biochanin a/infarkt

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Therapeutic potential of biochanin-A against isoproterenol -induced myocardial infarction in rats.

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This study determined the effect of Biochanin A (BCA) on isoproterenol (ISO) induced myocardial infarction (MI) in male Wistar rats.Animals (Weighing 150-180 g) were divided into four groups, with six animals in each group and pretreated with BCA (10mg/kg

Biochanin A attenuates myocardial ischemia/reperfusion injury through the TLR4/NF-κB/NLRP3 signaling pathway.

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Myocardial ischemia/reperfusion (Ml/R) injury is a leading cause of damage in cardiac tissues, with high rates of mortality and disability. Biochanin A (BCA) is a main constituent of Trifolium pratense L. This study was intended to explore the effect of BCA on Ml/R injury and explore

Biochanin A protects against focal cerebral ischemia/reperfusion in rats via inhibition of p38-mediated inflammatory responses.

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Logi sisse

Biochanin A, an O-methylated natural isoflavonoid classified as phytoestrogen, has been reported to show anti-tumorigenesis, anti-oxidation, and anti-inflammatory properties. However, little is known about the effects of biochanin A on cerebral ischemia/reperfusion. In this study, the

Biochanin A Provides Neuroprotection Against Cerebral Ischemia/Reperfusion Injury by Nrf2-Mediated Inhibition of Oxidative Stress and Inflammation Signaling Pathway in Rats.

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BACKGROUND Oxidative stress and neuroinflammation are 2 pivotal mechanisms in the progression of cerebral ischemia/reperfusion injury. Biochanin A, a natural phytoestrogen, has been reported to protect against ischemic brain injury in animal experiments, but the possible pharmacological mechanisms

Determination and pharmacokinetic study of taxifolin in rabbit plasma by high-performance liquid chromatography.

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Taxifolin has been widely used in the treatment of cerebral infarction and sequelae, cerebral thrombus, coronary heart disease and angina pectoris. A reliable sensitive reversed-phase high-performance liquid chromatography (RP-HPLC) method with UV detection for the pharmacokinetic study of taxifolin

17Beta-estradiol, its metabolites, and progesterone inhibit cardiac fibroblast growth.

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Postmenopausal women (PMW) have increased incidence of cardiovascular disease, and estrogen substitution therapy has been shown to have cardioprotective effects. Since abnormal growth of cardiac fibroblasts (CFs) is associated with hypertension and myocardial infarction and estrogen inhibits

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