DSA results showed that all aneurysms were completely occluded while in only one case the parent artery of the aneurysm was completely closed. OSCE in VBDAs patients is safe and effective. This technique showed favorable results in clinical and imaging follow-ups for non-ruptured and ruptured VBDAs.
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http://dx.doi.org/10.1080/01616412.2021.1922172DOI Listing
September 2021

Methane production from acetate, formate and H/CO under high ammonia level: Modified ADM1 simulation and microbial characterization.

Sci Total Environ 2021 Aug 7;783:147581. Epub 2021 May 7.

College of Chemical Engineering, Beijing University of Chemical Technology, Beijing 100029, China; Biomass Energy and Environmental Engineering Research Center, Beijing University of Chemical Technology, Beijing 100029, China. Electronic address:

This study evaluated the methanogenic performance of typical substrates (acetate, formate, H/CO, and glucose) under low and high ammonia levels and the Anaerobic Digestion Model No.1 (ADM1) was extended and modified for better simulation and understanding of the process. Formate-utilizing and hydrogen-utilizing methanogenesis showed stronger ammonia resistance than acetate-utilizing methanogenesis (13-23% vs. 34% decrease in methane production (MP)). Model extension, based on foundational experiments fed with three typical precursors (R > 0.92), was then validated with glucose degradation experiments, and satisfactory predictions of MP and total volatile fatty acids were obtained (R > 0.91). Based on the modified ADM1, the carbon fluxes of glucose degradation were determined, and formate-utilizing methanogenesis showed its importance with a 28-34% contribution of the total methanation, becoming the dominant pathway under high ammonia level. Formate-utilizing methanogenesis also had a thermodynamic advantage among the three pathways. 16S rRNA sequencing suggested a homology between the hydrogen-utilizing and formate-utilizing methanogens. Methanobacterium and Methanobrevibacter were found to be key methanogens, and their enrichment under high ammonia level confirmed the stronger ammonia tolerance of formate-utilizing and hydrogen-utilizing methanogenesis. The microbial characterization and modified ADM1 simulations supported each other.
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http://dx.doi.org/10.1016/j.scitotenv.2021.147581DOI Listing
August 2021

The Influence of NDRG1 Single Nucleotide Polymorphisms on Glioma Risk and Prognosis in Chinese Han Population.

Cell Mol Neurobiol 2022 Aug 12;42(6):1949-1964. Epub 2021 Mar 12.

Key Laboratory of Molecular Mechanism and Intervention Research for Plateau Diseases of Tibet Autonomous Region, School of Medicine, Xizang Minzu University, Xianyang, 712082, Shaanxi, China.

Glioma is a highly fatal malignant tumor with a high recurrence rate, poor clinical treatment effect, and prognosis. We aimed to determine the association between single nucleotide polymorphisms (SNPs) of NDRG1 and glioma risk and prognosis in the Chinese Han population. 5 candidate SNPs were genotyped by Agena MassARRAY in 558 cases and 503 controls; logistic regression was used to analyze the relationship between SNPs and glioma risk. We used multi-factor dimensionality reduction to analyze the interaction of 'SNP-SNP'; the prognosis analysis was performed by log-rank test, Kaplan-Meier analysis, and Cox regression model. Our results showed that the polymorphisms of rs3808599 was associated with the reduction of glioma risk in all participants (OR 0.41, p = 0.024) and the participants ≤ 40 years old (OR 0.30, p = 0.020). rs3802251 may reduce glioma risk in all participants (OR 0.79, p = 0.008), the male participants (OR 0.68, p = 0.033), and astrocytoma patients (OR 0.81, p = 0.023). rs3779941 was associated with poor glioma prognosis in all participants (HR = 2.59, p = 0.039) or astrocytoma patients (HR = 2.63, p = 0.038). We also found that the key factors for glioma prognosis may include surgical operation, radiotherapy, and chemotherapy. This study is the first to find that NDRG1 gene polymorphisms may have a certain association with glioma risk or prognosis in the Chinese Han population.
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http://dx.doi.org/10.1007/s10571-021-01075-6DOI Listing
August 2022

Ninjurin 2 rs118050317 gene polymorphism and endometrial cancer risk.

Cancer Cell Int 2021 Jan 4;21(1). Epub 2021 Jan 4.

The National Engineering Research Centre for Miniaturized Detection Systems, College of Life Science, Northwest University, #229 North TaiBai Road, Xi'an, 710069, Shaanxi, China.

Background: Endometrial cancer is one of the most common female reproductive system tumors. Ninjurin2 (NINJ2) is a new adhesion factor. As a vascular susceptibility gene, it is highly expressed in other cancers and promotes the growth of cancer cells. We conducted an association analysis between NINJ2 gene polymorphism and endometrial cancer risk.

Methods: Five SNPs rs118050317, rs75750647, rs7307242, rs10849390 and rs11610368 of NINJ2 gene were genotyped in 351 endometrial cancer patients and 344 healthy controls. The clinical index difference between cases and controls were tested by one-way analysis of variance. The allele and genotype frequency of cases and controls were been compared by Chi square test. The odds ratios (OR) with 95% confidence interval (95% CI) were examined by logistic regression analysis.

Results: The SNP rs118050317 mutant allele C and homozygote CC genotype were significant increased the endometrial cancer risk (OR 1.46, 95% CI 1.04-2.06, p = 0.028; OR 8.43, 95% CI 1.05-67.89, p = 0.045). In the clinical index analysis, there were significant higher quantities of CEA, CA125 and AFP in cases serum than controls.

Conclusion: The NINJ2 gene polymorphism loci rs118050317 mutant allele C was associated with an increased risk of endometrial cancer. CEA, CA125 and AFP quantities were significant higher in endometrial cancer patients.
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http://dx.doi.org/10.1186/s12935-020-01646-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7784262PMC
January 2021

TT01001 attenuates oxidative stress and neuronal apoptosis by preventing mitoNEET-mediated mitochondrial dysfunction after subarachnoid hemorrhage in rats.

Neuroreport 2020 08;31(11):845-850

Department of Neurosurgery, The First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang Province, People's Republic of China.

Oxidative stress and neuronal apoptosis are considered crucial therapeutic targets against early brain injury (EBI) after subarachnoid hemorrhage (SAH). Emerging evidence indicates that mitochondrial dysfunction is the main reason for oxidative stress and neuronal apoptosis. MitoNEET, an outer mitochondrial membrane protein, has been shown to regulate mitochondrial function. However, whether mitoNEET activation attenuates oxidative stress and neuronal apoptosis after SAH remains unknown. This study was therefore conducted to verify the neuroprotective role of mitoNEET in EBI after SAH in rats. A total of 93 rats were subjected to an endovascular perforation model of SAH. TT01001, a selective agonist of mitoNEET, was administered intraperitoneally 1 h after SAH induction. Neurological tests, immunofluorescence, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL) staining, dihydroergotamine (DHE) staining, and western blot experiments were performed. The results showed that MitoNEET is expressed in neurons, but significantly decreased at 24 h after SAH induction. Activating mitoNEET with TT01001 significantly improved the neurological deficits, and reduced oxidative stress and neuronal apoptosis as measured by DHE and TUNEL staining, when compared with the SAH+vehicle group. Furthermore, TT01001 treatment decreased the expression of the proapoptotic marker, Bax, while increasing the expression of the antiapoptotic marker, Bcl-2. Together, our results suggested that mitoNEET activation with TT01001 reduced oxidative stress injury and neuronal apoptosis by improving mitochondrial dysfunction in EBI after SAH.
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http://dx.doi.org/10.1097/WNR.0000000000001492DOI Listing
August 2020

DLPNet: A deep manifold network for feature extraction of hyperspectral imagery.

Neural Netw 2020 Sep 22;129:7-18. Epub 2020 May 22.

Key Laboratory of Optoelectronic Technology and Systems of the Education Ministry of China, Chongqing University, Chongqing 400044, China. Electronic address:

Deep learning has received increasing attention in recent years and it has been successfully applied for feature extraction (FE) of hyperspectral images. However, most deep learning methods fail to explore the manifold structure in hyperspectral image (HSI). To tackle this issue, a novel graph-based deep learning model, termed deep locality preserving neural network (DLPNet), was proposed in this paper. Traditional deep learning methods use random initialization to initialize network parameters. Different from that, DLPNet initializes each layer of the network by exploring the manifold structure in hyperspectral data. In the stage of network optimization, it designed a deep-manifold learning joint loss function to exploit graph embedding process while measuring the difference between the predictive value and the actual value, then the proposed model can take into account the extraction of deep features and explore the manifold structure of data simultaneously. Experimental results on real-world HSI datasets indicate that the proposed DLPNet performs significantly better than some state-of-the-art methods.
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http://dx.doi.org/10.1016/j.neunet.2020.05.022DOI Listing
September 2020

Ginsenoside Rb1 Alleviates Oxidative Low-Density Lipoprotein-Induced Vascular Endothelium Senescence via the SIRT1/Beclin-1/Autophagy Axis.

J Cardiovasc Pharmacol 2020 02;75(2):155-167

Department of Cardiology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.

Oxidative low-density lipoprotein (ox-LDL) induces endothelium senescence and promotes atherosclerosis. Ginsenoside Rb1 (gRb1) has been proved to protect human umbilical vein cells (HUVECs), but its effect on ox-LDL-induced endothelium senescence and the underlying mechanism remains unknown. This study is to explore the involvement of the SIRT1/Beclin-1/autophagy axis in the effect of gRb1 on protecting endothelium against ox-LDL-induced senescence. Hyperlipidemia of Sprague Dawley rats was induced by high-fat diet, and gRb1 was intraperitoneal injected. A senescence model of HUVECs induced by ox-LDL was also established. The results showed that gRb1 alleviated hyperlipidemia-induced endothelium senescence and ox-LDL-induced HUVECs senescence. GRb1 also restored the reductions in SIRT1 and autophagy, which were involved in the anti-senescence effects. Beclin-1 acetylation was reduced, and the correlation between SIRT1 and Beclin-1 was increased by gRb1. Results of our study demonstrated the anti-senescence function of gRb1 against hyperlipidemia in the endothelium, and the underlying mechanism involves the SIRT1/Beclin-1/autophagy axis.
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http://dx.doi.org/10.1097/FJC.0000000000000775DOI Listing
February 2020

MicroRNA‑576‑3p inhibits the migration and proangiogenic abilities of hypoxia‑treated glioma cells through hypoxia‑inducible factor‑1α.

Int J Mol Med 2019 Jun 4;43(6):2387-2397. Epub 2019 Apr 4.

Department of Neurosurgery, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi 330006, P.R. China.

The most common and aggressive type of brain cancer in adults is glioblastoma multiforme (GBM), and hypoxia is a common feature of glioblastoma. As the histological features of glioma include capillary endothelial cell proliferation, they are highly prone to invading the surrounding normal brain tissue, which is often one of the reasons for the failure of treatment. However, the mechanisms involved in this process are not fully understood. MicroRNAs (miRs) are a class of non‑coding RNA that are able to inhibit the malignant progression of tumor cells through the regulation of downstream genes. In the present study, the low expression of miR‑576‑3p was detected in glioma samples and hypoxia‑treated glioma cells using a reverse transcription‑quantitative polymerase chain reaction. The present study focused on the effects of miR‑576‑3p on hypoxia‑induced glioma. The results of the functional experiments revealed that the overexpression of miR‑576‑3p significantly inhibited the migration and pro‑angiogenic abilities of the glioma cells under hypoxic conditions (P<0.05) compared with in the lentivirus‑miR‑negative control group. Furthermore, luciferase reporter gene assays were used to validate the hypothesis that miR‑576‑3p interacts with the 3'‑untranslated region of hypoxia‑inducible factor‑1α (HIF‑1α) and induces a reduction in the protein levels of matrix metalloproteinase‑2 and vascular endothelial growth factor. Rescue experiments demonstrated that the restoration of HIF‑1α expression attenuated the effect of miR‑576‑3p on the migration and proangiogenic abilities of glioma cells. In conclusion, the present study confirms that miR‑576‑3p is a novel GBM inhibitor and its inhibition of the migration and proangiogenic capacity of hypoxia‑induced glioma cells is mediated by HIF‑1α.
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http://dx.doi.org/10.3892/ijmm.2019.4157DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6488173PMC
June 2019

Dimensionality Reduction of Hyperspectral Imagery Based on Spatial-Spectral Manifold Learning.

IEEE Trans Cybern 2020 Jun 29;50(6):2604-2616. Epub 2019 Mar 29.

The graph embedding (GE) methods have been widely applied for dimensionality reduction of hyperspectral imagery (HSI). However, a major challenge of GE is how to choose the proper neighbors for graph construction and explore the spatial information of HSI data. In this paper, we proposed an unsupervised dimensionality reduction algorithm called spatial-spectral manifold reconstruction preserving embedding (SSMRPE) for HSI classification. At first, a weighted mean filter (WMF) is employed to preprocess the image, which aims to reduce the influence of background noise. According to the spatial consistency property of HSI, SSMRPE utilizes a new spatial-spectral combined distance (SSCD) to fuse the spatial structure and spectral information for selecting effective spatial-spectral neighbors of HSI pixels. Then, it explores the spatial relationship between each point and its neighbors to adjust the reconstruction weights to improve the efficiency of manifold reconstruction. As a result, the proposed method can extract the discriminant features and subsequently improve the classification performance of HSI. The experimental results on the PaviaU and Salinas hyperspectral data sets indicate that SSMRPE can achieve better classification results in comparison with some state-of-the-art methods.
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http://dx.doi.org/10.1109/TCYB.2019.2905793DOI Listing
June 2020

TGF-β1-SOX9 axis-inducible COL10A1 promotes invasion and metastasis in gastric cancer via epithelial-to-mesenchymal transition.

Cell Death Dis 2018 08 28;9(9):849. Epub 2018 Aug 28.

Department of General Surgery, Nanfang Hospital, Southern Medical University, Guangzhou, China.

Molecular biomarkers that predict disease progression might promote drug development and therapeutic strategies in aggressive cancers, such as gastric cancer (GC). High-throughput mRNA sequencing (RNA-seq) revealed that collagen type X alpha 1 (COL10A1) is a disease progression-associated gene. Analysis of 103 GC patients showed that high COL10A1 mRNA expression was associated with GC metastasis and reduced survival. We analyzed the COL10A1 promoter using the UCSC genome website and JASPAR database, and we found potential SOX9 binding site. Here, we demonstrated that SOX9 and COL10A1 were both up-regulated in GC. We observed a positive correlation between the expression patterns of SOX9 and COL10A1 in GC cells and tissues. The results of electrophoretic mobility shift assay (EMSA), chromatin immunoprecipitation (ChIP) assay and promoter reporter indicated that SOX9 could directly bind to the COL10A1 gene promoter and activate its transcription. Biological function experiments showed that COL10A1 regulated the migration and invasion of GC cells. Knockdown COL10A1 inhibited lung and abdominal cavity metastasis in a nude mouse model. Moreover, transforming growth factor-β1 (TGF-β1) treatment up-regulated the phosphorylation of Smad2 and increased SOX9 and COL10A1 expression. COL10A1 was confirmed to be a potential inducer of epithelial-to-mesenchymal transition (EMT). SOX9 was essential for COL10A1-mediated EMT, and cell migration, invasion and metastasis. Co-expression of SOX9 and COL10A1 was associated with tumor progression and was strongly predictive of overall survival in GC patients. In summary, this study elucidated the mechanistic link between COL10A1 and the TGF-β1-SOX9 axis. These findings indicated that COL10A1 might play a crucial role in GC progression and serve as a potential biomarker and therapeutic target in GC patients.
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http://dx.doi.org/10.1038/s41419-018-0877-2DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6113209PMC
August 2018

Ginsenoside Rb1 inhibits free fatty acids‑induced oxidative stress and inflammation in 3T3‑L1 adipocytes.

Mol Med Rep 2017 Dec 4;16(6):9165-9172. Epub 2017 Oct 4.

Department of Cardiology, The Third Affiliated Hospital of Sun Yat‑sen University, Guangzhou, Guangdong 510630, P.R. China.

Free fatty acids (FFAs) increase in visceral fat and are inferred to be one of the underlying inducers of adipose tissue inflammation. In our previous study, it was demonstrated that ginsenoside Rb1 stimulates endothelial nitric oxide synthase (eNOS) and Sirtuin 1 to protect against endothelial cell senescence. In the present study, 3T3‑L1 adipocytes were exposed to 0.5 mM FFAs with or without Rb1 (10‑40 µM). Monocyte chemotactic protein‑1 (MCP‑1) and interleukin‑6 (IL‑6) secretion was measured using ELISA. Tumor necrosis factor‑α (TNF‑α) expression and nuclear factor‑κB (NF‑κB) p65 phosphorylation were detected using western blot analysis. Oxidative stress was determined via measuring intracellular reactive oxygen species (ROS) and nitric oxide (NO) production. The results demonstrated that MCP‑1 and IL‑6 secretion, as well as TNF‑α expression, were significantly increased following FFA treatment, which was attenuated by Rb1 in a dose‑dependent manner. Furthermore, Rb1 attenuated FFA‑induced NF‑κB phosphorylation, suggesting that the inhibitory effect of Rb1 on inflammatory cytokines was partially mediated through blockade of NF‑κB phosphorylation. Further experiments demonstrated that Rb1 ameliorated FFA‑induced ROS generation and NO reduction through upregulation of superoxide dismutase 2 and eNOS expression. Taken together, these results demonstrate proinflammatory and pro‑oxidant effects of FFA on 3T3‑L1 adipocytes, which are effectively ameliorated by Rb1. Suppression of inflammatory responses and oxidative stress may be a novel mechanism for attenuating the effect of Rb1 on adipocyte dysfunction.
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http://dx.doi.org/10.3892/mmr.2017.7710DOI Listing
December 2017
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