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  • 1
    Online Resource
    Online Resource
    Table9.XLSX
    Frontiers Media SA ; 2021
    In:  Frontiers in Pharmacology Vol. 12 ( 2021-11-26)
    Details
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 12 ( 2021-11-26)
    Abstract: The purpose of this study is to understand the mechanism of sodium arsenite (NaAsO 2 )-induced apoptosis of L-02 human hepatic cells, and how Dictyophora polysaccharide (DIP) protects L-02 cells from arsenic-induced apoptosis. The results revealed that DIP pretreatment inhibited NaAsO 2 induced L-02 cells apoptosis by increasing anti-apoptotic Bcl-2 expression and decreasing pro-apoptotic Bax expression. Proteomic analysis showed that arsenic treatment disrupted the expression of metabolism and apoptosis associated proteins, including ribosomal proteins (RPs). After pretreatment with DIP, the expression levels of these proteins were reversed or restored. For the first time, it was observed that the significant decrease of cytoplasmic RPs and the increase of mitochondrial RPs were related to human normal cell apoptosis induced by arsenic. This is also the first report that the protective effect of DIP on cells was related to RPs. The results highlight the relationship between RPs and apoptosis, as well as the relationship between RPs and DIP attenuating arsenic-induced apoptosis.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    URL: Article
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    URL: Article
    DOI: 10.3389/fphar.2021.749035
    DOI: 10.3389/fphar.2021.749035.s001
    DOI: 10.3389/fphar.2021.749035.s002
    DOI: 10.3389/fphar.2021.749035.s003
    DOI: 10.3389/fphar.2021.749035.s004
    DOI: 10.3389/fphar.2021.749035.s005
    DOI: 10.3389/fphar.2021.749035.s006
    DOI: 10.3389/fphar.2021.749035.s007
    DOI: 10.3389/fphar.2021.749035.s008
    DOI: 10.3389/fphar.2021.749035.s009
    DOI: 10.3389/fphar.2021.749035.s010
    DOI: 10.3389/fphar.2021.749035.s011
    DOI: 10.3389/fphar.2021.749035.s012
    DOI: 10.3389/fphar.2021.749035.s013
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
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  • 2
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    Assessing the Potential Value and Mechanism of Kaji-Ichigoside F1 on Arsenite-Induced Skin Cell Senescence
    Hindawi Limited ; 2022
    In:  Oxidative Medicine and Cellular Longevity Vol. 2022 ( 2022-1-11), p. 1-16
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2022 ( 2022-1-11), p. 1-16
    Abstract: Chronic exposure to inorganic arsenic is a major environmental public health issue worldwide affecting more than 220 million of people. Previous studies have shown the correlation between arsenic poisoning and cellular senescence; however, knowledge regarding the mechanism and effective prevention measures has not been fully studied. First, the associations among the ERK/CEBPB signaling pathway, oxidative stress, and arsenic-induced skin cell senescence were confirmed using the HaCaT cell model. In the arsenic-exposed group, the relative mRNA and protein expressions of ERK/CEBPB signaling pathway indicators (ERK1, ERK2, and CEBPB), cell cycle-related genes (p21, p16INK4a), and the secretion of SASP (IL-1α, IL-6, IL-8, TGF-β1, MMP-1, MMP-3, EGF, and VEGF) and the lipid peroxidation product (MDA) were significantly increased in cells ( P 〈 0.05 ), while the activity of antioxidant enzyme (SOD, GSH-Px, and CAT) was significantly decreased ( P 〈 0.05 ), and an increased number of cells accumulated in the G1 phase ( P 〈 0.05 ). Further Kaji-ichigoside F1 intervention experiments showed that compared to that in the arsenic-exposed group, the expression level of the activity of antioxidant enzyme was significantly increased in the Kaji-ichigoside F1 intervention group ( P 〈 0.05 ), but the indicators of ERK/CEBPB signaling pathway, cell cycle-related genes, and SASP were significantly decreased ( P 〈 0.05 ), and the cell cycle arrest relieved to a certain extent ( P 〈 0.05 ). Our study provides some limited evidence that the ERK/CEBPB signaling pathway is involved in low-dose arsenic-induced skin cell senescence, through regulating oxidative stress. The second major finding was that Kaji-ichigoside F1 can downregulate the ERK/CEBPB signaling pathway and regulate the balance between oxidation and antioxidation, alleviating arsenic-induced skin cell senescence. This study provides experimental evidence for further understanding of Kaji-ichigoside F1, a natural medicinal plant that may be more effective in preventing and controlling arsenic poisoning.
    Type of Medium: Online Resource
    ISSN: 1942-0994 , 1942-0900
    URL: Article
    DOI: 10.1155/2022/9574473
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2455981-7
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  • 3
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    Quantitative proteomics provides a new perspective on the mechanism of network structure depolymerization during egg white thinning
    Elsevier BV ; 2022
    In:  Food Chemistry Vol. 392 ( 2022-10), p. 133320-
    Details
    In: Food Chemistry, Elsevier BV, Vol. 392 ( 2022-10), p. 133320-
    Type of Medium: Online Resource
    ISSN: 0308-8146
    URL: Article
    DOI: 10.1016/j.foodchem.2022.133320
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 1483647-6
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  • 4
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    Genome-wide DNA methylation pattern in whole blood of patients with coal-burning arsenic poisoning
    Elsevier BV ; 2022
    In:  Ecotoxicology and Environmental Safety Vol. 248 ( 2022-12), p. 114323-
    Details
    In: Ecotoxicology and Environmental Safety, Elsevier BV, Vol. 248 ( 2022-12), p. 114323-
    Type of Medium: Online Resource
    ISSN: 0147-6513
    URL: Article
    DOI: 10.1016/j.ecoenv.2022.114323
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 1466969-9
    SSG: 24,1
    SSG: 12
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  • 5
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    Inorganic arsenic promotes apoptosis of human immortal keratinocytes through the TGF ‐β1/ ERK signaling pathway
    Wiley ; 2022
    In:  Environmental Toxicology Vol. 37, No. 6 ( 2022-06), p. 1321-1331
    Details
    In: Environmental Toxicology, Wiley, Vol. 37, No. 6 ( 2022-06), p. 1321-1331
    Abstract: Chronic exposure to high‐dose inorganic arsenic through groundwater, air, or food remains a major environmental public health issue worldwide. Apoptosis, a method of cell death, has recently become a hot topic of research in biology and medicine. Previous studies have demonstrated that extracellular signal‐regulated kinase (ERK) is related to arsenic‐induced apoptosis. However, the reports are contradictory, and the knowledge of the above‐mentioned mechanisms and their mutual regulation remains limited. In this study, the associations between the TGF‐β1/ERK signaling pathway and arsenic‐induced cell apoptosis were confirmed using the HaCaT cell model. The relative expressions of the indicators of the TGF‐β1/ERK signaling pathway, apoptosis‐related genes (cytochrome C, caspase‐3, caspase‐9, cleaved caspase‐3, cleaved caspase‐9, and Bax), the mitochondrial membrane potential, and the total apoptosis rate were significantly increased ( P  〈  .05), while the expression of the antiapoptosis gene Bcl‐2 was significantly decreased ( P  〈  .05) in cells of the group exposed to arsenic. Moreover, the results demonstrated that the ERK inhibitor (PD98059) and TGF‐β1 inhibitor (LY364947) could inhibit the activation of the ERK signaling pathway, thereby reducing the mitochondrial membrane potential, the total apoptosis rate, and the expression of pro‐apoptosis‐related genes in the cells, while the expression of the antiapoptosis gene Bcl‐2 was significantly increased ( P  〈  .05). By contrast, the recombinant human TGF‐β1 could promote apoptosis of the HaCaT cells by increasing the activation of the ERK signaling pathway ( P  〈  .05). These results indicate that inorganic arsenic promotes the apoptosis of human immortal keratinocytes through the TGF‐β1/ERK signaling pathway.
    Type of Medium: Online Resource
    ISSN: 1520-4081 , 1522-7278
    URL: Issue
    URL: Article
    DOI: 10.1002/tox.v37.6
    DOI: 10.1002/tox.23486
    Language: English
    Publisher: Wiley
    Publication Date: 2022
    detail.hit.zdb_id: 2027534-1
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  • 6
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    Screening and Identification of Antidepressant Active Ingredients from Puerariae Radix Extract and Study on Its Mechanism
    Hindawi Limited ; 2021
    In:  Oxidative Medicine and Cellular Longevity Vol. 2021 ( 2021-9-9), p. 1-18
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2021 ( 2021-9-9), p. 1-18
    Abstract: Objective. Depression is a common mental disease with long course and high recurrence rate. Previous studies showed that Puerariae Radix and its extracts have powerful antidepressant effects in recent years. The study proposed an integrated strategy, combining network pharmacology and molecular pharmacology experiment to investigate the mechanisms of the antidepressant active ingredients from Puerariae Radix. Methods. TCMSP database, GeneCards database, Venny 2.1, UniProt database, STRING database, Cytoscape 3.7.2, and Metascape database were used to screen the active chemical components, antidepressant-related genes, and core targets, convert the abbreviated gene names in batch, search and predict the interaction between proteins, and construct the PPI network of Puerariae Radix. KEGG pathway and GO biological process enrichment and biological annotation were used to select antidepressant core gene targets. The MTT method was used to detect the effect of puerarin on the damage of PC12 cells induced by corticosterone. The DCFH-DA probe and ROS assay kit were utilized to detect the production of ROS in PC12 cells. PI/Annexin V was used to detect the apoptotic rate of puerarin on PC12 cells. Western blotting was used to verify the regulation of puerarin on the key targets of AKT1, FOS, CASP3, STAT3, and TNF-α in PC12 cells. Results and Conclusion. Eight main active components, 64 potential antidepressant gene targets, and 15 core antidepressant gene targets were obtained. 35 signaling pathways and 52 biological processes related to antidepressant effect of Puerariae Radix were identified. Puerarin was the active ingredient derived from Puerariae Radix which exhibited the antidepression effect by improving the viability of cell, reducing cell apoptosis, regulating ROS production, increasing protein expressions of AKT1 and FOS, and reducing protein expressions of CASP3, STAT3, and TNF-α. The study revealed the pharmacodynamic material basis and possible antidepressant mechanism of Puerariae Radix and provided new theoretical basis and ideas for antidepressant research.
    Type of Medium: Online Resource
    ISSN: 1942-0994 , 1942-0900
    URL: Article
    DOI: 10.1155/2021/2230195
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2455981-7
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  • 7
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    Intervention Study of Dictyophora Polysaccharides on Arsenic-Induced Liver Fibrosis in SD Rats
    Hindawi Limited ; 2022
    In:  BioMed Research International Vol. 2022 ( 2022-3-30), p. 1-12
    Details
    In: BioMed Research International, Hindawi Limited, Vol. 2022 ( 2022-3-30), p. 1-12
    Abstract: Long-term arsenic (As) exposure can cause liver injury, hepatic cirrhosis, and cancer. Meanwhile, Dictyophora polysaccharides (DIP) have excellent antioxidation, anti-inflammation, and immune protection effects. There are currently few reports on the protection effects of DIP on As-induced hepatotoxicity and its pharmacological value. Therefore, this study was aimed at elucidating the protection of DIP on As-induced hepatotoxicity and exploring its preventive role in antifibrosis. In our study, the SD rat As poisoning model was established by the feeding method to explore the influence of As exposure on liver fibrosis. Then, DIP treatment was applied to the rats with As-induced liver fibrosis, and the changes of serum biochemical indexes and liver tissue pathology were observed. And the expression of fibrosis-related proteins TGF-β1, CTGF, and α-SMA levels was then determined to explore the DIP intervention function. The results demonstrated that through reduced pathological changes of hepatic and increased serum AST, ALT, TP, ALB, and A/G levels, DIP ameliorated liver fibrosis induced by As as reflected. And the administration of DIP decreased the concentration of HA, LN, PCIII, CIV, TBIL, and DBIL. In addition, the synthesis of TGF-β1 inhibited by DIP might regulate the expression of CTGF and decrease the proliferation of fibrinogen and fibroblasts, which reduced the synthesis of fibroblasts to transform into myofibroblasts. And a decrease of myofibroblasts downregulated the expression of α-SMA, which affected the synthesis and precipitation of ECM and alleviated the liver fibrosis caused by exposure to As. In conclusion, based on the pathological changes of liver tissue, serum biochemical indexes, and related protein expression, DIP can improve the As-induced liver fibrosis in rats and has strong medicinal value.
    Type of Medium: Online Resource
    ISSN: 2314-6141 , 2314-6133
    URL: Article
    DOI: 10.1155/2022/7509620
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2698540-8
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  • 8
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    Pirfenidone inhibits TGF‐β1‐induced metabolic reprogramming during epithelial‐mesenchymal transition in non‐small cell lung cancer
    Wiley ; 2024
    In:  Journal of Cellular and Molecular Medicine Vol. 28, No. 3 ( 2024-02)
    Details
    In: Journal of Cellular and Molecular Medicine, Wiley, Vol. 28, No. 3 ( 2024-02)
    Abstract: Metastasis is an important contributor to increased mortality rates in non‐small cell lung cancer (NSCLC). The TGF‐β signalling pathway plays a crucial role in facilitating tumour metastasis through epithelial‐mesenchymal transition (EMT). Glycolysis, a key metabolic process, is strongly correlated with NSCLC metastasis. Pirfenidone (PFD) has been shown to safely and effectively inhibit TGF‐β1 in patients with lung diseases. Furthermore, TGF‐β1 and glycolysis demonstrate an interdependent relationship within the tumour microenvironment. Our previous study demonstrated that PFD effectively inhibited glycolysis in NSCLC cells, prompting further investigation into its potential antitumour effects in this context. Therefore, the present study aims to investigate the potential antitumour effect of PFD in NSCLC and explore the relationship among TGF‐β1, glycolysis and EMT through further experimentation. The antitumour effects of PFD were evaluated using five different NSCLC cell lines and a xenograft tumour model. Notably, PFD demonstrated a significant antitumour effect specifically in highly glycolytic H1299 cells. To elucidate the underlying mechanism, we compared the efficacy of PFD after pretreatment with either TGF‐β1 or a TGF‐β receptor inhibitor (LY2109761). The energy metabolomics analysis of tumour tissue demonstrated that PFD, a chemosensitizing agent, reduced lactate and ATP production, thereby inhibiting glycolysis and exerting synergistic antineoplastic effects. Additionally, PFD combined with cisplatin targeted TGF‐β1 to inhibit glycolysis during EMT and enhanced the chemosensitization of A549 and H1299 cells. The magnitude of the anticancer effect exhibited by PFD was intricately linked to its metabolic properties.
    Type of Medium: Online Resource
    ISSN: 1582-1838 , 1582-4934
    URL: Issue
    URL: Article
    DOI: 10.1111/jcmm.v28.3
    DOI: 10.1111/jcmm.18059
    Language: English
    Publisher: Wiley
    Publication Date: 2024
    detail.hit.zdb_id: 2076114-4
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