44 results on '"Zhong, Yufang"'
Search Results
2. A comprehensive evaluation of pre- and post-processing sperm parameters for predicting successful pregnancy rate following intrauterine insemination with the husband’s sperms
- Author
-
Luo, Yumei, Liu, Mingxing, Wu, Shunhong, Zhang, Mimi, Yuan, Jingru, Zhong, Yufang, Li, Qing, Sun, Xiaofang, Xu, Xia, and Zhu, Detu
- Published
- 2022
- Full Text
- View/download PDF
3. Altered effective connectivity patterns of the default mode network in Alzheimer's disease: An fMRI study
- Author
-
Zhong, Yufang, Huang, Liyu, Cai, Suping, Zhang, Yun, von Deneen, Karen M, Ren, Aifeng, Ren, Junchan, and Initiative, Alzheimer's Disease Neuroimaging
- Subjects
Biological Psychology ,Psychology ,Neurosciences ,Aging ,Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD) ,Acquired Cognitive Impairment ,Alzheimer's Disease ,Neurodegenerative ,Dementia ,Brain Disorders ,Clinical Research ,2.1 Biological and endogenous factors ,Aetiology ,Neurological ,Aged ,Aged ,80 and over ,Alzheimer Disease ,Brain ,Brain Mapping ,Female ,Humans ,Magnetic Resonance Imaging ,Male ,Middle Aged ,Nerve Net ,Default mode network ,Alzheimer's disease ,Independent component analysis ,Multivariate Granger causality analysis ,Alzheimer's Disease Neuroimaging Initiative ,Cognitive Sciences ,Biochemistry and cell biology ,Biological psychology - Abstract
The aim of this work is to investigate the differences of effective connectivity of the default mode network (DMN) in Alzheimer's disease (AD) patients and normal controls (NC). The technique of independent component analysis (ICA) was applied to identify DMN components and multivariate Granger causality analysis (mGCA) was used to explore an effective connectivity pattern. We found that: (i) connections in AD were decreased than those in NC, in terms of intensity and quantity. Posterior cingulated cortex (PCC) exhibited significant activity in NC as it connected with most of the other regions within the DMN. Besides, the PCC was the convergence center which only received interactions from other regions; (ii) right inferior temporal cortex (rITC) in the NC exhibited stronger interactions with other regions within the DMN compared with AD patients; and (iii) interactions between medial prefrontal cortex (MPFC) and bilateral inferior parietal cortex (IPC) in the NC were weaker than those in AD patients. These findings may implicate a brain dysfunction in AD patients and reveal more pathophysiological characteristics of AD.
- Published
- 2014
4. Cytotoxicity comparison between fine particles emitted from the combustion of municipal solid waste and biomass
- Author
-
Shang, Yu, Wu, Meiying, Zhou, Jizhi, Zhang, Xing, Zhong, Yufang, An, Jing, and Qian, Guangren
- Published
- 2019
- Full Text
- View/download PDF
5. Interactions between oxidative stress, autophagy and apoptosis in A549 cells treated with aged black carbon
- Author
-
An, Jing, Zhou, Qian, Wu, Meiying, Wang, Lu, Zhong, Yufang, Feng, Jialiang, Shang, Yu, and Chen, Yingjun
- Published
- 2019
- Full Text
- View/download PDF
6. Endoplasmic reticulum stress participates in apoptosis of HeLa cells exposed to TPHP and OH-TPHP via the eIF2α-ATF4/ATF3-CHOP-DR5/P53 signaling pathway.
- Author
-
An, Jing, Du, Chenyang, Xue, Wanlei, Huang, Jin, Zhong, Yufang, Ren, Guofa, Shang, Yu, and Xu, Bingye
- Subjects
HELA cells ,ENDOPLASMIC reticulum ,P53 antioncogene ,CELLULAR signal transduction ,APOPTOSIS ,DEATH receptors - Abstract
Purpose: Triphenyl phosphate (TPHP) is a widely used organophosphate flame retardant, which can be transformed in vivo into diphenyl phosphate (DPHP) and 4-hydroxyphenyl phosphate (diphenyl) ester (OH-TPHP) through biotransformation process. Accumulation of TPHP and its derivatives in biological tissues makes it necessary to investigate their toxicity and molecular mechanism. Methods: The present study evaluated the cellular effects of TPHP, DPHP, and OH‐TPHP on cell survival, cell membrane damage, oxidative damage, and cell apoptosis using HeLa cells as in vitro model. RNA sequencing and bioinformatics analysis were conducted to monitor the differently expressed genes, and then RT-qPCR and Western bolt were used to identify potential molecular mechanisms and key hub genes. Results: Results showed that OH-TPHP had the most significant cytotoxic effect in HeLa cells, followed by TPHP; and no significant cytotoxic effects were observed for DPHP exposure within the experimental concentrations. Biological function enrichment analysis suggested that TPHP and OH-TPHP exposure may induce endoplasmic reticulum stress (ERS) and cell apoptosis. The nodes filtering revealed that ERS and apoptosis related genes were involved in biological effects induced by TPHP and OH-TPHP, which may be mediated through the eukaryotic translation initiation factor 2α/activating transcription factor 4 (ATF4)/ATF3- CCAAT/ enhancer-binding protein homologous protein (CHOP) cascade pathway and death receptor 5 (DR5) /P53 signaling axis. Conclusion: Above all, these findings indicated that ERS-mediated apoptosis might be one of potential mechanisms for cytotoxicity of TPHP and OH-TPHP. Graphical Abstract [ABSTRACT FROM AUTHOR]
- Published
- 2023
- Full Text
- View/download PDF
7. Airborne nitro-PAHs induce Nrf2/ARE defense system against oxidative stress and promote inflammatory process by activating PI3K/Akt pathway in A549 cells
- Author
-
Shang, Yu, Zhou, Qian, Wang, Tiantian, Jiang, Yuting, Zhong, Yufang, Qian, Guangren, Zhu, Tong, Qiu, Xinghua, and An, Jing
- Published
- 2017
- Full Text
- View/download PDF
8. Partial melting of an ancient sub-continental lithospheric mantle in the early Paleozoic intracontinental regime and its contribution to petrogenesis of the coeval peraluminous granites in South China
- Author
-
Zhong, Yufang, Wang, Lianxun, Zhao, Junhong, Liu, Lei, Ma, Changqian, Zheng, Jianping, Zhang, Zejun, and Luo, Biji
- Published
- 2016
- Full Text
- View/download PDF
9. Dual-templating synthesis of multi-shelled mesoporous silica nanoparticles as catalyst and drug carrier
- Author
-
Wu, Lu, Zhang, Haijiao, Wu, Minghong, Zhong, Yufang, Liu, Xingwen, and Jiao, Zheng
- Published
- 2016
- Full Text
- View/download PDF
10. Hexabromocyclododecane and polychlorinated biphenyls increase resistance of hepatocellular carcinoma cells to cisplatin through the phosphatidylinositol 3-kinase/protein kinase B pathway
- Author
-
An, Jing, Wang, Xiu, Guo, Panpan, Zhong, Yufang, Zhang, Xinyu, and Yu, Zhiqiang
- Published
- 2014
- Full Text
- View/download PDF
11. Ordovician appinites in the Wugongshan Domain of the Cathaysia Block, South China: Geochronological and geochemical evidence for intrusion into a local extensional zone within an intracontinental regime
- Author
-
Zhong, Yufang, Ma, Changqian, Liu, Lei, Zhao, Junhong, Zheng, Jianping, Nong, Junnian, and Zhang, Zejun
- Published
- 2014
- Full Text
- View/download PDF
12. Oligomeric proanthocyanidins alleviate hexabromocyclododecane-induced cytotoxicity in HepG2 cells through regulation on ROS formation and mitochondrial pathway
- Author
-
An, Jing, Chen, Cen, Wang, Xiu, Zhong, Yufang, Zhang, Xinyu, Yu, Yingxin, and Yu, Zhiqiang
- Published
- 2014
- Full Text
- View/download PDF
13. Zircon U–Pb age, Hf isotopic compositions and geochemistry of the Silurian Fengdingshan I-type granite Pluton and Taoyuan mafic–felsic Complex at the southeastern margin of the Yangtze Block
- Author
-
Zhong, Yufang, Ma, Changqian, Zhang, Chao, Wang, Shiming, She, Zhenbing, Liu, Lei, and Xu, Haijin
- Published
- 2013
- Full Text
- View/download PDF
14. The toxic effects of Aroclor 1254 exposure on the osteoblastic cell line MC3T3-E1 and its molecular mechanism
- Author
-
An, Jing, Zou, Wen, Zhong, Yufang, Zhang, Xinyu, Wu, Minghong, Yu, Zhiqiang, and Ye, Tianwen
- Published
- 2012
- Full Text
- View/download PDF
15. The hormesis effect of BDE-47 in HepG2 cells and the potential molecular mechanism
- Author
-
Wang, Liulin, Zou, Wen, Zhong, Yufang, An, Jing, Zhang, Xinyu, Wu, Minghong, and Yu, Zhiqiang
- Published
- 2012
- Full Text
- View/download PDF
16. The combined effects of BDE47 and BaP on oxidatively generated DNA damage in L02 cells and the possible molecular mechanism
- Author
-
An, Jing, Yin, Lingling, Shang, Yu, Zhong, Yufang, Zhang, Xinyu, Wu, Minghong, Yu, Zhiqiang, Sheng, Guoying, Fu, Jiamo, and Huang, Yuecheng
- Published
- 2011
- Full Text
- View/download PDF
17. Ag2Te Colloidal Quantum Dots for Near-Infrared-II Photodetectors.
- Author
-
Ouyang, Jianying, Graddage, Neil, Lu, Jianping, Zhong, Yufang, Chu, Ta-Ya, Zhang, Yanguang, Wu, Xiaohua, Kodra, Oltion, Li, Zhao, Tao, Ye, and Ding, Jianfu
- Abstract
Ag
2 Te colloidal quantum dots (QDs) are an excellent nanomaterial for applications in the second near-infrared window (NIR-II, 1000–1700 nm). However, synthesis with narrow size distribution and high photoluminescence quantum yield (PL QY) is challenging. In this study, we systematically investigate critical synthesis parameters affecting an organic phase process. We show that high Ag/Te feed ratio leads to smaller size and higher PL QY; under 4:1 Ag/Te feed molar ratio, addition of secondary phosphine leads to narrower size distribution and excellent colloidal stability; under 6:1 Ag/Te feed molar ratio, excess 1-dodecanethiol as a strong ligand slows the nucleation and results in fewer nuclei, leading to a broad size distribution and poor optical properties; additional trioctylphosphine as a weak ligand provides better colloidal stability; and another weak ligand tributylphosphine improves QD colloidal stability, focuses size distribution, and enhances PL QY. A noninjection method maintains narrow size distribution in upscaling syntheses. After optimization, relatively large Ag2 Te QDs with distinct excitonic absorption peaks (∼1050–1450 nm) and PL emission peak 1.3–1.7 μm (QY up to 6.2%) were obtained. NIR-II photodetection has been demonstrated with a responsivity of ∼1.5 mA/W at 1400 nm. [ABSTRACT FROM AUTHOR]- Published
- 2021
- Full Text
- View/download PDF
18. Modifications of autophagy influenced the Alzheimer-like changes in SH-SY5Y cells promoted by ultrafine black carbon.
- Author
-
Shang, Yu, Liu, Mingyuan, Wang, Tiantian, Wang, Lu, He, Huixin, Zhong, Yufang, Qian, Guangren, An, Jing, Zhu, Tong, Qiu, Xinghua, Shang, Jing, and Chen, Yingjun
- Subjects
SOOT ,OXIDATIVE stress ,PROTEIN kinase B ,ALZHEIMER'S disease ,CARBONACEOUS aerosols ,CELL-mediated cytotoxicity - Abstract
Abstract Ambient ultrafine black carbon (uBC) can potentially cross blood-brain barrier, however, very little is currently known about the effects they may have on central nervous system. This study aimed to explore the roles of autophagy in Alzheimer-like pathogenic changes promoted by uBC in SH-SY5Y cells. We firstly found uBC could cause cytotoxicity and oxidative stress in SH-SY5Y cells. Additionally we found uBC initiated progressive development of Alzheimer's disease (AD) associated features, mainly including neuro-inflammation and phosphorylation of tau protein (p-Tau) accumulation. Meanwhile, autophagy process was activated by uBC probably through phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) pathway. RNA interference and autophagosome-lysosome fusion inhibitor were applied to block autophagy process at different stages. Autophagy dysfunction at the initial membrane expansion stage could aggravate p-Tau accumulation and other Alzheimer-like changes in SH-SY5Y cells promoted by uBC. However, autophagy inhibition at the final stage could alleviate p-Tau accumulation caused by uBC. This suggested that inhibition of the infusion of autophagosome and lysosome could possibly activate ubiquitination degradation pathway to regulate p-Tau equilibrium in SH-SY5Y cells. Our findings further raise the concerns about the effects of uBC on the risk of AD and indicate potential roles of autophagy in early Alzheimer-like pathogenic changes caused by ambient uBC. Graphical abstract Image 1 Highlights • Ultrafine black carbon (uBC) caused early Alzheimer-like pathogenic changes. • Autophagy related to these Alzheimer-like pathogenic changes induced by uBC. • Autophagy inhibition at initial membrane expansion stage aggravated p-Tau accumulation. • Autophagy dysfunction at final stage alleviate p-Tau accumulation. Autophagy regulated Alzheimer-like pathogenic changes promoted by uBC. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
19. Fresh and ozonized black carbon promoted DNA damage and repair responses in A549 cells.
- Author
-
An, Jing, He, Huixin, Wang, Lu, Jin, Yingying, Kong, Jiexing, Zhong, Yufang, Liu, Mingyuan, and Shang, Yu
- Subjects
DNA damage ,DNA repair ,SOOT ,APOPTOSIS ,GENE expression - Abstract
Nano-sized ambient black carbon (BC) is hypothesized to pose a serious threat to human health. After emission into the air, the atmospheric oxidation process can modify its physiochemical properties and change its biological responses. In this study, we aimed to compare different DNA damage and repair responses promoted by fresh BC (FBC) and ozone oxidized-BC (OBC). The cell apoptosis, cell arrest, DNA damage and repair were investigated in A549 cells after treatment with FBC and OBC. Associated gene expressions were measured with the reverse transcription quantitative polymerase chain reaction (RT-qPCR) method. Both FBC and OBC could induce cell apoptosis in A549 cells with up-regulated gene of promyelocytic leukemia protein (pml) and down-regulated gene of anti-apoptotic B-cell lymphoma-2 (bcl-2). FBC caused cell cycle arrest at S and G2/M phases, which was associated with up-regulated ataxia telangiectasia mutated (atm), checkpoint kinase 2 (chk2), structural maintenance of chromosomes 1 (smc1) and cell division cycle 25 homolog A (cdc25a) genes. OBC promoted cell cycle arrest at the S phase with up-regulated genes of atm, chk2 and smc1. Both FBC and OBC induced oxidative DNA damage and time-dependent DNA repair responses with increased gene expressions of breast cancer susceptibility protein 1 (brca1), recombination protein A paralog B (rad51b), methyl methanesulfonate-sensitivity protein 22-like and tonsoku-like (mms22l). Compared to FBC, OBC could cause more sufficient DNA damage repair responses through cell cycle arrest at the S phase, resulting in relatively weaker DNA damages. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
20. Comparison of hepatotoxicity and mechanisms induced by triclosan (TCS) and methyl-triclosan (MTCS) in human liver hepatocellular HepG2 cells.
- Author
-
Wang, Lu, Mao, Boyu, He, Huixin, Shang, Yu, Zhong, Yufang, Yu, Zhiqiang, Yang, Yiting, Li, Hui, and An, Jing
- Subjects
TRICLOSAN ,LIVER cancer ,APOPTOSIS ,CANCER cell proliferation ,CELL cycle - Abstract
Triclosan (TCS) is used as an antimicrobial agent and has been widely dispersed and detected in the environment and organisms including human samples. Methyl-triclosan (MTCS) is the predominant bacterial TCS metabolite. At present, the toxicological effects and mechanism of TCS and MTCS are still not fully understood. In this study, the cytotoxic effects of TCS and MTCS in HepG2 cells were investigated in terms of cell proliferation, comet assay, cell cycle, and apoptosis. In addition, the expressions of related proteins were detected with western blotting analysis. The results showed that TCS could significantly inhibit cell proliferation, while MTCS had no obvious effect on cell growth. Both TCS and MTCS caused oxidative injury associated with HO-1 induction and increased DNA strand breaks, which consequently initiated the damage repair process via up-regulation of DNA-PKcs. In addition, TCS blocked the HepG2 cells in S and G2/M phases of cell cycle through down-regulation of cyclin A2 and CDK; while MTCS induced cell cycle arrest at the S phase through up-regulation of cyclin A2 and CDK. Furthermore, TCS activated p53 mediated apoptosis in HepG2 cells in a caspase-independent manner, while MTCS induced apoptosis was dependent on caspase. Moreover, TCS exposure exhibited more severe toxicity in HepG2 cells as compared with MTCS exposure, indicating that the replacement of the ionizable proton in TCS by the methyl group in MTCS is correlated with the cellular toxicity and the molecular mechanism. [ABSTRACT FROM AUTHOR]
- Published
- 2019
- Full Text
- View/download PDF
21. Tributylphosphate (TBP) and tris (2-butoxyethyl) phosphate (TBEP) induced apoptosis and cell cycle arrest in HepG2 cells.
- Author
-
Ren, Guofa, Hu, Jingwen, Shang, Yu, Zhong, Yufang, Yu, Zhiqiang, and An, Jing
- Subjects
OXIDATIVE stress ,APOPTOSIS ,MITOCHONDRIAL membranes ,C-Jun N-terminal kinases ,CYCLIN-dependent kinase inhibitors - Abstract
The purpose of this study was to investigate the cytotoxic effects of tributylphosphate (TBP) and tris (2-butoxyethyl) phosphate (TBEP) and to explore the underlying molecular mechanism focusing on oxidative stress, apoptosis, and cell cycle arrest. The results showed that TBP and TBEP could inhibit cell proliferation, induce cellular reactive oxidative stress, and suppress the mitochondrial membrane potential in HepG2 cells. TBP and TBEP could induce both mitochondrial and p53 mediated apoptosis through different mitogen-activated protein kinase (MAPK) signal pathways. TBP activated the c-Jun N-terminal kinase (JNK) and extracellular regulated protein kinase (ERK1/2) pathways, while TBEP activated the JNK pathway. Furthermore, TBP and TBEP caused a concentration-dependent decrease of cyclin D1 expression and an increase of cyclin-dependent kinase (CDK) inhibitor proteins such as p21 and p27, resulting in significant cell cycle arrest in the G0/G1 phase. Taken together, the toxicity of TBP and TBEP on the HepG2 cells was associated with apoptosis and cell cycle arrest induced by oxidative stress. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF
22. Chemical treatment of contaminated sediment for phosphorus control and subsequent effects on ammonia-oxidizing and ammonia-denitrifying microorganisms and on submerged macrophyte revegetation.
- Author
-
Lin, Juan, Song, Chaofeng, Zhong, Yufang, Fan, Hua, Yu, Chao, Gao, Yue, Xiong, Xiong, Wu, Chenxi, and Liu, Jiantong
- Subjects
TOXICOLOGY of phosphorus ,CHEMICAL treatment of hazardous substances ,CONTAMINATED sediment analysis ,AMMONIA-oxidizing bacteria ,MACROPHYTES ,REVEGETATION ,DENITRIFICATION ,EUTROPHICATION - Abstract
In this work, sediments were treated with calcium nitrate, aluminum sulfate, ferric sulfate, and Phoslock®, respectively. The impact of treatments on internal phosphorus release, the abundance of nitrogen cycle-related functional genes, and the growth of submerged macrophytes were investigated. All treatments reduced total phosphorus (TP) and soluble reactive phosphorus (SRP) in interstitial water, and aluminum sulfate was most efficient. Aluminum sulfate also decreased TP and SRP in overlying water. Treatments significantly changed P speciations in the sediment. Phoslock® transformed other P species into calcium-bound P. Calcium nitrate, ferric sulfate, and Phoslock® had negative influence on ammonia oxidizers, while four chemicals had positive influence on denitrifies, indicating that chemical treatment could inhibit nitrification but enhance denitrification. Aluminum sulfate had decreased chlorophyll content of the leaves of submerged macrophytes, while ferric sulfate and Phoslock® treatment would inhibit the growth of the root. Based on the results that we obtained, we emphasized that before application of chemical treatment, the effects on submerged macrophyte revegetation should be taken into consideration. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF
23. The cytotoxicity of organophosphate flame retardants on HepG2, A549 and Caco-2 cells.
- Author
-
An, Jing, Hu, Jingwen, Shang, Yu, Zhong, Yufang, Zhang, Xinyu, and Yu, Zhiqiang
- Subjects
CELL-mediated cytotoxicity ,CHOLINESTERASE reactivators ,FIREPROOFING agents ,LUNG cancer ,DNA damage - Abstract
In order to elucidate the cytotoxicity of organophosphate flame retardants (OPFRs), three human in vitro models, namely the HepG2 hepatoma cells, the A549 lung cancer cells and the Caco-2 colon cancer cells, were chosen to investigate the toxicity of triphenyl phosphate (TPP), tributylphosphate (TBP), tris(2-butoxyexthyl) phosphate (TBEP) and tris (2-chloroisopropyl) phosphate (TCPP). Cytotoxicity was assayed in terms of cell viability, DNA damage status, reactive oxygen species (ROS) level and lactate dehydrogenase (LDH) leakage. The results showed that all these four OPFRs could inhibit cell viability, overproduce ROS level, induce DNA lesions and increase the LDH leakage. In addition, the toxic effects of OPFRs in Caco-2 cells were relatively severer than those in HepG2 and A549 cells, which might result from some possible mechanisms apart from oxidative stress pathway. In conclusion, TBP, TPP, TBEP and TCPP could induce cell toxicity in various cell lines at relatively high concentrations as evidenced by suppression of cell viability, overproduction of ROS, induction of DNA lesions and increase of LDH leakage. Different cell types seemed to have different sensitivities and responses to OPFRs exposure, as well as the underlying potential molecular mechanisms. [ABSTRACT FROM AUTHOR]
- Published
- 2016
- Full Text
- View/download PDF
24. A soft–hard template approach towards hollow mesoporous silica nanoparticles with rough surfaces for controlled drug delivery and protein adsorption.
- Author
-
Zhang, Haijiao, Xu, Huijuan, Wu, Minghong, Zhong, Yufang, Wang, Donghai, and Jiao, Zheng
- Abstract
In this work, a novel type of hollow mesoporous silica nanoparticle (HMSN) with a rough surface has been successfully prepared via a facile soft–hard template route by using a carbon nanosphere as a hard template and cetyltrimethylammonium bromide (CTAB) as a soft template, respectively. This method involves the preparation of a carbon nanosphere, sequential coating of double SiO
2 layers, and the removal of the inner carbon core and CTAB to produce HMSNs. The obtained HMSNs possess spherical morphology, a mesoporous shell, and crumpled surfaces. The controlled experiments prove that the addition of 3-ammonia propyl triethoxy silane (APTES) is very crucial for the formation of desired HMSNs. The cell tests indicate that HMSNs show a good biocompatibility. As a result, the potential applications of HMSNs are further explored for drug delivery and protein adsorption, using doxorubicin hydrochloride (DOX) and Cytochrome c (Cyt c) as the model drug and protein, respectively. The HMSNs exhibit high drug loading and protein adsorption capacity, as well as the controlled pH-responsive release behavior for DOX. Therefore, the HMSNs prepared are ideal candidates for various applications such as nanoreactors, drug delivery and protein adsorption. [ABSTRACT FROM AUTHOR]- Published
- 2015
- Full Text
- View/download PDF
25. Transcriptomics changes and the candidate pathway in human macrophages induced by different PM2.5 extracts.
- Author
-
An, Jing, Tang, Waner, Wang, Lu, Xue, Wanlei, Yao, Weiwei, Zhong, Yufang, Qiu, Xinghua, Li, Yi, Chen, Yingjun, Wang, Hongli, and Shang, Yu
- Subjects
POLYCYCLIC aromatic hydrocarbons ,MACROPHAGES ,PARTICULATE matter ,CELL cycle ,TRANSCRIPTOMES - Abstract
Ambient fine particulate matter (PM 2.5) is a worldwide environmental problem and is posing a serious threat to human health. Until now, the molecular toxicological mechanisms and the crucial toxic components of PM 2.5 remain to be clarified. This study investigated the whole transcriptomic changes in THP-1 derived macrophages treated with different types of PM 2.5 extracts using RNA sequencing technique. Bioinformatics analyses covering biological functions, signal pathways, protein networks and node genes were performed to explore the candidate pathways and critical genes, and to find the potential molecular mechanisms. Results of Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes pathway (KEGG), and protein-protein interaction (PPI) networks revealed that water extracts (WEs) of PM 2.5 obviously influenced genes and molecular pathways responded to oxidative stress and inflammation. Dichloromethane extracts (DEs) specifically affected genes and signal cascades related to cell cycle progress process. Furthermore, compared with WEs collected in heating season, non-heating season WEs induced much higher expression levels of Ca-associated genes (including phosphodiesterase 4B and cyclooxygenase-2), which may consequently result in more severe inflammatory responses. While, for DEs exposure, the heating season (DH) group showed extensive induction of deferentially expressed genes (DEGs) related to cell cycle pathway, which may be caused by the higher polycyclic aromatic hydrocarbons (PAHs) contents in DH samples than those from non-heating season. In conclusion, the oxidative stress and inflammation response are closely correlated with cellular responses in THP-1 derived macrophages induced by water soluble components of PM 2.5 , and cell cycle dysregulation may play an important role in biological effects induced by organic components. The different transcriptomic changes induced by seasonal PM 2.5 extracts may partially depend on the contents of PAHs and metal ions, respectively. [Display omitted] • The oxidative stress and inflammation response are closely correlated with water soluble components-induced cytotoxicity. • Cell cycle dysregulation may play an important role in biological effects induced by organic components of PM 2.5. • The transcriptomic changes induced by seasonal PM 2.5 extracts partially depend on the contents of PAHs and metal ions. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
26. The cytotoxic effects of synthetic 6-hydroxylated and 6-methoxylated polybrominated diphenyl ether 47 (BDE47).
- Author
-
An, Jing, Li, Shuhui, Zhong, Yufang, Wang, Yipei, Zhen, Kewen, Zhang, Xinyu, Wang, Yangjun, Wu, Minghong, Yu, Zhiqiang, Sheng, Guoying, Fu, Jiamo, and Huang, Yuecheng
- Subjects
ENDOCRINE disruptors ,METABOLITES ,DNA damage ,ANTIOXIDANTS ,APOPTOSIS - Abstract
Polybrominated diphenyl ethers (PBDE) have been widely applied as flame retardants in plastics, polyurethane foam, paints, and synthetic fabrics. The rising PBDE level in human tissues and environment has led to concern about the health impact of exposure to PBDE. The 2,2′,4,4′-tetrabromodiphenyl ether (BDE47), the dominant PBDE congener found in the environment and human tissues, has been shown to be an endocrine disruptor. It has also been reported to cause liver and neurodevelopmental toxicity. BDE47 can be metabolized to 6-OH-BDE47 and 6-MeO-BDE47. So far little has been reported on the cytotoxicity of the metabolites. In the present study, the cytotoxicity of the two metabolites was investigated by exposing human hepatoma cell line HepG2 to different doses of 6-OH-BDE47 and 6-MeO-BDE47. The cell viability, cell cycle, apoptosis, DNA damage, micronucleus levels, and oxidative stress response were studied. The results indicated that both metabolites could markedly inhibit the proliferation of HepG2 cells with 6-OH-BDE47 showing a stronger effect, and significantly increase the micronucleus level and apoptosis rate in a dose-dependant manner. Moreover, treatment with 6-OH-BDE47 (≥0.5 μM) resulted in a marked cell cycle block. The SCGE experiments revealed that both metabolites could cause DNA damage in a dose-dependant manner. Analysis of the oxidative stress response showed that 6-OH-BDE47 treatment (≥2.0 μM) significantly increased intracellular ROS levels as indicated by GSH depletion and elevation of SOD level, whereas 6-MeO-BDE47 showed a weaker effect, suggesting that oxidative stress might play a role in the cytotoxic effects. We concluded that 6-OH-BDE47 or 6-MeO-BDE47 exposure was able to induce inhibition of cell viability, increase of apoptosis rate, cell cycle block, and DNA damages, which might involve the alterated oxidative stress response due to the elevated free radicals and impaired antioxidative system. © 2010 Wiley Periodicals, Inc. Environ Toxicol, 2011. [ABSTRACT FROM AUTHOR]
- Published
- 2011
- Full Text
- View/download PDF
27. The cytotoxic and genetoxic effects of dust and soil samples from E-waste recycling area on L02 cells.
- Author
-
Wang Liulin, Hou Meiling, An Jing, Zhong Yufang, Wang Xuetong, Wang Yangjun, Wu Minghong, Bi Xinhui, Sheng Guoying, and Fu Jiamo
- Subjects
CELL-mediated cytotoxicity ,GENETIC toxicology ,DUST ,ELECTRONIC waste ,WASTE recycling ,SOIL pollution ,CELL proliferation ,REACTIVE oxygen species ,DNA damage - Abstract
Electrical and electronic waste (E-waste) has now become the fastest growing solid waste around the world. Primitive recycling operations for E-waste have resulted in severe contamination of toxic metals and organic chemicals in the related areas. In this study, six dust and soil samples collected from E-waste recycling workshops and open-burning sites in Longtang were analyzed to investigate their cytotoxicity and genotoxicity on L02 cells. These six samples were: dust No. 1 collected at the gate of the workshop; dust No. 2 collected from air conditioning compressor dismantling site; dust No. 3 collected from where some motors, wires, and aluminium products since the 1980s were dismantled; soil No. 1 collected at the circuit board acid washing site; soil No. 2 collected from a wire open-burning site; soil No. 3 collected near a fiber open-burning site. At the same time, two control soil samples were collected from farmlands approximately 8 km away from the dismantling workshops. The results showed that all of these samples could inhibit cell proliferation and cause cell membrane lesion, among which dust No. 3 and soil No. 2 had the strongest toxicity. Moreover, the comet assay showed that the dust No. 3 had the most significant capability to cause DNA single-strand beaks (SSB), while the road dust (dust No. 1) collected at the gate of the workshop, a relatively farer site, showed the slightest capability to induce DNA SSB. The intracellular reactive oxygen species (ROS) detection showed that ROS level was elevated with the increase of dust and soil samples concentration. Dust No. 3 and soil No. 2 had the highest ROS level, followed by dust No. 2 and 1, soil No. 3 and 1. All of the above results indicated that polluted soil and dust from the E-waste area had cytotoxicity and genotoxicity on L02 cells, the mechanism might involve the increased ROS level and consequent DNA SSB. [ABSTRACT FROM PUBLISHER]
- Published
- 2011
- Full Text
- View/download PDF
28. Polystyrene nanoparticles induced neurodevelopmental toxicity in Caenorhabditis elegans through regulation of dpy-5 and rol-6.
- Author
-
Shang, Yu, Wang, Siyan, Jin, Yingying, Xue, Wanlei, Zhong, Yufang, Wang, Hongli, An, Jing, and Li, Hui
- Subjects
CAENORHABDITIS elegans ,POLYSTYRENE ,SURVIVAL rate ,GAIT disorders ,REACTIVE oxygen species - Abstract
Micro- and nano- polystyrene particles have been widely detected in environment, posing potential threats to human health. This study was designed to evaluate the neurodevelopmental toxicity of polystyrene nanoparticles (NPs) in Caenorhabditis elegans (C. elegans), to screen crucial genes and investigate the underlying mechanism. In wild-type C. elegans , polystyrene NPs (diameter 50 nm) could concentration-dependently induce significant inhibition in body length, survival rate, head thrashes, and body bending, accompanying with increase of reactive oxygen species (ROS) production, lipofuscin accumulation, and apoptosis and decrease of dopamine (DA) contents. Moreover, pink-1 mutant was demonstrated to alleviate the locomotion disorders and oxidative damage induced by polystyrene NPs, indicating involvement of pink-1 in the polystyrene NPs-induced neurotoxicity. RNA sequencing results revealed 89 up-regulated and 56 down-regulated differently expressed genes (DEGs) response to polystyrene NPs (100 μg/L) exposure. Gene Ontology (GO) enrichment analysis revealed that predominant enriched DEGs were correlated with biological function of cuticle development and molting cycle. Furthermore, mutant strains test showed that the neurodevelopmental toxicity and oxidative stress responses induced by 50 nm polystyrene NPs were regulated by dpy-5 and rol-6. In general, polystyrene NPs induced obvious neurodevelopmental toxicity in C. elegans through oxidative damage and dopamine reduction. Crucial genes dpy-5 and rol-6 might participate in polystyrene NPs-induced neurodevelopmental toxicity through regulation on synthesis and deposition of cuticle collagen. [Display omitted] • Polystyrene NPs induced oxidative stress, potentially resulting in cellular damages and neurodevelopmental toxicity. • The biological functions related with cuticle development were the predominant biological events of polystyrene NPs. • Dpy-5 and rol-6 were involved in regulation of polystyrene NPs-induced neurodevelopmental toxicity and oxidative damage. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
29. Causal Interactions Between the Default Mode Network and Central Executive Network in Patients with Major Depression.
- Author
-
Li, Jiaming, Liu, Jian, Zhong, Yufang, Wang, Huaning, Yan, Baoyu, Zheng, Kaizhong, Wei, Lei, Lu, Hongbing, and Li, Baojuan
- Subjects
- *
FRONTOPARIETAL network , *DEFAULT mode network , *MENTAL depression , *CAUSAL models - Abstract
• Causal interactions between the CEN and DMN in depressed patients were investigated by spectral dynamic causal modeling. • Inhibitory influences from the CEN to the DMN were detected with node-level PEB analyses. • Patients with MDD showed increased effective connectivity within the CEN. • Decreased connectivity from regions of the CEN to DMN was found in the patients. Two different but interacting neural systems exist in the human brain: the task positive networks and task negative networks. One of the most important task positive networks is the central executive network (CEN), while the task negative network generally refers to the default mode network (DMN), which usually demonstrates task-induced deactivation. Although previous studies have clearly shown the association of both the CEN and DMN with major depressive disorder (MDD), how the causal interactions between these two networks change in depressed patients remains unclear. In the current study, 99 subjects (43 patients with MDD and 56 healthy controls) were recruited with their resting-state fMRI data collected. After data preprocessing, spectral dynamic causal modeling (spDCM) was used to investigate the causal interactions within and between the DMN and CEN. Group commonalities and differences in causal interaction patterns within and between the CEN and DMN in patients and controls were assessed by a parametric empirical Bayes (PEB) model. Both subject groups demonstrated significant effective connectivity between regions of the CEN and DMN. In particular, we detected inhibitory influences from the CEN to the DMN with node-level PEB analyses, which may help to explain the anticorrelations between these two networks consistently reported in previous studies. Compared with healthy controls, patients with MDD showed increased effective connectivity within the CEN and decreased connectivity from regions of the CEN to DMN, suggesting impaired control of the DMN by the CEN in these patients. These findings might provide new insights into the neural substrates of MDD. [ABSTRACT FROM AUTHOR]
- Published
- 2021
- Full Text
- View/download PDF
30. GW26-e2274 AVE 0991, Nonpeptide angiotensin-(1-7) analogue, modulates cardiac hypertrophy via reducing oxidative stress.
- Author
-
Chen, Yili, Zhong, Yufang, Lin, Chunxi, Lu, Guiying, Huang, Huiling, and Ma, Yuedong
- Subjects
- *
CARDIAC hypertrophy , *ANGIOTENSINS , *OXIDATIVE stress , *NADPH oxidase , *PROTEIN expression - Published
- 2015
- Full Text
- View/download PDF
31. The hormesis effect of BDE-47 in HepG2 cells and the potential molecular mechanism
- Author
-
Wang, Liulin, Zou, Wen, Zhong, Yufang, An, Jing, Zhang, Xinyu, Wu, Minghong, and Yu, Zhiqiang
- Subjects
- *
HORMESIS , *POLYBROMINATED diphenyl ethers , *BROMINE , *ENDOCRINE diseases , *IMMUNOTOXICOLOGY , *DNA damage , *CELL proliferation - Abstract
Abstract: Polybrominated diphenyl ethers (PBDEs) had been used extensively in electrical and electronic products as brominated flame retardants. PBDEs are widely distributed in environment media and wildlife since they are lipophilic and persistent, resulting in bioaccumulation and bioamplification through food chains. Accumulation of PBDEs in the environment and human tissues will consequently cause potential negative effects on the ecological environment and human health. To date, some in vitro and in vivo studies have reported that PBDEs possess neurotoxicity, hepatotoxicity, immunotoxicity, reproduction toxicity, endocrine disrupting activity and carcinogenicity. BDE-47 is one of the most predominant PBDE congeners detected in human tissues. The objective of this study is to investigate whether low concentration of BDE-47 could cause hormesis effect in the human hepatoma HepG2 cells, and to explore the possible molecular mechanism. The results showed that low concentration of BDE-47 (10−10, 10−9 and 10−8 M) could promote cell proliferation and cause no obvious change in DNA damage or cell apoptosis, while the high concentration significantly inhibit cell proliferation. Meanwhile, the reactive oxygen species (ROS) in low concentration BDE-47 (10−10, 10−9 and 10−8 M) treated groups significantly elevated compared with the control group. After low concentration BDE-47 treatment, the expression of proliferating cell nuclear antigen (PCNA), Cyclin D1, DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and phosphorylated protein kinase B (p-Akt) in the HepG2 cells was markedly up-regulated. However, in DNA-PKcs inhibited cells, the promotion effect on cell proliferation was significantly suppressed. Cell cycle analysis showed a significant decrease in G1 phase after exposure to low concentration of BDE-47. Moreover, pre-exposure to low concentration BDE-47 seemed alleviate the negative effects of high concentration (50μM) exposure to cause DNA damage and apoptosis. These results suggested that BDE-47 has a hormesis effect in HepG2 cells and DNA-PKcs/Akt pathway may be involved in regulation of cell proliferation and apoptosis. [Copyright &y& Elsevier]
- Published
- 2012
- Full Text
- View/download PDF
32. The transepithelial transport mechanism of polybrominated diphenyl ethers in human intestine determined using a Caco-2 cell monolayer.
- Author
-
Yu, Yingxin, Wang, Mengmeng, Zhang, Kaiqiong, Yang, Dan, Zhong, Yufang, An, Jing, Lei, Bingli, and Zhang, Xinyu
- Subjects
- *
POLYBROMINATED diphenyl ethers , *GUT microbiome , *PH effect , *PROTEIN transport , *CHEMICAL kinetics - Abstract
Oral ingestion plays an important role in human exposure to polybrominated diphenyl ethers (PBDEs). The uptake of PBDEs primarily occurs in the small intestine. The aim of the present study is to investigate the transepithelial transport characteristics and mechanisms of PBDEs in the small intestine using a Caco-2 cell monolayer model. The apparent permeability coefficients of PBDEs indicated that tri- to hepta-BDEs were poorly absorbed compounds. A linear increase in transepithelial transport was observed with various concentrations of PBDEs, which suggested that passive diffusion dominated their transport at the concentration range tested. In addition, the pseudo-first-order kinetics equation can be applied to the transepithelial transport of PBDEs. The rate-determining step in transepithelial transport of PBDEs was trans-cell transport including the trans-pore process. The significantly lower transepithelial transport rates at low temperature for bidirectional transepithelial transport suggested that an energy-dependent transport mechanism was involved. The efflux transporters (P-glycoprotein, multidrug resistance-associated protein, and breast cancer resistance protein) and influx transporters (organic cation transporters) participated in the transepithelial transport of PBDEs. In addition, the transepithelial transport of PBDEs was pH sensitive; however, more information is required to understand the influence of pH. [ABSTRACT FROM AUTHOR]
- Published
- 2017
- Full Text
- View/download PDF
33. In vitro study on the biotransformation and cytotoxicity of three hexabromocyclododecane diastereoisomers in liver cells.
- Author
-
Huang, Xiaomei, Chen, Cen, Shang, Yu, Zhong, Yufang, Ren, Guofa, Yu, Zhiqiang, and An, Jing
- Subjects
- *
HEXABROMOCYCLODODECANE , *DIASTEREOISOMERS , *CELL-mediated cytotoxicity , *BIOTRANSFORMATION (Metabolism) , *LIVER cells , *DNA damage , *IN vitro studies - Abstract
In order to clarify the cytotoxicity of hexabromocyclododecane (HBCD) diastereoisomers, and to investigate the correlation of cytotoxicity and biotransformation of HBCDs, the immortalized human liver cells L02 and human hepatoma cells HepG2 were exposed to individual HBCD diastereoisomer (α-, β- and γ-HBCD). Cytotoxicity was assayed in terms of cell viability, reactive oxygen species (ROS) level and DNA damage. Metabolic rate, bioisomerization and enantiomer fractions were analyzed using the liquid chromatograph coupled to triple quadrupole mass spectrometer (LC-MS/MS). The α-, β- and γ-HBCD all had cytotoxicity in L02 and HepG2 cells with the toxicity order β-HBCD ≥ γ-HBCD > α-HBCD according to the results of proliferation assay. The cytotoxicity mechanism between the two cells seemed different: a) the stability of intracellular redox state plays an important role in inducing cell toxicity in HepG2 cells. b) DNA damage status is central to inhibit proliferation in L02 cells. The metabolic capability of HepG2 was superior to L02 for HBCD diastereoisomers, which may explain the greater toxicity of HBCDs in HepG2 cells. The bioisomerization and enantiomer enrichment were also detected in this study, although the results were inconsistent with other reports, which might result from species-specific differences in HBCDs metabolism or experimental conditions. The cytotoxicity and metabolic mechanism of individual enantiomers must be further investigated to evaluate the health risks of HBCDs. [ABSTRACT FROM AUTHOR]
- Published
- 2016
- Full Text
- View/download PDF
34. GW26-e1586 AMPK attenuates proliferation of cardiac fibroblast via regulating TGF-β1/Smad pathways.
- Author
-
Chen, Yili, Lin, Chunxi, Zhong, Yufang, Lu, Guiying, Ma, Yuedong, and Huang, Huiling
- Subjects
- *
PROTEIN kinases , *FIBROBLASTS , *CARDIOMYOPATHIES , *CELL proliferation , *TRANSFORMING growth factors , *SMAD proteins - Published
- 2015
- Full Text
- View/download PDF
35. The “adaptive responses” of low concentrations of HBCD in L02 cells and the underlying molecular mechanisms.
- Author
-
An, Jing, Guo, Panpan, Shang, Yu, Zhong, Yufang, Zhang, Xinyu, Yu, Yingxin, and Yu, Zhiqiang
- Subjects
- *
HEXABROMOCYCLODODECANE , *ENVIRONMENTAL chemistry , *LIVER cells , *POLYBROMINATED diphenyl ethers , *REACTIVE oxygen species , *DNA damage - Abstract
This study aimed to investigate the “adaptive responses” of hexabromocyclododecanes (HBCD) at environmentally relevant concentrations in human hepatocytes L02. L02 cells were pre-treated with low concentrations of HBCD (10 −13 –10 −11 M), followed by treatment with high concentrations of HBCD, α-hexachlorocyclohexane (α-HCH), polychlorinated biphenyls (PCBs), or polybrominated diphenyl ether-47 (BDE47). The results showed that the pre-treatment with low concentrations of HBCD induced “adaptive responses” to high concentrations of HBCD/α-HCH exposure (but not to PCBs and BDE47), as evidenced by attenuation of survival inhibition, reactive oxygen species (ROS) over-production, and deoxyribonucleic acid (DNA) damage induction. The “adaptive responses” induced by low concentrations of HBCD, which depended on the activation of the phosphatidylinositide 3-kinase/protein kinase B (PI3K/Akt) pathway, reduced the phosphorylation of adenosine monophosphate-activated kinase (AMPK) and enhanced the phosphorylation of p38 mitogen-activated protein kinases (p38 MAPK). The observations were further confirmed by the experiments with inhibitors. Moreover, the evaluation on the changes of metabolic enzymes revealed that HBCD and α-HCH shared a similar pattern of cytochrome P450 induction (CYP2B6), which was different from those of PCBs and BDE47 (CYP1A1 and CYP2B6). These results indicated that low concentrations of HBCD could induce “adaptive responses” to the subsequent treatment with high concentrations of HBCD/α-HCH in L02 cells, which was associated with the PI3K/Akt pathway, and AMPK and p38 MAPK signaling. The “adaptive responses” seemed to be dependent on the types of chemicals in terms of the metabolic patterns and chemical structures. [ABSTRACT FROM AUTHOR]
- Published
- 2016
- Full Text
- View/download PDF
36. Sperm DNA integrity is critically impacted by male age but does not influence outcomes of artificial insemination by husband in the Chinese infertile couples.
- Author
-
Luo Y, Wu S, Zhang M, Zhou H, Yuan J, Yang Y, Zhong Y, Li Q, Sun X, Xu X, and Zhu D
- Subjects
- China, Chromatin, DNA, DNA Fragmentation, Female, Humans, Insemination, Artificial, Male, Pregnancy, Retrospective Studies, Spermatozoa, Infertility, Spouses
- Abstract
The sperm chromatin structure assay (SCSA) is crucial for assessing male fertility. However, the predictive value of the SCSA parameters, including the DNA fragment indices (DFI) and the percentages of high DNA stainability (HDS), for outcomes of artificial insemination by husband (AIH) remains controversial. This study aims to evaluate the correlations between SCSA parameters and male aging as well as other routine semen parameters, and explore their prognostic powers on AIH outcomes of the Chinese infertile couples. A total of 809 AIH cycles were retrospectively analyzed. The results showed that DFI in the age groups < 35 years were significantly lower than that in the age groups ≥ 35 years (P < 0.001). Meanwhile, there was no statistical difference in HDS between the age groups (P = 0.063). DFI and HDS are negatively correlated with most routine semen parameters (all P < 0.05). The chi-square and generalized linear model tests indicated that neither DFI nor HDS influenced the clinical pregnancy rate of AIH. In summary, this study found that aging is a critical factor leading to increased sperm DFI but not HDS. DFI and HDS are negatively correlated with most semen parameters but do not significantly influence AIH outcomes.
- Published
- 2022
- Full Text
- View/download PDF
37. Gratitude Intervention Evokes Indebtedness: Moderated by Perceived Social Distance.
- Author
-
He W, Qiu J, Chen Y, and Zhong Y
- Abstract
Previous study suggests that gratitude intervention evokes indebtedness among people from an interdependent society. This study furtherly hypothesized that perceived social distance moderates the effect of gratitude intervention on felt indebtedness. A total of 275 adolescents were randomly assigned to three gratitude intervention conditions, namely, writing gratitude to significant others, the health of one's own, or nothing. After completing the writing task, they rated their experienced emotions on ten dimensions, including gratitude and indebtedness. They also reported perceived social distance from surrounding people and other demographical information. Results indicated that participants in the condition of writing about gratitude to significant others felt indebted regardless of perceived social distance, while those in the condition of writing about gratitude to his/her own health and those in the control condition experienced lesser indebtedness as the perceived social distance with others becomes closer. Gratitude increases as perceived social connectedness increases across all conditions. Theoretical and practical implications were discussed., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 He, Qiu, Chen and Zhong.)
- Published
- 2022
- Full Text
- View/download PDF
38. Transcriptomics changes and the candidate pathway in human macrophages induced by different PM 2.5 extracts.
- Author
-
An J, Tang W, Wang L, Xue W, Yao W, Zhong Y, Qiu X, Li Y, Chen Y, Wang H, and Shang Y
- Subjects
- Humans, Macrophages, Particulate Matter analysis, Particulate Matter toxicity, Transcriptome, Air Pollutants analysis, Air Pollutants toxicity, Polycyclic Aromatic Hydrocarbons toxicity
- Abstract
Ambient fine particulate matter (PM
2.5 ) is a worldwide environmental problem and is posing a serious threat to human health. Until now, the molecular toxicological mechanisms and the crucial toxic components of PM2.5 remain to be clarified. This study investigated the whole transcriptomic changes in THP-1 derived macrophages treated with different types of PM2.5 extracts using RNA sequencing technique. Bioinformatics analyses covering biological functions, signal pathways, protein networks and node genes were performed to explore the candidate pathways and critical genes, and to find the potential molecular mechanisms. Results of Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes pathway (KEGG), and protein-protein interaction (PPI) networks revealed that water extracts (WEs) of PM2.5 obviously influenced genes and molecular pathways responded to oxidative stress and inflammation. Dichloromethane extracts (DEs) specifically affected genes and signal cascades related to cell cycle progress process. Furthermore, compared with WEs collected in heating season, non-heating season WEs induced much higher expression levels of Ca-associated genes (including phosphodiesterase 4B and cyclooxygenase-2), which may consequently result in more severe inflammatory responses. While, for DEs exposure, the heating season (DH) group showed extensive induction of deferentially expressed genes (DEGs) related to cell cycle pathway, which may be caused by the higher polycyclic aromatic hydrocarbons (PAHs) contents in DH samples than those from non-heating season. In conclusion, the oxidative stress and inflammation response are closely correlated with cellular responses in THP-1 derived macrophages induced by water soluble components of PM2.5 , and cell cycle dysregulation may play an important role in biological effects induced by organic components. The different transcriptomic changes induced by seasonal PM2.5 extracts may partially depend on the contents of PAHs and metal ions, respectively., (Copyright © 2021 Elsevier Ltd. All rights reserved.)- Published
- 2021
- Full Text
- View/download PDF
39. Evaluation of Prognostic Factors for Clinical Pregnancy Rate Following Artificial Insemination by Husband in the Chinese Population.
- Author
-
Luo Y, Wu S, Yuan J, Zhou H, Zhong Y, Zhang M, Li Q, Xu X, Sun X, and Zhu D
- Abstract
Background: To determine the independent prognostic factors and develop a multivariate logistic regression model for predicting successful pregnancy following artificial insemination by husband (AIH) in infertile Chinese couples. Methods: A total of 3,015 AIH cycles with superovulation from 1,853 infertile Chinese couples were retrospectively analyzed. The clinical characteristics and sperm parameters were compared between the pregnant and non-pregnant groups. Multivariate logistic regression analysis was performed to remove the confounding factors and create an equation to predict the successful pregnancy. Receiver operating characteristic (ROC) curves were constructed for evaluating the abilities for prognostic classification of the independent predictors and the equation. Results: The overall pregnancy rate was 13.0%. The pregnancy rate of double intrauterine insemination (IUI) (18.9%) was significantly higher than that of single IUI (11.4%). The pregnancy rate of the stimulated cycle (14.4%) was significantly higher than that of the natural cycle (9.0%). The pregnancy rates of the age groups <40 years are ~3 times higher than that of the ≥40 years age group. Among sperm parameters, the influencing factors included straight-line velocity (VSL), sperm deformity index (SDI), and normal form rate (all P < 0.05). A multivariate logistic regression equation was created based on the above influencing factors. ROC analysis showed that the prognostic power of the equation is better than those of individual predictors. Conclusion: Cycle treatment options, single/double IUI, female age, sperm VSL, SDI, and normal form rate could predict successful pregnancy following AIH in China. The multivariate logistic regression equation exhibited a greater value for prognostic classification than single predictors., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Luo, Wu, Yuan, Zhou, Zhong, Zhang, Li, Xu, Sun and Zhu.)
- Published
- 2021
- Full Text
- View/download PDF
40. Fresh and ozonized black carbon promoted DNA damage and repair responses in A549 cells.
- Author
-
An J, He H, Wang L, Jin Y, Kong J, Zhong Y, Liu M, and Shang Y
- Abstract
Nano-sized ambient black carbon (BC) is hypothesized to pose a serious threat to human health. After emission into the air, the atmospheric oxidation process can modify its physiochemical properties and change its biological responses. In this study, we aimed to compare different DNA damage and repair responses promoted by fresh BC (FBC) and ozone oxidized-BC (OBC). The cell apoptosis, cell arrest, DNA damage and repair were investigated in A549 cells after treatment with FBC and OBC. Associated gene expressions were measured with the reverse transcription quantitative polymerase chain reaction (RT-qPCR) method. Both FBC and OBC could induce cell apoptosis in A549 cells with up-regulated gene of promyelocytic leukemia protein ( pml ) and down-regulated gene of anti-apoptotic B-cell lymphoma-2 ( bcl-2 ). FBC caused cell cycle arrest at S and G2/M phases, which was associated with up-regulated ataxia telangiectasia mutated ( atm ), checkpoint kinase 2 ( chk2 ), structural maintenance of chromosomes 1 ( smc1 ) and cell division cycle 25 homolog A ( cdc25a ) genes. OBC promoted cell cycle arrest at the S phase with up-regulated genes of atm , chk2 and smc1 . Both FBC and OBC induced oxidative DNA damage and time-dependent DNA repair responses with increased gene expressions of breast cancer susceptibility protein 1 ( brca1 ), recombination protein A paralog B ( rad51b ), methyl methanesulfonate-sensitivity protein 22-like and tonsoku-like ( mms22l ). Compared to FBC, OBC could cause more sufficient DNA damage repair responses through cell cycle arrest at the S phase, resulting in relatively weaker DNA damages.
- Published
- 2018
- Full Text
- View/download PDF
41. Comparison of hepatotoxicity and mechanisms induced by triclosan (TCS) and methyl-triclosan (MTCS) in human liver hepatocellular HepG2 cells.
- Author
-
Wang L, Mao B, He H, Shang Y, Zhong Y, Yu Z, Yang Y, Li H, and An J
- Abstract
Triclosan (TCS) is used as an antimicrobial agent and has been widely dispersed and detected in the environment and organisms including human samples. Methyl-triclosan (MTCS) is the predominant bacterial TCS metabolite. At present, the toxicological effects and mechanism of TCS and MTCS are still not fully understood. In this study, the cytotoxic effects of TCS and MTCS in HepG2 cells were investigated in terms of cell proliferation, comet assay, cell cycle, and apoptosis. In addition, the expressions of related proteins were detected with western blotting analysis. The results showed that TCS could significantly inhibit cell proliferation, while MTCS had no obvious effect on cell growth. Both TCS and MTCS caused oxidative injury associated with HO-1 induction and increased DNA strand breaks, which consequently initiated the damage repair process via up-regulation of DNA-PKcs. In addition, TCS blocked the HepG2 cells in S and G2/M phases of cell cycle through down-regulation of cyclin A2 and CDK; while MTCS induced cell cycle arrest at the S phase through up-regulation of cyclin A2 and CDK. Furthermore, TCS activated p53 mediated apoptosis in HepG2 cells in a caspase-independent manner, while MTCS induced apoptosis was dependent on caspase. Moreover, TCS exposure exhibited more severe toxicity in HepG2 cells as compared with MTCS exposure, indicating that the replacement of the ionizable proton in TCS by the methyl group in MTCS is correlated with the cellular toxicity and the molecular mechanism.
- Published
- 2018
- Full Text
- View/download PDF
42. Aroclor 1254 inhibits cell viability and induces apoptosis of human A549 lung cancer cells by modulating the intracellular Ca(2+) level and ROS production through the mitochondrial pathway.
- Author
-
Zhong Y, Guo P, Wang X, and An J
- Subjects
- Cell Line, Tumor, Cell Survival drug effects, Cytochromes c metabolism, Humans, Lung Neoplasms metabolism, Membrane Potential, Mitochondrial drug effects, Mitochondria drug effects, Reactive Oxygen Species metabolism, Apoptosis drug effects, Calcium metabolism, Chlorodiphenyl (54% Chlorine) pharmacology, Lung Neoplasms drug therapy, Lung Neoplasms pathology, Mitochondria metabolism
- Abstract
To study the acute toxic effects of PCBs on airway exposure, the cell viability, apoptosis and mitochondrial functions of human lung cancer cell line A549 were measured and compared after Aroclor 1254 exposure for different time. The results showed that Aroclor 1254 could inhibit cell viability and increase cell apoptosis in a concentration- and time-dependent manner. The mitochondrial apoptosis pathway was confirmed playing an important role. ROS elevation was an early response within 1h treatment of Aroclor 1254. Then after 4 h of Aroclor 1254 exposure, the intracellular calcium level increased and mitochondrial transmembrane potential (ΔΨm) collapsed, accompanying with Cytochrome c (Cyt-c) leakage, boosting expression of Bax, Apaf-1 and miRNA155, which were involved in the mitochondrial apoptosis pathway. After 24 h of Aroclor 1254 exposure, ROS returned to normal level, but cell apoptosis rate was higher than that at 4 h with ΔΨm continued collapsing and intracellular calcium increased. In conclusion, Aroclor 1254 could suppress cell viability and induce apoptosis in A549 cells, which was associated with ROS over-production and elevated cellular Ca(2+) level, which may result in mitochondrial dysfunction, inducing expression of Bax/Cyt-c/Apaf-1 and miRNA155.
- Published
- 2015
- Full Text
- View/download PDF
43. Altered effective connectivity patterns of the default mode network in Alzheimer's disease: an fMRI study.
- Author
-
Zhong Y, Huang L, Cai S, Zhang Y, von Deneen KM, Ren A, and Ren J
- Subjects
- Aged, Aged, 80 and over, Brain Mapping, Female, Humans, Magnetic Resonance Imaging, Male, Middle Aged, Alzheimer Disease physiopathology, Brain physiopathology, Nerve Net physiopathology
- Abstract
The aim of this work is to investigate the differences of effective connectivity of the default mode network (DMN) in Alzheimer's disease (AD) patients and normal controls (NC). The technique of independent component analysis (ICA) was applied to identify DMN components and multivariate Granger causality analysis (mGCA) was used to explore an effective connectivity pattern. We found that: (i) connections in AD were decreased than those in NC, in terms of intensity and quantity. Posterior cingulated cortex (PCC) exhibited significant activity in NC as it connected with most of the other regions within the DMN. Besides, the PCC was the convergence center which only received interactions from other regions; (ii) right inferior temporal cortex (rITC) in the NC exhibited stronger interactions with other regions within the DMN compared with AD patients; and (iii) interactions between medial prefrontal cortex (MPFC) and bilateral inferior parietal cortex (IPC) in the NC were weaker than those in AD patients. These findings may implicate a brain dysfunction in AD patients and reveal more pathophysiological characteristics of AD., (Copyright © 2014 Elsevier Ireland Ltd. All rights reserved.)
- Published
- 2014
- Full Text
- View/download PDF
44. PI3K/Akt pathway mediates Nrf2/ARE activation in human L02 hepatocytes exposed to low-concentration HBCDs.
- Author
-
Zou W, Chen C, Zhong Y, An J, Zhang X, Yu Y, Yu Z, and Fu J
- Subjects
- Cell Nucleus drug effects, Cell Nucleus metabolism, Cell Proliferation drug effects, DNA-Activated Protein Kinase metabolism, Gene Expression Regulation drug effects, Gene Silencing drug effects, Heme Oxygenase-1 metabolism, Hepatocytes drug effects, Hepatocytes enzymology, Humans, NF-E2-Related Factor 2 genetics, Nuclear Proteins metabolism, Protein Transport drug effects, Antioxidant Response Elements genetics, Hepatocytes metabolism, Hydrocarbons, Brominated toxicity, NF-E2-Related Factor 2 metabolism, Phosphatidylinositol 3-Kinases metabolism, Proto-Oncogene Proteins c-akt metabolism, Signal Transduction drug effects
- Abstract
We investigated the effects of hexabromocyclododecanes (HBCDs) at environmentally relevant concentrations on human L02 hepatocytes and explored possible underlying molecular mechanism(s), focusing on functional interactions between the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) and nuclear factor-erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) pathways. The results showed that low concentrations of HBCDs could stimulate cell proliferation in a "DNA-dependent protein kinase catalytic subunit" (DNA-PKcs)-dependent manner, increase protein levels and nuclear translocation of transcription factor Nrf2, and upregulate expression of its target gene heme oxygenase-1 (HO-1). Electrophoretic mobility-shift assays (EMSAs) showed that ARE was a prominent element for HO-1 induction after low-concentration HBCDs exposure. The relationship between PI3K/Akt pathway and Nrf2/HO-1 axis was demonstrated by the finding that pretreatment with PI3K inhibitors (wortmannin, LY294002) attenuated the upregulation of Nrf2 expression induced by HBCDs exposure. Furthermore, knock-down of DNA-PKcs through small interfering RNA blocked Nrf2/HO-1 axis activation in L02 cells exposed to low-concentration HBCDs. Moreover, DNA-PKcs and phosphorylated Akt at Ser(473) proved to be crucial in regulating the Nrf2-ARE pathway. Thus, the PI3K/Akt pathway is essential in regulating Nrf2-ARE pathway activation in L02 cells induced by low-concentration HBCDs.
- Published
- 2013
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.