Aucubin promotes angiogenesis via estrogen receptor beta in a mouse model of hindlimb ischemia

Chen, Lu; Yang, Yue; Zhang, Lusha; Li, Chunxiao; Coffie, Joel Wake; Geng, Xiao; Qiu, Li-Zhen; You, Xingyu; Fang, Zhirui; Song, Min; Gao, Xiumei; Wang, Hong

doi:10.1016/j.jsbmb.2017.07.007

Cited by 17 publications

(12 citation statements)

References 54 publications

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“…In the treatment of estrogen receptor-positive breast cancer, selective estrogen receptor modulators can effectively inhibit angiogenesis [7]. During the ischemia-reperfusion injury of lower extremity muscles, estrogen receptor β (ER β )-mediated pathways can promote blood vessel formation [8]. Previous studies have confirmed that estrogen receptors are closely related to angiogenesis in a variety of cancers and cardiovascular diseases, such as breast cancer [9, 10].…”

Section: Introductionmentioning

confidence: 99%

Angiogenesis Changes in Ovariectomized Rats with Osteoporosis Treated with Estrogen Replacement Therapy

Zhang

Fang

Ding

et al. 2019

BioMed Research International

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To investigate whether angiogenesis changes in early menopausal osteoporosis treated with estrogen replacement therapy, 120 rats were randomly divided into five groups: sham operation group (SHAM), ovariectomy group (OVX), and ovariectomy plus three different estrogen doses replacement therapy groups (OVX + E2). We detected the bone microarchitecture and measured the expression levels of estrogen receptor beta (ERβ), vascular endothelial growth factor (VEGF), osteoprotegerin (OPG), and receptor activator of NF-κB ligand (RANKL). CD31 immunofluorescence and silica gel perfusion imaging were used to analyze the vascular distribution. We confirmed that the femur BMD of ovariectomized rats was significantly lower than SHAM group and OVX+E2 groups. After estrogen therapy, the local microvascular formation increased after estrogen treatment in a dose dependent manner. ERβ was downregulated and VEGF was upregulated, positively correlated with estrogen dosage. We successfully constructed an osteoporosis model of ovariectomized rats with estrogen replacement therapy. We also found angiogenesis changed in early menopausal osteoporosis treated with estrogen replacement therapy. We indicated that estrogen replacement therapy increased angiogenesis through VEGF upregulation. However, we observed that, at the highest doses of estrogen studied, increased angiogenesis was associated with a decrease in BMD, the underlying mechanisms of which remain unclear.

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Section: Introductionmentioning

confidence: 99%

Angiogenesis Changes in Ovariectomized Rats with Osteoporosis Treated with Estrogen Replacement Therapy

Zhang

Fang

Ding

et al. 2019

BioMed Research International

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“…Moreover, it reportedly downregulates expression of HIF-1α-independent VEGF and angiogenesis thereby inhibiting the TLR4/MyD88 signaling pathway [24,25]. Aucubin has been shown to alleviate inflammation and H 2 O 2 -induced neuron cell apoptosis through Nrf2-mediated signaling activity, to exert proangiogenic effects through the ERβ-mediated VEGF signaling pathway [26,27]. On the other hand, salidroside was found to attenuate neuroinflammation and alleviate apoptosis in PC12 cells, thereby suppressing complications of brain ischemic injury [28].…”

Section: Discussionmentioning

confidence: 99%

Serum Pharmacochemistry Combining Network Pharmacology to Discover the Active Constituents and Effect of Xijiao Dihuang Tang Prescription for Treatment of Blood-Heat and Blood-Stasis Syndrome-Related Disease

Chen

Dai

Xia

et al. 2022

Oxidative Medicine and Cellular Longevity

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Xijiao Dihuang Tang (XDT), a classic TCM prescription, has been used to clinically treat blood-heat and blood-stasis syndrome- (BHSS-) related diseases, including hemorrhagic stroke and sepsis. However, the active constituents and mechanism of XDT in the treatment of BHSS-related diseases have not been elucidated due to the lack of appropriate methodologies. In this study, serum pharmacochemistry and network pharmacology were used to explore the active constituents and the mechanism of XDT in the treatment of BHSS-related diseases. The effects of XDT were evaluated using dry yeast-induced rats as rat models with BHSS, which demonstrated the antipyretic and anticoagulant properties of XDT. The HPLC-QTOF/MS/MS assay was used to identify 60 serum constituents of XDT (SCXDT). Then, 338 targets of 60 SCXDT were predicted by integrating multiple databases and the MACCS fingerprint similarity prediction method. The degree of topological properties with targets of 19 key active constituents in SCXDT was identified and evaluated in glutamate-induced PC12 cells. Subsequently, 338 targets of 60 SCXDT were mainly involved in biological processes such as inflammation, coagulation, cell proliferation, and apoptosis, as well as oxidative contingencies via compound-target-disease network analysis. The core targets including IL-1β, IL-6, TNF, NOS3, and MAPK1 were identified using protein-protein interaction network analysis, whereas dozens of signaling pathways such as the p38MAPK signaling pathway were identified using functional pathway enrichment analysis. The results indicated that XDT has broad therapeutic and neuroprotective effects on inflammation, coagulation, oxidative stress, cell proliferation, and apoptosis in dry yeast-induced rats with BHSS and glutamate-induced PC12 cells by regulating the p38MAPK signaling pathway. This study not only discovered the active constituents of XDT but also elaborated its mechanisms in the treatment of BHSS-related diseases by intervening in a series of targets, signaling pathways, and biological processes such as inflammation, coagulation, oxidative stress, neuroprotection. The findings in this study provide a novel strategy for exploring the therapeutic efficacy of TCM prescriptions.

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“…Accumulated β-Catenin enters the nucleus to bind to transcription factor 3/lymphoid enhancing binding factor 1 (TCF3/LEF1), enhancing VEGF expression ( 45 ). ERα and ERβ also directly bind to the VEGF promoter region and increase VEGF expression upon E2 activation ( 46 – 48 ).…”

Section: Factors For Endometriosis-associated Angiogenesismentioning

confidence: 99%

Endometriosis-Associated Angiogenesis and Anti-angiogenic Therapy for Endometriosis

Chung

Han

2022

Front. Glob. Womens Health

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Endometriosis is a known estrogen-dependent inflammatory disease affecting reproductive-aged women. Common symptoms include pelvic pain, dysmenorrhea, dyspareunia, heavy menstrual bleeding, and infertility. The exact etiology of endometriosis is largely unknown, and, thus, the diagnosis and treatment of endometriosis are challenging. A complex interplay of many molecular mechanisms is thought to aid in the progression of endometriosis, most notably angiogenesis. This mini-review examines our current knowledge of the molecular etiology of endometriosis-associated angiogenesis and discusses anti-angiogenic therapy, in the blockade of endometriosis-associated angiogenesis, as potential non-hormonal therapy for the treatment of endometriosis.

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Aucubin promotes angiogenesis via estrogen receptor beta in a mouse model of hindlimb ischemia

Cited by 17 publications

References 54 publications

Angiogenesis Changes in Ovariectomized Rats with Osteoporosis Treated with Estrogen Replacement Therapy

Angiogenesis Changes in Ovariectomized Rats with Osteoporosis Treated with Estrogen Replacement Therapy

Serum Pharmacochemistry Combining Network Pharmacology to Discover the Active Constituents and Effect of Xijiao Dihuang Tang Prescription for Treatment of Blood-Heat and Blood-Stasis Syndrome-Related Disease

Endometriosis-Associated Angiogenesis and Anti-angiogenic Therapy for Endometriosis

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