Schizandrin B attenuates angiotensin II induced endothelial to mesenchymal transition in vascular endothelium by suppressing NF-κB activation

You, Shengban; Qian, Jianchang; Wu, Gaojun; Qian, Yuanyuan; Wang, Zhengxian; Chen, Taiwei; Wang, Jingying; Huang, Weijian; Liang, Guang

doi:10.1016/j.phymed.2019.152955

Cited by 27 publications

(16 citation statements)

References 34 publications

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“…EndMT leads to vascular damage during angiotensin-IItreated chronic inflammation, which can be prevented by treatment with schisandrin B. Schisandrin B is a natural product derived from Schisandra chinensis that can inhibit the activation of NF-κB. Schisandrin B was also found to suppress inflammation/ROS-mediated EndMT by inhibiting NF-κB 48 . Hypoxia is the main factor promoting the occurrence of EndMT.…”

Section: Role Of Oxidative Stress and Hypoxia In Endmtmentioning

confidence: 99%

Endothelial-to-mesenchymal transition in anticancer therapy and normal tissue damage

et al. 2020

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Endothelial-to-mesenchymal transition (EndMT) involves the phenotypic conversion of endothelial-to-mesenchymal cells, and was first discovered in association with embryonic heart development. EndMT can regulate various processes, such as tissue fibrosis and cancer. Recent findings have shown that EndMT is related to resistance to cancer therapy, such as chemotherapy, antiangiogenic therapy, and radiation therapy. Based on the known effects of EndMT on the cardiac toxicity of anticancer therapy and tissue damage of radiation therapy, we propose that EndMT can be targeted as a strategy for overcoming tumor resistance while reducing complications, such as tissue damage. In this review, we discuss EndMT and its roles in damaging cardiac and lung tissues, as well as EndMT-related effects on tumor vasculature and resistance in anticancer therapy. Modulating EndMT in radioresistant tumors and radiationinduced tissue fibrosis can especially increase the efficacy of radiation therapy. In addition, we review the role of hypoxia and reactive oxygen species as the main stimulating factors of tissue damage due to vascular damage and EndMT. We consider drugs that may be clinically useful for regulating EndMT in various diseases. Finally, we argue the importance of EndMT as a therapeutic target in anticancer therapy for reducing tissue damage.

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Section: Role Of Oxidative Stress and Hypoxia In Endmtmentioning

confidence: 99%

Endothelial-to-mesenchymal transition in anticancer therapy and normal tissue damage

et al. 2020

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“…And it belongs to dibenzocyclooctadiene derivatives chemically. In general, Schisandrin B has shown various benefits in different organs and diseases, such as osteoarthritis, renal fibrosis, and myocardial ischemia ( Ran et al, 2018 ; Zhao et al, 2018 ; Cao et al, 2019 ), and it has been reported to regulate several signaling pathways, including NF-κB, MAPK, PI3K/AKT, and Nrf2/HO-1 pathways ( Zhu et al, 2017 ; Feng et al, 2018 ; Zhao et al, 2018 ; You et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

“…Schisandrin B is a bioactive component isolated from the traditional Chinese medicine named Schisandra chinensis. Schisandrin B has shown varieties of biological and pharmacological properties, including antiinflammation and antioxidative activities ( Ding et al, 2018 ; You et al, 2019 ). For instance, Schisandrin B has been reported to ameliorate chondrocytes inflammation and osteoarthritis by repression of MAPK and NF-κB pathways ( Ran et al, 2018 ), indicating the potential mechanism of its antiinflammation property.…”

Section: Introductionmentioning

confidence: 99%

Schisandrin B Inhibits Osteoclastogenesis and Protects Against Ovariectomy-Induced Bone Loss

et al. 2020

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Osteoporosis is a systemic skeletal disease which is highly prevalent worldwide and considered to be associated with excessive bone resorption mediated by osteoclast. Osteoclast differentiation is featured by the activation of inflammation-related pathways and the generation of reactive oxygen species. Schisandrin B is a bioactive compound with strong antiinflammation and antioxidative properties, we thus speculated that Schisandrin B might serve as a potential candidate for osteoporosis. In the present study, we found that the formation and` function of osteoclasts were dramatically suppressed by Schisandrin B. And consistent with the in vitro results, treatment with Schisandrin B attenuated ovariectomy-induced bone loss in mice. Moreover, Schisandrin B notably inhibited the activation of mitogen activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) pathways and scavenged ROS by activating nuclear factor E2 p45-related factor 2 (Nrf2) signaling. In conclusion, our study indicates that Schisandrin B is an effective approach to treat osteoporosis and other osteoclast-related diseases.

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“…The NF-κB-EGFP NRK-52E stable cell line was prepared by lentiviral infection as described in our previous publication. 15,16 During the experiment, the NFκB-EGFP NRK-52E stable cells were incubated with LPS (0.5 μg/mL) for 6 h. Mean fluorescence intensity was analyzed by flow cytometry.…”

Section: Nf-κb Activity Assaymentioning

confidence: 99%

<p>AZD4547 Attenuates Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting Inflammation: The Role of FGFR1 in Renal Tubular Epithelial Cells</p>

Zhang

Zhao

et al. 2020

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Introduction: Inflammation plays an important role in the pathogenesis of acute kidney injury (AKI). Fibroblast growth factor receptor 1 (FGFR1) signaling is implicated in kidney pathology. AZD4547 is a small molecule inhibitor of FGFR1. Materials and Methods: Here, we investigated whether AZD4547 could mitigate inflammatory responses in AKI. C57BL/6 mice were injected with lipopolysaccharide (LPS) to induce AKI. FGFR1 was blocked using AZD4547 or CRISPR/Cas9 genome editing. After immunofluorescent double-staining of kidney tissues showing that P-FGFR1 was localized to renal tubular epithelial cells, a tubular epithelial cell line (NRK-52E) was used for in vitro analysis. Results: AZD4547 significantly reduced renal inflammation, cell apoptosis, and kidney dysfunction in AKI mice. In vitro, treatment of NRK-52E cells with AZD4547 attenuated LPS-induced inflammatory responses and was associated with downregulated P-FGFR1 levels. These findings were further confirmed in NRK-52E cells by knocking down the expression of FGFR1. Conclusion: Our findings provide direct evidence that FGFR1 mediates LPS-induced inflammation leading to renal dysfunction. We also show that AZD4547 is a potential therapeutic agent to reduce inflammatory responses in AKI. Both FGFR1 and AZD4547 may interesting therapeutic options to combat AKI.

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Schizandrin B attenuates angiotensin II induced endothelial to mesenchymal transition in vascular endothelium by suppressing NF-κB activation

Cited by 27 publications

References 34 publications

Endothelial-to-mesenchymal transition in anticancer therapy and normal tissue damage

Endothelial-to-mesenchymal transition in anticancer therapy and normal tissue damage

Schisandrin B Inhibits Osteoclastogenesis and Protects Against Ovariectomy-Induced Bone Loss

<p>AZD4547 Attenuates Lipopolysaccharide-Induced Acute Kidney Injury by Inhibiting Inflammation: The Role of FGFR1 in Renal Tubular Epithelial Cells</p>

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