2020
DOI: 10.1016/j.biopha.2020.110766
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TMEM16A-encoded anoctamin 1 inhibition contributes to chrysin-induced coronary relaxation

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Cited by 5 publications
(4 citation statements)
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“…This activity could be used in the treatment of diseases with an etiology associated with vasomotor dysfunctions, such as hypertension or stroke. In addition, chrysin in mitoxantrone cardiotoxicity studies in a mouse model reduced cardiomyocyte apoptosis and loss of intermediate filaments, which may indicate its anti-apoptotic properties and their importance in cardioprotective action [24,42,43].…”
Section: Cardioprotective Activitymentioning
confidence: 94%
“…This activity could be used in the treatment of diseases with an etiology associated with vasomotor dysfunctions, such as hypertension or stroke. In addition, chrysin in mitoxantrone cardiotoxicity studies in a mouse model reduced cardiomyocyte apoptosis and loss of intermediate filaments, which may indicate its anti-apoptotic properties and their importance in cardioprotective action [24,42,43].…”
Section: Cardioprotective Activitymentioning
confidence: 94%
“…According to the previous experimental method ( Ma et al, 2020 ), we evaluated the effects of DBD, ASR, and AR on MCA contraction induced by the release of internal Ca 2+ from organelles such as the endoplasmic reticulum and mitochondria into the cytoplasmic matrix ([Ca 2+ ] in ). After incubating the MCA vessels with EGTA containing the Ca 2+ -free PSS fluid for 10 min to remove intracellular Ca 2+ , the vessels were then administered with the EGTA- and Ca 2+ -free PSS fluids containing DBD, ASR, and AR (64 mg/ml) for 10 min.…”
Section: Methodsmentioning
confidence: 99%
“…This indicates that CSS can exert effects similar to the antidepressant venlafaxine by regulating BDNF expression levels ( Zhang and Liu, 2020 ). Tropomyosin receptor kinase B (TrkB) is a specific receptor for BDNF, and it has been confirmed that activating BDNF-TrkB signaling can have an antidepressant effect ( Ma et al, 2020 ). Figure 4 After intervening with CSS in depression model rats, it was found that compared to the model group, rats in the CSS group exhibited significantly increased expression of BDNF and its receptor TrkB in the hippocampus, prefrontal cortex, and amygdala, suggesting that the mechanism through which CSS alleviates depressive states might be related to the increased expression of BDNF and its receptor TrkB in these brain regions ( Ying et al, 2011 ).…”
Section: The Antidepressant Mechanisms Of Cssmentioning
confidence: 99%