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  • Xue, Xinyan  (7)
  • 1
    Online Resource
    Online Resource
    Hindawi Limited ; 2022
    In:  Oxidative Medicine and Cellular Longevity Vol. 2022 ( 2022-1-5), p. 1-17
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2022 ( 2022-1-5), p. 1-17
    Abstract: Hepatic stellate cells (HSCs) activation is an important step in the process of hepatic fibrosis. NOX4 and reactive oxygen species expressed in HSCs play an important role in liver fibrosis. Forsythiaside A (FA), a phenylethanoid glycoside extracted and isolated from Forsythiae Fructus, has significant antioxidant activities. However, it is not clear whether FA can play a role in inhibiting the HSCs activation through regulating NOX4/ROS pathway. Therefore, our purpose is to explore the effect and mechanism of FA on HSCs activation to alleviate liver fibrosis. LX2 cells were activated by TGF-β1 in vitro. MTT assay and Wound Healing assay were used to investigate the effect of FA on TGF-β1-induced LX2 cell proliferation and migration. Elisa kit was used to measure the expression of MMP-1 and TIMP-1. Western blot and RT-qPCR were used to investigate the expression of fibrosis-related COLI, α-SMA, MMP-1 and TIMP-1, and inflammation-related TNF-α, IL-6 and IL-1β. The hydroxyproline content was characterized using a biochemical kit. The mechanism of FA to inhibit HSCs activation and apoptosis was detected by DCF-DA probe, RT-qPCR, western blot and flow cytometry. NOX4 siRNA was used to futher verify the effect of FA on NOX4/ROS pathway. The results showed that FA inhibited the proliferation and migration of LX2 cells and adjusted the expression of MMP-1, TIMP-1, COLI, α-SMA, TNF-α, IL-6 and IL-1β as well as promoted collagen metabolism to show potential in anti-hepatic fibrosis. Mechanically, FA down-regulated NOX4/ROS signaling pathway to improve oxidation imbalances, and subsequently inhibited PI3K/Akt pathway to suppress proliferation. FA also promoted the apoptosis of LX2 cells by Bax/Bcl2 pathway. Furthermore, the effects of FA on TGF-β1-induced increased ROS levels and α-SMA and COLI expression were weaken by silencing NOX4. In conclusion, FA had potential in anti-hepatic fibrosis at least in part by remolding of extracellular matrix and improving oxidation imbalances to inhibit the activation of HSCs and promote HSCs apoptosis.
    Type of Medium: Online Resource
    ISSN: 1942-0994 , 1942-0900
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2022
    detail.hit.zdb_id: 2455981-7
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  • 2
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2021 ( 2021-8-3), p. 1-12
    Abstract: Thrombus is considered to be the pathological source of morbidity and mortality of cardiovascular disease and thrombotic complications, while oxidative stress is regarded as an important factor in vascular endothelial injury and thrombus formation. Therefore, antioxidative stress and maintaining the normal function of vascular endothelial cells are greatly significant in regulating vascular tension and maintaining a nonthrombotic environment. Leonurine (LEO) is a unique alkaloid isolated from Leonurus japonicus Houtt (a traditional Chinese medicine (TCM)), which has shown a good effect on promoting blood circulation and removing blood stasis. In this study, we explored the protective effect and action mechanism of LEO on human umbilical vein endothelial cells (HUVECs) after damage by hydrogen peroxide (H2O2). The protective effects of LEO on H2O2-induced HUVECs were determined by measuring the cell viability, cell migration, tube formation, and oxidative biomarkers. The underlying mechanism of antioxidation of LEO was investigated by RT-qPCR and western blotting. Our results showed that LEO treatment promoted cell viability; remarkably downregulated the intracellular generation of reactive oxygen species (ROS), malondialdehyde (MDA) production, and lactate dehydrogenase (LDH); and upregulated the nitric oxide (NO) and superoxide dismutase (SOD) activity in H2O2-induced HUVECs. At the same time, LEO treatment significantly promoted the phosphorylation level of angiogenic protein PI3K, Akt, and eNOS and the expression level of survival factor Bcl2 and decreased the expression level of death factor Bax and caspase3. In conclusion, our findings suggested that LEO can ameliorate the oxidative stress damage and insufficient angiogenesis of HUVECs induced by H2O2 through activating the PI3K/Akt-eNOS signaling pathway.
    Type of Medium: Online Resource
    ISSN: 1942-0994 , 1942-0900
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2455981-7
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  • 3
    In: Phytomedicine, Elsevier BV, Vol. 91 ( 2021-10), p. 153694-
    Type of Medium: Online Resource
    ISSN: 0944-7113
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 2040195-4
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  • 4
    In: Journal of Ethnopharmacology, Elsevier BV, Vol. 293 ( 2022-07), p. 115322-
    Type of Medium: Online Resource
    ISSN: 0378-8741
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2022
    detail.hit.zdb_id: 1491279-X
    SSG: 15,3
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  • 5
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 12 ( 2021-11-4)
    Abstract: Thrombosis is a general pathological phenomenon during severe disturbances to homeostasis, which plays an essential role in cardiovascular and cerebrovascular diseases. Leonurine (LEO), isolated from Leonurus japonicus Houtt, showes a crucial role in anticoagulation and vasodilatation. However, the properties and therapeutic mechanisms of this effect have not yet been systematically elucidated. Therefore, the antithrombotic effect of LEO was investigated in this study. Hematoxylin-Eosin staining was used to detect the thrombosis of zebrafish tail. Fluorescence probe was used to detect the reactive oxygen species. The biochemical indexes related to oxidative stress (lactate dehydrogenase, malondialdehyde, superoxide dismutase and glutathione) and vasodilator factor (endothelin-1 and nitric oxide) were analyzed by specific commercial assay kits. Besides, we detected the expression of related genes (fga, fgb, fgg, pkcα, pkcβ, vwf, f2) and proteins (PI3K, phospho-PI3K, Akt, phospho-Akt, ERK, phospho-ERK FIB) related to the anticoagulation and fibrinolytic system by quantitative reverse transcription and western blot. Beyond that, metabolomic analyses were carried out to identify the expressions of metabolites associated with the anti-thrombosis mechanism of LEO. Our in vivo experimental results showed that LEO could improve the oxidative stress injury, abnormal platelet aggregation and coagulation dysfunction induced by adrenalin hydrochloride. Moreover, LEO restored the modulation of amino acids and inositol metabolites which are reported to alleviate the thrombus formation. Collectively, LEO attenuates adrenalin hydrochloride-induced thrombosis partly via modulating oxidative stress, coagulation cascade and platelet activation and amino acid and inositol metabolites.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
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  • 6
    Online Resource
    Online Resource
    Bentham Science Publishers Ltd. ; 2022
    In:  Current Pharmaceutical Design Vol. 28, No. 9 ( 2022-03), p. 727-742
    In: Current Pharmaceutical Design, Bentham Science Publishers Ltd., Vol. 28, No. 9 ( 2022-03), p. 727-742
    Abstract: Quercetin is the main dietary flavonoid with a wide range of pharmacological activities. However, the poor gastrointestinal absorption and low bioavailability of quercetin curtails its clinical applications.. Enhancement the bioavailability of quercetin focuses on the application of delivery systems technologies such as microparticle delivery systems, solid dispersions, encapsulation, phospholipid complexes, and hydrogels , which have been systematically reviewed .And theirapplications in vitro and in vivo animal experiments also been described, promoting the development and optimization of dr ug delivery system for clinical applications.
    Type of Medium: Online Resource
    ISSN: 1381-6128
    Language: English
    Publisher: Bentham Science Publishers Ltd.
    Publication Date: 2022
    SSG: 15,3
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  • 7
    Online Resource
    Online Resource
    Bentham Science Publishers Ltd. ; 2022
    In:  Current Pharmaceutical Design Vol. 28, No. 12 ( 2022-04), p. 993-999
    In: Current Pharmaceutical Design, Bentham Science Publishers Ltd., Vol. 28, No. 12 ( 2022-04), p. 993-999
    Abstract: Inflammation, as a complex immunopathological process, is the organism's natural defense response against harmful, foreign, and destructive immune or non-immune factors. It is the main pathological form of various diseases, such as tumors, neurodegenerative diseases, periodontitis, alcoholic steatohepatitis, asthma, and other diseases. The P2X7 receptor (P2X7R) is widely distributed in vivo and up-regulated in various inflammatory pathological states. Studies have shown that milder chronic inflammation is related to a deficiency or inhibition of P2X7R, which is an indispensable part of the pro-inflammatory mechanism in vivo. P2X7R, a unique subtype of seven purinergic P2X receptors, is an ATP-gated non-selective cationic channel. P2X7R will promote the influx of Ca2+ and the outflow of K+ after being stimulated. The influx of Ca2+ is essential for activating the body's innate immune response and inducing the production of inflammatory factors. This paper reviews the regulation of P2X7R in inflammation from the perspectives of innate immunity and adaptive immunity.
    Type of Medium: Online Resource
    ISSN: 1381-6128
    Language: English
    Publisher: Bentham Science Publishers Ltd.
    Publication Date: 2022
    SSG: 15,3
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