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  • 1
    Online Resource
    Online Resource
    Assessing the potential value and mechanism of Ginkgo biloba L . On coal-fired arsenic-induced skin damage: In vitro and human evidence
    SAGE Publications ; 2021
    In:  Human & Experimental Toxicology Vol. 40, No. 12 ( 2021-12), p. 2113-2122
    Details
    In: Human & Experimental Toxicology, SAGE Publications, Vol. 40, No. 12 ( 2021-12), p. 2113-2122
    Abstract: Exposure through arsenic-contaminated air and food caused by the burning of coal is a major environmental public health concern in Guizhou Province of China. Previous studies have shown that immunological dysfunction is involved in the pathogenesis and carcinogenesis of arsenic; however, knowledge regarding effective prevention measures have not been fully examined. The effect of Ginkgo biloba extract (EGb761) on arsenic-induced skin damage of human immortalized keratinocyte cells (HaCaT) was first evaluated in this study. The results showed that 200 μg/mL EGb761 can reduce the expression of miR-155-5p, and the indicators reflecting arsenic-induced skin damage (Krt1, Krt6c and Krt10) in arsenic-exposed cells ( P 〈 0.05), the expression levels of NF-AT1; the indicators reflecting arsenic-induced immunological dysfunction (IL-2, IFN-γ) in cells; and the levels of secreted IL-2 and IFN-γ in cell supernatants were significantly increased ( P 〈 0.05). Further randomized controlled double-blind experiments showed that compared to the placebo control group, the expression level of miR-155-5p in the plasma of the Ginkgo biloba intervention group, the indicators in the serum reflecting arsenic-induced skin damage (Krt1, Krt6c, and Krt10) and the epithelial-mesenchymal transformation (EMT) vimentin were significantly reduced ( P 〈 0.05), but the levels of NF-AT1 and the indicators reflecting arsenic-induced immunological dysfunction (IL-2, IFN-γ) and EMT (E-cadherin) in serum were significantly increased ( P 〈 0.05). Our study provides some limited evidence that Ginkgo biloba L. can increase the expression of NF-AT1 by downregulating the level of miR-155-5p, alleviating immunological dysfunction, and decreasing the expression of EMT biomarkers, thus indirectly improving arsenic-induced skin damage.
    Type of Medium: Online Resource
    ISSN: 0960-3271 , 1477-0903
    URL: Article
    DOI: 10.1177/09603271211021887
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2021
    detail.hit.zdb_id: 1483723-7
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  • 2
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    Assessing the risk of coal-burning arsenic-induced liver damage: a population-based study on hair arsenic and cumulative arsenic
    Springer Science and Business Media LLC ; 2021
    In:  Environmental Science and Pollution Research Vol. 28, No. 36 ( 2021-09), p. 50489-50499
    Details
    In: Environmental Science and Pollution Research, Springer Science and Business Media LLC, Vol. 28, No. 36 ( 2021-09), p. 50489-50499
    Type of Medium: Online Resource
    ISSN: 0944-1344 , 1614-7499
    URL: Article
    DOI: 10.1007/s11356-021-14273-y
    RVK:
    AR 10100
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2014192-0
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  • 3
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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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  • 4
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    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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    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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  • 5
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    Semaphorin 4A antibody alleviates arsenic-induced hepatotoxicity in mice via inhibition of AKT2/NF-κB inflammatory signaling
    Elsevier BV ; 2021
    In:  Toxicology and Applied Pharmacology Vol. 410 ( 2021-01), p. 115364-
    Details
    In: Toxicology and Applied Pharmacology, Elsevier BV, Vol. 410 ( 2021-01), p. 115364-
    Type of Medium: Online Resource
    ISSN: 0041-008X
    URL: Article
    DOI: 10.1016/j.taap.2020.115364
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 1471923-X
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  • 6
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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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  • 7
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    Presentation_1.pdf
    Frontiers Media SA ; 2023
    In:  Frontiers in Nutrition Vol. 10 ( 2023-2-7)
    Details
    In: Frontiers in Nutrition, Frontiers Media SA, Vol. 10 ( 2023-2-7)
    Abstract: Grifola frondosa is an edible medicinal mushroom that has been proven to have a variety of health benefits. The main active ingredients of this mushroom are polysaccharides. In this study, ultrasonic-assisted extraction was used to obtain crude Grifola frondosa polysaccharides (GFPs). Then, purified GFP was obtained after purification. The optimum extraction conditions were an extraction time of 71 min, an extraction temperature of 90°C in a solid-to-liquid ratio of 1:37 g/mL, and an ultrasonic power of 500 W. GFP was purified using DEAE-52 and Sephadex G-100. The structural characterization of GFP was performed using Fourier transform infrared spectroscopy (FT-IR), X-ray diffraction (XRD), ion chromatography (IC), and ultraviolet (UV) visible photometry. The morphology of GFP was analyzed by scanning electron microscopy (SEM), thermogravimetric differential scanning calorimetry (TG-DSC), and Congo red testing. In addition, the administration of GFP in oxazolone (OXZ)-induced ulcerative colitis (UC) in mice was found to prevent weight loss. Different doses of GFP (80, 160, and 320 mg/kg body weight) were used, and sulfapyridine (SASP) was used as a positive control (370 mg/kg body weight) for the treatment of OXZ-induced UC. After treatment, the mice were killed, and blood and colon tissue samples were collected. GFP was found to prevent decreases in colon length and the levels of leukocytes, platelets, and neutrophils in UC mice. Moreover, GFP also decreased the expression of pro-inflammatory cytokines [tumor necrosis factor (TNF)-α and interleukin (IL)-1 β], increased IL-10, and reduced colon injury in UC mice. The results showed that Under these conditions, the predicted polysaccharide yield was 21.72%, and the actual extraction rate was 21.13%. The polysaccharide composition (molar ratio) was composed of fucose (0.025), glucosamine hydrochloride (0.004), galactose (0.063), glucose (0.869), and mannose (0.038). GFP was also found to have a typical absorption peak, and the GFP extracted using the ultrasound-assisted extraction protocol was mainly β-glucan. These results indicate that ultrasound-assisted extraction of GFP could reduce OXZ-induced intestinal inflammation as a promising candidate for the treatment of UC, with the potential for development as a food supplement to improve intestinal diseases.
    Type of Medium: Online Resource
    ISSN: 2296-861X
    URL: Article
    URL: Article
    DOI: 10.3389/fnut.2023.1078868
    DOI: 10.3389/fnut.2023.1078868.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2776676-7
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  • 8
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    Extraction and Purification of Flavonoids from Buddleja officinalis Maxim and Their Attenuation of H2O2-Induced Cell Injury by Modulating Oxidative Stress and Autophagy
    MDPI AG ; 2022
    In:  Molecules Vol. 27, No. 24 ( 2022-12-16), p. 8985-
    Details
    In: Molecules, MDPI AG, Vol. 27, No. 24 ( 2022-12-16), p. 8985-
    Abstract: Cataracts are an ailment representing the leading cause of blindness in the world. The pathogenesis of cataracts is not clear, and there is no effective treatment. An increasing amount of evidence shows that oxidative stress and autophagy in lens epithelial cells play a key role in the occurrence and development of cataracts. Buddleja officinalis Maxim flavonoids (BMF) are natural antioxidants and regulators that present anti-inflammatory and anti-tumor effects, among others. In this study, we optimized the extraction method of BMFs and detected three of their main active monomers (luteolin, apigenin, and acacetin). In addition, a model of oxidative damage model using rabbit lens epithelial cells induced by hydrogen peroxide (H2O2). By detecting the levels of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), and OH (OH), the expression of autophagosomes and autolysosomes were observed after MRFP-GFP-LC3 adenovirus was introduced into the cells. Western blotting was used to detect the expression of Beclin-1 and P62. Our research results showed that the optimal extraction parameters to obtain the highest yield of total flavonoids were a liquid–solid ratio of 1:31 g/mL, an ethanol volume fraction of 67%, an extraction time of 2.6 h, and an extraction temperature of 58 °C. Moreover, the content of luteolin was 690.85 ppb, that of apigenin was 114.91 ppb, and the content of acacetin was 5.617 ppb. After oxidative damage was induced by H2O2, the cell survival rate decreased significantly. BMFs could increase the levels of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and decrease the levels of malondialdehyde (MDA) and OH (OH). After the MRFP-GFP-LC3 virus was introduced into rabbit lens epithelial cells and detecting the expression of P62 and Beclin-1, we found that the intervention of BMF could promote the binding of autophagosomes to lysosomes. Compared with the model group, the level of P62 in the low-, middle-, and high-dose groups of BMF was significantly down-regulated, the level of Beclin-1 was significantly increased, and the difference was statistically significant (p 〈 0.05). In other words, the optimized extraction method was better than others, and the purified BMF contained three main active monomers (luteolin, apigenin, and acacetin). In addition, BMFs could ameliorate the H2O2-induced oxidative damage to rabbit lens cells by promoting autophagy and regulating the level of antioxidation.
    Type of Medium: Online Resource
    ISSN: 1420-3049
    URL: Article
    DOI: 10.3390/molecules27248985
    Language: English
    Publisher: MDPI AG
    Publication Date: 2022
    detail.hit.zdb_id: 2008644-1
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  • 9
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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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  • 10
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    Assessing the Role of Nrf2/GPX4-Mediated Oxidative Stress in Arsenic-Induced Liver Damage and the Potential Application Value of Rosa roxburghii Tratt [Rosaceae]
    Hindawi Limited ; 2022
    In:  Oxidative Medicine and Cellular Longevity Vol. 2022 ( 2022-4-25), p. 1-15
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2022 ( 2022-4-25), p. 1-15
    Abstract: Arsenic poisoning is a geochemical disease that seriously endangers human health. The liver is one of the important target organs for arsenic poisoning, several studies have shown that oxidative stress plays an important role in arsenic-induced liver damage. However, the specific mechanism of arsenic-induced oxidative stress has not yet been fully elucidated, and currently, there are no effective intervention measures for the prevention and treatment of arsenic-induced liver damage. In this study, the effect of the Nrf2/GPX4 signaling pathway and oxidative stress in the arsenic-induced liver damage was first evaluated. The results show that arsenic can activate the Nrf2/GPX4 signaling pathway and increase the oxidative stress, which in turn promotes arsenic-induced liver damage in MIHA cells. Moreover, when we applied the Nrf2 inhibitor, the promoting effect of arsenic on liver damage was alleviated by inhibiting the activation of the Nrf2/GPX4 signaling pathway. Subsequently, the Rosa roxburghii Tratt [Rosaceae] (RRT) intervention experiments in cells and arsenic poisoning population were designed. The results revealed that RRT can inhibit Nrf2/GPX4 signaling pathway to reduce oxidative stress, thereby alleviates arsenic-induced liver damage. This study provides some limited evidence that arsenite can activate Nrf2/GPX4 signaling pathway to induce oxidative stress, which in turn promotes arsenic-induced liver damage in MIHA cells. The second major finding was that Kaji-ichigoside F1 may be a potential bioactive compound of RRT, which can inhibit Nrf2/GPX4 signaling pathway to reduce oxidative stress, thereby alleviates arsenic-induced liver damage. Our study will contribute to a deeper understanding of the mechanisms in arsenic-induced liver damage, these findings will identify a possible natural medicinal food dual-purpose fruit, RRT, as a more effective prevention and control strategies for arsenic poisoning.
    Type of Medium: Online Resource
    ISSN: 1942-0994 , 1942-0900
    URL: Article
    DOI: 10.1155/2022/9865606
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2455981-7
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