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Article ; Online: Effects of 50 Hz magnetic field exposure on metabolism of cerebral cortex in APP/PS1 transgenic mice

ZHANG Yanwen / MA Qinlong / GAO Peng / DENG Ping / PI Huifeng

陆军军医大学学报, Vol 45, Iss 4, Pp 277-

2023 Volume 290

Abstract: Objective To study the effects of 50 Hz magnetic field exposure on metabolism of cerebral cortex in APP/PS1 transgenic mice. Methods Twelve 12-week-old male APP/PS1 double transgenic mice were randomly divided into the control group (C group) and the 50 ... ...

Abstract	Objective To study the effects of 50 Hz magnetic field exposure on metabolism of cerebral cortex in APP/PS1 transgenic mice. Methods Twelve 12-week-old male APP/PS1 double transgenic mice were randomly divided into the control group (C group) and the 50 Hz magnetic field exposure group (MF group) (n=6). The mice in the MF group were exposed to 1.0 mT 50 Hz magnetic field 2 h/d for 3 weeks (21 d). The mice in the sham exposure group had the same conditions as those in the MF group, except for no magnetic field exposure. After exposure, the cerebral cortex tissues of mice were taken according to the standard method for high-resolution untargeted metabonomics tests, including sample metabolite extraction, sample LC-MS/MS mass spectrometry analysis, metabolite qualitative and quantitative analysis and data analysis. Results The growth of APP/PS1 double transgenic mice were not affected after 50 Hz magnetic field exposure. The high-resolution untargeted metabonomics showed 1 068 metabolites were identified. Based on fold change analysis (FC>1.5 or FC < 0.67, P < 0.05), 22 significant changed metabolites were identified in cerebral cortex of mice after 50 Hz magnetic field exposure, and 11-keto-beta-boswellic acid was the most increased metabolite (FC=80.68), and 5-aminolevulinic acid was the most decreased metabolite (FC=0.34). Based on the variable importance in the projection (VIP) value of each variable in the orthogonal partial least-squares discriminant analysis (OPLS-DA) model (VIP>1, P < 0.05), 30 identified significant changed metabolites were screened in cerebral cortex of mice after 50 Hz magnetic field exposure. And the top 3 significant changed metabolites in VIP value were 2-oleoyl-1-palmitoyl-sn-glycero-3-phosphocholine (VIP=19.76, FC=0.52), dehydroascorbic acid (VIP=12.71, FC=0.72) and inosine (VIP=10.64, FC=1.05). The analyses of hierarchical clustering, correlation and Kyoto Encyclopedia of Genes and Genomes (KEGG) showed that the 30 VIP significant changed metabolites may be involved ...
Keywords	50 hz magnetic field ; app/ps1 transgenic mice ; cerebral cortex ; untargeted metabolomics ; Medicine (General) ; R5-920
Subject code	572
Language	Chinese
Publishing date	2023-02-01T00:00:00Z
Publisher	Editorial Office of Journal of Army Medical University
Document type	Article ; Online
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Article: Editorial: Autophagy in diseases-From basic to clinic.

Yang, Jie / Ni, Zhenhong / Pi, Huifeng / Bohnert, Adam / Deng, Zhiqiang

Frontiers in physiology

2023 Volume 13, Page(s) 1115511

Language	English
Publishing date	2023-01-04
Publishing country	Switzerland
Document type	Editorial
ZDB-ID	2564217-0
ISSN	1664-042X
ISSN	1664-042X
DOI	10.3389/fphys.2022.1115511
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Article ; Online: Effect of KIF5A mediated lysosomal functions in cadmium exposure-induced neurotoxicity in vitro

DENG Ping / CHEN Menyan / XIE Jia / TIAN Li / YU Zhengping / PI Huifeng

Di-san junyi daxue xuebao, Vol 44, Iss 4, Pp 320-

2022 Volume 328

Abstract: Objective To investigate the effect of kinesin family member 5A (KIF5A) mediated lysosomal functions in cadmium (Cd) exposure-induced neurotoxicity. Methods Primary cortical neurons isolated and primarily cultured from specific pathogen free (SPF) C57BL/ ... ...

Abstract	Objective To investigate the effect of kinesin family member 5A (KIF5A) mediated lysosomal functions in cadmium (Cd) exposure-induced neurotoxicity. Methods Primary cortical neurons isolated and primarily cultured from specific pathogen free (SPF) C57BL/6J mice were used and divided into control and Cd-exposed groups. The 50% inhibitory concentration (IC50) of cortical neurons after 24 h of Cd exposure was measured. Furthermore, the neurons were treated with 1, 2 and 3 μmol/L cadmium chloride (CdCl2) for 24 h, and then cell viability, neuronal differentiation and lysosomal function were measured. RT-qPCR and Western blotting were used to detect the changes of KIF5A expression at mRNA and protein levels. The effects of overexpression of KIF5A by adenoviral vector on cell viability, neuronal differentiation and lysosomal function were also investigated in the Cd-exposed cortical neurons. Results The IC50 value in neurons exposure to CdCl2 for 24 h was determined to be 2.9 μmol/L. Compared with the control group, the cell viability was inhibited (P < 0.01) and the total length of protrusion growth and the number of branching points were obviously reduced (P < 0.01) after 2 and 3 μmol/L CdCl2 exposure for 24 h. In addition, 2 and 3 μmol/L CdCl2 treatment also resulted in dramatically decreased lysosomal activity of cathepsin B (CTSB) and altered acidic environment when compared with the control group (P < 0.01). However, the activity cathepsin D(CTSD) was not significantly changed in CdCl2-exposed neuronal cells. More importantly, the mRNA and protein levels of KIF5A were remarkably decreased after Cd exposure (P < 0.01). Overexpression of KIF5A effectively increased the CTSB activity, stabilized the lysosomal pH value, and antagonized the inhibitory effect on cell viability and protrusion growth induced by Cd exposure (P < 0.01). Conclusion Cd exposure significantly reduces KIF5A protein expression in neurons, and thereby impairs lysosomal function and inhibits neuronal cell viability and protrusion ...
Keywords	cdcl2 ; neurotoxicity ; kinesin family member 5a ; lysosomal function ; Medicine (General) ; R5-920
Subject code	571
Language	Chinese
Publishing date	2022-02-01T00:00:00Z
Publisher	Editorial Office of Journal of Third Military Medical University
Document type	Article ; Online
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Article ; Online: Microarray analysis of the mechanism of liver injury induced by acute cadmium exposure in rats

DENG Ping / CHEN Mengyan / XIE Jia / TIAN Li / YU Zhengping / PI Huifeng

Di-san junyi daxue xuebao, Vol 42, Iss 16, Pp 1641-

2020 Volume 1647

Abstract: Objective To explore the mechanism of acute cadmium (Cd) exposure-induced liver injury in rats. Methods Sixteen male SD rats were randomly divided into control group and acute cadmium exposure group (n=8), and received a single peritoneal injection of ... ...

Abstract	Objective To explore the mechanism of acute cadmium (Cd) exposure-induced liver injury in rats. Methods Sixteen male SD rats were randomly divided into control group and acute cadmium exposure group (n=8), and received a single peritoneal injection of normal saline and 1.25 mg/kg CdCl2 dissolved in normal saline, respectively. The rats were euthanized at 24 h after the injection for histopathological assessment using HE staining and detection of serum alanine transaminase (ALT) and aspartate transaminase (AST) activities using a biochemical analyzer. The tissue microarray GSE65198 dataset from the GEO database was analyzed for the gene expression profiles in the liver tissues of rats receiving identical treatments, and online analysis with GEO2R was performed to compare the data between the control and daily 1.25 mg/kg cadmium exposure group to identify the differentially expressed genes (DEGs). The functions and pathway enrichment of the DEGs were analyzed using Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis. The hub genes were identified by protein-protein interactions (PPIs) network and Cytoscape software, and their expression levels in the liver tissues of the rats were verified by qRT-PCR. Results Compared with the control rats, the rats with acute Cd exposure showed marked elevations of serum AST and ALT levels (P < 0.01) without exhibiting obvious pathologies in the liver tissues, where no ballooning hepatocyte degeneration, focal necrosis or inflammatory cell infiltration was found. GO and KEGG enrichment analysis confirmed that the DEGs were highly enriched in cell cycle arrest (the Top 1 signaling pathway). Cdc20, Ccnb1, Cdk1, Top2a, and Ube2c were the hub genes in the PPI network of the DEGs, all of which showed decreased expression at the mRNA level in the liver of rats with acute Cd exposure (P < 0.01). Only Cdk1 out of the 3 hub genes involved in cell cycle (Cdc20, Ccnb1, and Cdk1) was significantly down-regulated following cadmium exposure in rats (P < ...
Keywords	cdcl2 ; rats ; hepatoxicity ; microarray ; cell cycle ; Medicine (General) ; R5-920
Subject code	610
Language	Chinese
Publishing date	2020-08-01T00:00:00Z
Publisher	Editorial Office of Journal of Third Military Medical University
Document type	Article ; Online
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Article ; Online: Radiofrequency radiation reshapes tumor immune microenvironment into antitumor phenotype in pulmonary metastatic melanoma by inducing active transformation of tumor-infiltrating CD8

Jiao, Jia-Zheng / Zhang, Yang / Zhang, Wen-Juan / He, Min-di / Meng, Meng / Liu, Tao / Ma, Qin-Long / Xu, Ya / Gao, Peng / Chen, Chun-Hai / Zhang, Lei / Pi, Hui-Feng / Deng, Ping / Wu, Yong-Zhong / Zhou, Zhou / Yu, Zheng-Ping / Deng, You-Cai / Lu, Yong-Hui

Acta pharmacologica Sinica

2024

Abstract: Immunosuppression by the tumor microenvironment is a pivotal factor contributing to tumor progression and immunotherapy resistance. Priming the tumor immune microenvironment (TIME) has emerged as a promising strategy for improving the efficacy of cancer ... ...

Abstract	Immunosuppression by the tumor microenvironment is a pivotal factor contributing to tumor progression and immunotherapy resistance. Priming the tumor immune microenvironment (TIME) has emerged as a promising strategy for improving the efficacy of cancer immunotherapy. In this study we investigated the effects of noninvasive radiofrequency radiation (RFR) exposure on tumor progression and TIME phenotype, as well as the antitumor potential of PD-1 blockage in a model of pulmonary metastatic melanoma (PMM). Mouse model of PMM was established by tail vein injection of B16F10 cells. From day 3 after injection, the mice were exposed to RFR at an average specific absorption rate of 9.7 W/kg for 1 h per day for 14 days. After RFR exposure, lung tissues were harvested and RNAs were extracted for transcriptome sequencing; PMM-infiltrating immune cells were isolated for single-cell RNA-seq analysis. We showed that RFR exposure significantly impeded PMM progression accompanied by remodeled TIME of PMM via altering the proportion and transcription profile of tumor-infiltrating immune cells. RFR exposure increased the activation and cytotoxicity signatures of tumor-infiltrating CD8
Language	English
Publishing date	2024-03-27
Publishing country	United States
Document type	Journal Article
ZDB-ID	1360774-1
ISSN	1745-7254 ; 0253-9756 ; 1671-4083
ISSN (online)	1745-7254
ISSN	0253-9756 ; 1671-4083
DOI	10.1038/s41401-024-01260-5
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Article ; Online: Melatonin ameliorates atherosclerosis by suppressing S100a9-mediated vascular inflammation.

Chen, Liyuan / Wang, Xue / Liu, Chang / Deng, Ping / Pan, Lina / Yang, Lingling / Cheng, Juan / Zhang, Xutao / Reiter, Russel J / Yu, Zhengping / Pi, Huifeng / Zhou, Zhou / Hu, Houyuan

European journal of pharmacology

2023 Volume 957, Page(s) 175965

Abstract: Atherosclerosis (AS)-associated cardiovascular diseases are predominant causes of morbidity and mortality worldwide. Melatonin, a circadian hormone with anti-inflammatory activity, may be a novel therapeutic intervention for AS. However, the exact ... ...

Abstract	Atherosclerosis (AS)-associated cardiovascular diseases are predominant causes of morbidity and mortality worldwide. Melatonin, a circadian hormone with anti-inflammatory activity, may be a novel therapeutic intervention for AS. However, the exact mechanism is unclear. This research intended to investigate the mechanism of melatonin in treating AS. Melatonin (20 mg/kg/d) was intraperitoneally administered in a high-fat diet (HFD)-induced AS model using apolipoprotein E-deficient (ApoE
MeSH term(s)	Animals ; Mice ; Melatonin/pharmacology ; Melatonin/therapeutic use ; NF-kappa B ; Atherosclerosis/drug therapy ; Apolipoproteins E/genetics ; Inflammation/drug therapy
Chemical Substances	Melatonin (JL5DK93RCL) ; NF-kappa B ; Apolipoproteins E
Language	English
Publishing date	2023-08-23
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2023.175965
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Article ; Online: Chronic cadmium exposure induces Parkinson-like syndrome by eliciting sphingolipid disturbance and neuroinflammation in the midbrain of C57BL/6J mice.

Xu, Yudong / Hong, Huihui / Lin, Xiqin / Tong, Tong / Zhang, Jingjing / He, Haotian / Yang, Lingling / Mao, Gaofeng / Hao, Rongrong / Deng, Ping / Yu, Zhengping / Pi, Huifeng / Cheng, Yong / Zhou, Zhou

Environmental pollution (Barking, Essex : 1987)

2023 Volume 337, Page(s) 122606

Abstract: Cadmium (Cd) is known as a widespread environmental neurotoxic pollutant. Cd exposure is recently recognized as an etiological factor of Parkinson's disease (PD) in humans. However, the mechanism underlying Cd neurotoxicity in relation to Parkinsonism ... ...

Abstract	Cadmium (Cd) is known as a widespread environmental neurotoxic pollutant. Cd exposure is recently recognized as an etiological factor of Parkinson's disease (PD) in humans. However, the mechanism underlying Cd neurotoxicity in relation to Parkinsonism pathogenesis is unclear. In our present study, C57BL/6 J mice were exposed to 100 mg/L CdCl
MeSH term(s)	Humans ; Mice ; Animals ; Cadmium/toxicity ; Sphingolipids ; Neuroinflammatory Diseases ; Parkinson Disease ; Sphingomyelins ; Mice, Inbred C57BL ; Chromatography, Liquid ; Tandem Mass Spectrometry ; Mesencephalon ; Ceramides ; RNA, Messenger ; Biomarkers
Chemical Substances	Cadmium (00BH33GNGH) ; Sphingolipids ; Sphingomyelins ; Ceramides ; RNA, Messenger ; Biomarkers
Language	English
Publishing date	2023-09-22
Publishing country	England
Document type	Journal Article
ZDB-ID	280652-6
ISSN	1873-6424 ; 0013-9327 ; 0269-7491
ISSN (online)	1873-6424
ISSN	0013-9327 ; 0269-7491
DOI	10.1016/j.envpol.2023.122606
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Article ; Online: Long-term exposure to polystyrene microplastics induces hepatotoxicity by altering lipid signatures in C57BL/6J mice.

Tao, Jiawen / Deng, Ping / Lin, Min / Chen, Chunhai / Ma, Qinlong / Yang, Lingling / Zhang, Wenjuan / Luo, Yan / Chen, Siyu / Pi, Huifeng / Zhou, Zhou / Yu, Zhengping

Chemosphere

2023 Volume 347, Page(s) 140716

Abstract: It is estimated that the life of plastics is hundreds to thousands of years, their lasting properties making plastic debris absorbing toxic chemicals and degrading into microplastics (MPs). The purpose of this study was to explore the effects of exposure ...

Abstract	It is estimated that the life of plastics is hundreds to thousands of years, their lasting properties making plastic debris absorbing toxic chemicals and degrading into microplastics (MPs). The purpose of this study was to explore the effects of exposure to different size (0.08 and 0.5 μm) polystyrene (PS) in mice. After 16 weeks of exposure, it was found that PS-MPs could be identified in the liver. No effect of PS-MPs treatment on body weight was observed. PS-MPs exposure disturbed lipids and lipid-like molecule metabolisms and perturbed the citrate cycle and oxidative phosphorylation. Meanwhile, isocitrate dehydrogenase (ICDHc), nicotinamide adenine dinucleotide -malate dehydrogenase (NAD-MDH), succinate dehydrogenase (SDH), α ketoglutarate dehydrogenase (α-KGDH) activities and adenosine triphosphate (ATP) level were obviously affected by PS-MPs treatment. In addition, significant differences were recorded in catalase (CAT) and malondialdehyde (MDA) levels, indicating that PS-MPs exposure induced an oxidative stress in the liver. In conclusion, our present study provided the first evidence of: (a) long-term exposure to PS-MPs lead to PS-MPs accumulated in the liver and results in liver injury; (b) long-term exposure to PS-MPs disturbs lipids and lipid-like molecule metabolisms; (c) long-term exposure to PS-MPs perturbs citrate cycle and oxidative phosphorylation and leads to oxidative stress in the liver.
MeSH term(s)	Animals ; Mice ; Mice, Inbred C57BL ; Microplastics/toxicity ; Plastics ; Polystyrenes/toxicity ; Citrates ; Citric Acid ; Chemical and Drug Induced Liver Injury/etiology ; Lipids
Chemical Substances	Microplastics ; Plastics ; Polystyrenes ; Citrates ; Citric Acid (2968PHW8QP) ; Lipids
Language	English
Publishing date	2023-11-16
Publishing country	England
Document type	Journal Article
ZDB-ID	120089-6
ISSN	1879-1298 ; 0045-6535 ; 0366-7111
ISSN (online)	1879-1298
ISSN	0045-6535 ; 0366-7111
DOI	10.1016/j.chemosphere.2023.140716
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Article ; Online: Manganese overexposure induces Parkinson-like symptoms, altered lipid signature and oxidative stress in C57BL/6 J mouse.

Lu, Muxue / Deng, Ping / Yang, Lingling / Wang, Xue / Mei, Xiang / Zhou, Chao / Chen, Mengyan / Zhou, Zhou / Pi, Huifeng / Wu, Lichuan / Yu, Zhengping

Ecotoxicology and environmental safety

2023 Volume 263, Page(s) 115238

Abstract: Although adequate intake of manganese (Mn) is essential to humans, Mn in excess is neurotoxic. Exposure to extremely high doses of Mn results in "manganism", a condition that exhibits Parkinson-like symptoms. However, the mechanisms underlying its ... ...

Abstract	Although adequate intake of manganese (Mn) is essential to humans, Mn in excess is neurotoxic. Exposure to extremely high doses of Mn results in "manganism", a condition that exhibits Parkinson-like symptoms. However, the mechanisms underlying its neurotoxic effects in Mn-induced parkinsonism pathogenesis are unclear. In this study, 8-week-old male C57BL/6 J mice were injected intraperitoneally with saline and 50 mg/kg MnCl
MeSH term(s)	Male ; Humans ; Animals ; Mice ; Manganese/toxicity ; Parkinson Disease ; Mice, Inbred C57BL ; Oxidative Stress ; Parkinsonian Disorders/chemically induced ; Lipids
Chemical Substances	Manganese (42Z2K6ZL8P) ; Lipids
Language	English
Publishing date	2023-07-11
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	436536-7
ISSN	1090-2414 ; 0147-6513
ISSN (online)	1090-2414
ISSN	0147-6513
DOI	10.1016/j.ecoenv.2023.115238
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Article ; Online: Cadmium exposure disturbs myocardial lipid signature and induces inflammation in C57BL/6J mice.

Lin, Xiqin / Xu, Yudong / Tong, Tong / Zhang, Jingjing / He, Haotian / Yang, Lingling / Deng, Ping / Yu, Zhengping / Pi, Huifeng / Hong, Huihui / Zhou, Zhou

Ecotoxicology and environmental safety

2023 Volume 265, Page(s) 115517

Abstract: Cadmium is a highly ubiquitous environmental pollutant that poses a serious threat to human health. In this study, we assessed the cardiotoxicity of Cd exposure and explored the possible mechanisms by which Cd exerts its toxic effects. The results ... ...

Abstract	Cadmium is a highly ubiquitous environmental pollutant that poses a serious threat to human health. In this study, we assessed the cardiotoxicity of Cd exposure and explored the possible mechanisms by which Cd exerts its toxic effects. The results demonstrated that exposure to Cd via drinking water containing CdCl
Language	English
Publishing date	2023-09-28
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	436536-7
ISSN	1090-2414 ; 0147-6513
ISSN (online)	1090-2414
ISSN	0147-6513
DOI	10.1016/j.ecoenv.2023.115517
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