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  • 11
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    Online Resource
    Emodin alleviates LPS ‐induced myocardial injury through inhibition of NLRP3 inflammasome activation
    Wiley ; 2021
    In:  Phytotherapy Research Vol. 35, No. 9 ( 2021-09), p. 5203-5213
    Details
    In: Phytotherapy Research, Wiley, Vol. 35, No. 9 ( 2021-09), p. 5203-5213
    Abstract: Myocardial injury and cardiovascular dysfunction are serious consequences of sepsis and contribute to high mortality. Currently, the pathogenesis of myocardial injury in sepsis is still unclear, and therapeutic approaches are limited. In this study, we investigated the protective effect of emodin on septic myocardial injury and the underlying mechanism. Lipopolysaccharide (LPS)‐induced C57BL/6 mice and cardiomyocytes were used as models of sepsis in vivo and in vitro, respectively. The results showed that emodin alleviated cardiac dysfunction, myocardial injury and improved survival rate in LPS‐induced septic mice. Emodin attenuated the levels of inflammatory cytokines and cardiac inflammation induced by LPS. Emodin reduced NOD‐like receptor protein 3 (NLRP3) and Gasdermin D (GSDMD) expression in the heart tissue of LPS‐induced septic mice. In vitro, emodin alleviated LPS‐induced cell injury and inflammation in cardiomyocytes by inhibiting NLRP3 inflammasome activation. In addition, an NLRP3 inhibitor was used to further confirm the function of the NLRP3 inflammasome in LPS‐induced myocardial injury. Taken together, our findings suggest that emodin improves LPS‐induced myocardial injury and cardiac dysfunction by alleviating the inflammatory response and cardiomyocyte pyroptosis by inhibiting NLRP3 inflammasome activation, which provides a feasible strategy for preventing and treating myocardial injury in sepsis.
    Type of Medium: Online Resource
    ISSN: 0951-418X , 1099-1573
    URL: Issue
    URL: Article
    DOI: 10.1002/ptr.v35.9
    DOI: 10.1002/ptr.7191
    Language: English
    Publisher: Wiley
    Publication Date: 2021
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  • 12
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    Disordered farnesoid X receptor signaling is associated with liver carcinogenesis in Abcb11 ‐deficient mice
    Wiley ; 2021
    In:  The Journal of Pathology Vol. 255, No. 4 ( 2021-12), p. 412-424
    Details
    In: The Journal of Pathology, Wiley, Vol. 255, No. 4 ( 2021-12), p. 412-424
    Abstract: ABCB11 encodes the bile salt export pump (BSEP), a key regulator in maintaining bile acid (BA) homeostasis. Although inherited ABCB11 mutations have previously been linked to primary liver cancer, whether ABCB11 deficiency leads to liver cancer remains unknown. Here, we analyzed ABCB11 mRNA expression levels in liver tumor specimens [29 with hepatocellular carcinoma (HCC), one with intrahepatic cholangiocarcinoma (ICC), and one with mixed HCC/ICC] with adjacent normal specimens and published human datasets. Liver tissues obtained from Abcb11 ‐deficient ( Abcb11 −/− ) mice and wild‐type mice at different ages were compared by histologic, RNA‐sequencing, and BA analyses. ABCB11 was significantly downregulated in human liver tumors compared with normal controls. Abcb11 −/− mice demonstrated progressive intrahepatic cholestasis and liver fibrosis, and spontaneously developed HCC and ICC over 12 months of age. Abcb11 deficiency increased BAs in the liver and serum in mice, most of which are farnesoid X receptor (FXR) antagonists/non‐agonists. Accordingly, the hepatic expression and transcriptional activity of FXR were downregulated in Abcb11 −/− mouse livers. Administration of the FXR agonist obeticholic acid reduced liver injury and tumor incidence in Abcb11 −/− mice. In conclusion, ABCB11 is aberrantly downregulated and plays a vital role in liver carcinogenesis. The cholestatic liver injury and liver tumors developed in Abcb11 −/− mice are associated with increased FXR antagonist BAs and thereby decreased activation of FXR. FXR activation might be a therapeutic strategy in ABCB11 deficiency diseases. © 2021 The Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
    Type of Medium: Online Resource
    ISSN: 0022-3417 , 1096-9896
    URL: Issue
    URL: Article
    DOI: 10.1002/path.v255.4
    DOI: 10.1002/path.5780
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 1475280-3
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  • 13
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    Growth arrest‐specific 5 attenuates cisplatin‐induced apoptosis in cervical cancer by regulating STAT3 signaling via miR‐21
    Wiley ; 2019
    In:  Journal of Cellular Physiology Vol. 234, No. 6 ( 2019-06), p. 9605-9615
    Details
    In: Journal of Cellular Physiology, Wiley, Vol. 234, No. 6 ( 2019-06), p. 9605-9615
    Abstract: Cervical cancer is the most common cause of female cancer‐related mortality worldwide. Decreased expression of long noncoding RNA growth arrest‐specific 5 (GAS5) is found in human cervical cancer tissues and associated with poor prognosis. However, the studies on associations between GAS5 level and malignant phenotypes, as well as sensitivity to chemotherapeutic drug in cervical cancer cells are limited. In this study, overexpression of GAS5 in cervical cancer cells resulted in prohibited cell proliferation and colony formation, which were promoted by siGAS5. Enhanced GAS5 increased cell percentage in the G0/G1 phase and decreased cells percentage in the S phase, whereas reduced expression did not. The malignant behaviors of cervical cancer cells, manifested by cell migration and invasion, could be weakened by the GAS5 overexpression and enhanced by siGAS5. Furthermore, in cisplatin‐induced cell, overexpression of GAS5 reduced cells viability and enhanced apoptosis, whereas in cells transfected with siGAS5, apoptosis eliminated. We have reported the upregulation of microRNA‐21 (miR‐21) and its oncogenetic roles in cervical cancer previously. In this study, we found the negative relationship between the GAS5 and miR‐21. Moreover, the decrease of miR‐21 associated proteins phosphorylated STAT3 and E2F3 was seen in GAS5 overexpressed cells, both of which could be increased by siGAS5. The GAS5 deficiency also reduced miR‐21 target proteins TIMP3 and PDCD4 expressions. Taken together, the GAS5 expression level is inversely associated with malignancy, but positively associated with sensitivity to cisplatin‐induced apoptosis, suggesting that GAS5 could be a biomarker of cisplatin‐resistance in clinical therapy of human cervical cancer.
    Type of Medium: Online Resource
    ISSN: 0021-9541 , 1097-4652
    URL: Issue
    URL: Article
    DOI: 10.1002/jcp.v234.6
    DOI: 10.1002/jcp.27647
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 1478143-8
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  • 14
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    Optimized Animal Model of Cyclophosphamide‐induced Bone Marrow Suppression
    Wiley ; 2016
    In:  Basic & Clinical Pharmacology & Toxicology Vol. 119, No. 5 ( 2016-11), p. 428-435
    Details
    In: Basic & Clinical Pharmacology & Toxicology, Wiley, Vol. 119, No. 5 ( 2016-11), p. 428-435
    Abstract: Myelosuppression is one of the serious side effects of anticancer chemotherapeutic drugs that deteriorate the bodily functions of patients, thereby affecting the quality of life considerably. Prevention of myelosuppression in anticancer chemotherapy is an important research topic. A stabilized chemotherapy‐induced myelosuppression animal model is necessary in experimental research. This study aimed to establish an optimized animal model of chemotherapy‐induced bone marrow suppression. After C57 BL /6 mice were treated with intermediate‐ and high‐dose (25/50 mg/kg) cyclophosphamide ( CTX ) for 10 days, the body‐weight, changes in thymus and spleen, number of white blood cells ( WBC s), red blood cells ( RBC s), and platelets ( PLT s) and changes in bone marrow in the mice were systematically evaluated at the next 2, 7 and 14 days. Our results demonstrated that CTX treatments could significantly decrease the body‐weight of mice, as well as the ratios of the weights of thymus and spleen to body‐weight. The physiological structures of thymus and spleen were destroyed by CTX treatments. The number of WBC s and RBC s significantly declined after CTX treatments; however, the number of PLT s increased. Moreover, the expression of Sca1 in bone marrow cells decreased on Day 2 but increased on Day 14. The expression of CD 34 decreased in bone marrow cells after CTX treatments. In conclusion, mice models, with high‐dose CTX treatments for 10 days, can be an optimized animal model for chemotherapy‐induced bone marrow suppression.
    Type of Medium: Online Resource
    ISSN: 1742-7835 , 1742-7843
    URL: Issue
    URL: Article
    DOI: 10.1111/bcpt.2016.119.issue-5
    DOI: 10.1111/bcpt.12600
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2151592-X
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  • 15
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    An Effective Machine Learning Approach for Prognosis of Paraquat Poisoning Patients Using Blood Routine Indexes
    Wiley ; 2017
    In:  Basic & Clinical Pharmacology & Toxicology Vol. 120, No. 1 ( 2017-01), p. 86-96
    Details
    In: Basic & Clinical Pharmacology & Toxicology, Wiley, Vol. 120, No. 1 ( 2017-01), p. 86-96
    Abstract: The early identification of toxic paraquat ( PQ ) poisoning in patients is critical to ensure timely and accurate prognosis. Although plasma PQ concentration has been reported as a clinical indicator of PQ poisoning, it is not commonly applied in practice due to the inconvenient necessary instruments and operation. In this study, we explored the use of blood routine indexes to identify the degree of PQ toxicity and/or diagnose PQ poisoning in patients via machine learning approach. Specifically, we developed a method based on support vector machine combined with the feature selection technique to accurately predict PQ poisoning risk status, then tested the method on 79 (42 male and 37 female; 41 living and 38 deceased) patients. The detection method was rigorously evaluated against a real‐world data set to determine its accuracy, sensitivity and specificity. Feature selection was also applied to identify the factors correlated with risk status, and the results showed that there are significant differences in blood routine indexes between dead and living PQ ‐poisoned individuals ( p ‐value 〈 0.01). Feature selection also showed that the most important correlated indexes are white blood cell and neutrophils. In conclusion, the toxicity or prognosis of PQ poisoning can be preliminarily ascertained by blood routine testing without PQ concentration data, representing an additional tool and innovative approach to assess the prognosis of PQ poisoning.
    Type of Medium: Online Resource
    ISSN: 1742-7835 , 1742-7843
    URL: Issue
    URL: Article
    DOI: 10.1111/bcpt.2017.120.issue-1
    DOI: 10.1111/bcpt.12638
    Language: English
    Publisher: Wiley
    Publication Date: 2017
    detail.hit.zdb_id: 2151592-X
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  • 16
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    Species‐ and gender‐dependent differences in the glucuronidation of a flavonoid glucoside and its aglycone determined using expressed UGT enzymes and microsomes
    Wiley ; 2015
    In:  Biopharmaceutics & Drug Disposition Vol. 36, No. 9 ( 2015-12), p. 622-635
    Details
    In: Biopharmaceutics & Drug Disposition, Wiley, Vol. 36, No. 9 ( 2015-12), p. 622-635
    Abstract: Flavonoids occur naturally as glucosides and aglycones. Their common phenolic hydroxyl groups may trigger extensive UDP‐glucuronosyltransferase (UGT)‐ catalysed metabolism. Unlike aglycones, glucosides contain glucose moieties. However, the influence of these glucose moieties on glucuronidation of glucosides and aglycones remains unclear. In this study, the flavonoid glucoside tilianin and its aglycone acacetin were used as model compounds. The glucuronidation characteristics and enzyme kinetics of tilianin and acacetin were compared using human UGT isoforms, liver microsomes and intestinal microsomes obtained from different animal species. Tilianin and acacetin were metabolized into different glucuronides, with UGT1A8 produced as the main isoform. Assessment of enzyme kinetics in UGT1A8, human liver microsomes and human intestinal microsomes revealed that compared with tilianin, acacetin displayed lower K m (0.6‐, 0.7‐ and 0.6‐fold, respectively), higher V max (20‐, 60‐ and 230‐fold, respectively) and higher clearance (30‐, 80‐ and 300‐fold, respectively). Furthermore, glucuronidation of acacetin and tilianin showed significant species‐ and gender‐dependent differences. In conclusion, glucuronidation of flavonoid aglycones is faster than that of glucosides in the intestine and the liver. Understanding the metabolism and species‐ and gender‐dependent differences between glucosides and aglycones is crucial for the development of drugs from flavonoids. Copyright © 2015 John Wiley & Sons, Ltd.
    Type of Medium: Online Resource
    ISSN: 0142-2782 , 1099-081X
    URL: Issue
    URL: Article
    DOI: 10.1002/bdd.v36.9
    DOI: 10.1002/bdd.1989
    Language: English
    Publisher: Wiley
    Publication Date: 2015
    detail.hit.zdb_id: 1496395-4
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  • 17
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    Probabilistic routing algorithm based on contact duration and message redundancy in delay tolerant network
    Wiley ; 2016
    In:  International Journal of Communication Systems Vol. 29, No. 16 ( 2016-11-10), p. 2416-2426
    Details
    In: International Journal of Communication Systems, Wiley, Vol. 29, No. 16 ( 2016-11-10), p. 2416-2426
    Abstract: The Delay Tolerant Network (DTN) is a novel Wireless Sensor Network architecture for an opportunistic network environment, in which environment end‐to‐end connection cannot be set up constantly between source and destination nodes pairs. In this paper, we have proposed a novel routing algorithm based on a hybrid of message delivery probability and message redundancy to reduce the communication overhead while keeping the high message delivery ratio. In this algorithm, the message delivery probability is calculated by the combined impact of meeting frequency and length of contact duration. Further, the maximum number of copies of the message is designated in the source node, and the forwarding task of message copies is assigned to relay nodes based on the pattern of a binary tree, so that multi‐path parallel transmission can be implemented on message forwarding. Simulated results showed that the proposed routing algorithm can achieve a higher efficiency of message delivery than the related existing routing algorithms and it can also reduce the communication overhead significantly in general DTNs. Copyright © 2015 John Wiley & Sons, Ltd.
    Type of Medium: Online Resource
    ISSN: 1074-5351 , 1099-1131
    URL: Issue
    URL: Article
    DOI: 10.1002/dac.v29.16
    DOI: 10.1002/dac.3030
    Language: English
    Publisher: Wiley
    Publication Date: 2016
    detail.hit.zdb_id: 2024893-3
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  • 18
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    Age‐related changes in hepatic expression and activity of drug metabolizing enzymes in male wild‐type and breast cancer resistance protein knockout mice
    Wiley ; 2018
    In:  Biopharmaceutics & Drug Disposition Vol. 39, No. 7 ( 2018-07), p. 344-353
    Details
    In: Biopharmaceutics & Drug Disposition, Wiley, Vol. 39, No. 7 ( 2018-07), p. 344-353
    Abstract: This study aimed to reveal age‐related changes in the expression and activity of seven hepatic drug metabolizing enzymes (DMEs) in male wild‐type and breast cancer resistance protein knockout (Bcrp1 −/− ) FVB mice. The protein expression of four cytochrome P450 (Cyps) (Cyp3a11, 2d22, 2e1, and 1a2), and three UDP‐glucuronosyltransferases (Ugts) (Ugt1a1, 1a6a, and 1a9) in liver microsomes of wild‐type and Bcrp1 −/− FVB mice at different ages were determined using a validated ultra high performance liquid chromatography with tandem mass spectrometry (UHPLC–MS/MS) method. The activities and mRNA levels of these DMEs were measured using the probe substrates method and real‐time PCR, respectively. In the liver of wild‐type FVB mice, Cyp3a11, 2d22, 2e1, 1a2, Ugt1a1, and 1a6a displayed maximum protein levels at 6–9 weeks of age. Cyp1a2, Ugt1a1, 1a6a, and 1a9 showed maximum activities at 6–9 weeks of age, whereas Cyp3a11, 2d22, and 2e1 showed maximum activities in 1–3‐week‐old mice. Additionally, most of the DMEs showed maximum mRNA levels in 17‐week‐old mice liver. Compared with wild‐type FVB mice, the protein levels of these DMEs showed no significant changes in Bcrp1 −/− FVB mice liver. However, the activity of Cyp2e1 was increased and that of Cyp2d22 was decreased. In conclusion, t he seven hepatic DMEs in FVB mice liver showed significant alterations in an isoform‐specific manner with increased age. Although the protein levels of these DMEs showed no significant changes, the activities of Cyp2e1 and 2d22 were changed in Bcrp1 −/− mice.
    Type of Medium: Online Resource
    ISSN: 0142-2782 , 1099-081X
    URL: Issue
    URL: Article
    DOI: 10.1002/bdd.v39.7
    DOI: 10.1002/bdd.2151
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 1496395-4
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  • 19
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    Gene coexpression analysis offers important modules and pathway of human lung adenocarcinomas
    Wiley ; 2020
    In:  Journal of Cellular Physiology Vol. 235, No. 1 ( 2020-01), p. 454-464
    Details
    In: Journal of Cellular Physiology, Wiley, Vol. 235, No. 1 ( 2020-01), p. 454-464
    Abstract: Lung adenocarcinomas injured greatly on the people worldwide. Although clinic experiments and gene profiling analyses had been well performed, to our knowledge, systemic coexpression analysis of human genes for this cancer is still limited to date. Here, using the published data GSE75037, we built the coexpression modules of genes by Weighted Gene Co‐Expression Network Analysis (WGCNA), and investigated function and protein–protein interaction network of coexpression genes by Database for Annotation, visualization, and Integrated Discovery (DAVID) and String database, respectively. First, 11 coexpression modules were conducted for 5,000 genes in the 83 samples recently. Number of genes for each module ranged from 90 to 1,260, with the mean of 454. Second, interaction relationships of hub‐genes between pairwise modules showed great differences, suggesting relatively high scale independence of the modules. Third, functional enrichment of the coexpression modules showed great differences. We found that genes in modules 8 significantly enriched in the biological process and/or pathways of cell adhesion, extracellular matrix (ECM)–receptor interaction, focal adhesion, and PI3K‐Akt signaling pathway, and so forth. It was inferred as the key module underlying lung adenocarcinomas. Furthermore, PPI analysis revealed that the genes COL1A1, COL1A2, COL3A1, CTGF , and BGN owned the largest number of adjacency genes, unveiling that they may functioned importantly during the occurrence of lung adenocarcinomas. To summary, genes involved in cell adhesion, ECM–receptor interaction, focal adhesion, and PI3K‐Akt signaling pathway play crucial roles in human lung adenocarcinomas.
    Type of Medium: Online Resource
    ISSN: 0021-9541 , 1097-4652
    URL: Issue
    URL: Article
    DOI: 10.1002/jcp.v235.1
    DOI: 10.1002/jcp.28985
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 1478143-8
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  • 20
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    Long non‐coding RNA TDRG1 aggravates lung cancer stemness by binding to Sox2 mRNA
    Wiley ; 2023
    In:  Environmental Toxicology Vol. 38, No. 3 ( 2023-03), p. 645-653
    Details
    In: Environmental Toxicology, Wiley, Vol. 38, No. 3 ( 2023-03), p. 645-653
    Abstract: The roles of long non‐coding RNA TDRG1 have been revealed in several tumors, especially its roles in CSC progression have been recently elucidated; However, its effects in lung CSC progression have not been revealed. In the present study, we collected 3D non‐adherent spheres as the CSC model to measure lncRNA TDRG1 level in lung CSC and the parental lung cancer cells, and found that TDRG1 level was significantly upregulated in lung CSCs compared to that of parental lung cancer cells. Then we constructed the lung CSCs with or without TDRG1 stable knockdown and lung cancer cells with or without TDRG1 stable overexpression. It was found that TDRG1 positively regulated lung cancer stemness. Mechanistically, we identified that TDRG1 directly bound to Sox2 mRNA, which is a critical stemness regulator, enhanced its mRNA stability, and thus increased Sox2 expression. Indeed, we demonstrated that TDRG1 aggravated lung cancer stemness dependent on Sox2 expression. Thus, this study suggests that TDRG1 is a critical stemness promoter of lung cancer cells by acting as a stabilizer for Sox2 mRNA.
    Type of Medium: Online Resource
    ISSN: 1520-4081 , 1522-7278
    URL: Issue
    URL: Article
    DOI: 10.1002/tox.v38.3
    DOI: 10.1002/tox.23714
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2027534-1
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