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baicalin/infarction
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Baicalin attenuates acute myocardial infarction of rats via mediating the mitogen-activated protein kinase pathway.
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Baicalin is a bioactive ingredient from the herb and has possessed various pharmacological actions. The present study was performed to evaluate the cardioprotective potential of baicalin against myocardial infarction and explore the potential mechanism. Baicalin was intraperitoneally injected into
Protective Effects of Baicalin on Experimental Myocardial Infarction in Rats.
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OBJECTIVE
This study aimed to investigate the protective effects of baicalin on myocardial infarction in rats and explore the related mechanisms.
METHODS
Fifty Sprague Dawley rats were randomly divided into the control, model, and low-, medium- and high-dose baicalin groups. The latter 3 groups were
Baicalin ameliorates isoproterenol-induced acute myocardial infarction through iNOS, inflammation and oxidative stress in rat.
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Baicalin belongs to glucuronic acid glycosides and after hydrolysis baicalein and glucuronic acid come into being. It has such effects as clearing heat and removing toxicity, anti-inflammation, choleresis, bringing high blood pressure down, diuresis, anti-allergic reaction and so on. In this study,
Baicalin ameliorates isoproterenol-induced acute myocardial infarction through iNOS, inflammation, oxidative stress and P38MAPK pathway in rat.
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Baicalin is one of the active ingredients in the skullcap, with a variety of pharmacological effects, such as blood pressure reduction, sedation, liver-protection, gallbladder-protection, anti-bacteria, anti-inflammation, etc. The aim of this study was to investigate the potential cardioprotective
Baicalin inhibiting cerebral ischemia/hypoxia-induced neuronal apoptosis via MRTF-A-mediated transactivity.
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Baicalin has been shown to provide the neuroprotective effect by alleviating cerebral ischemia injury. However, little's known about the underlying mechanism. Here, a cerebral artery occlusion (MACO)/reperfusion rat model and rat primary cortical neuron culture exposed to hydrogen peroxide (H2O2)
Gene expression profile induced by oral administration of baicalin and gardenin after focal brain ischemia in rats.
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OBJECTIVE
To investigate differential gene expression and the pharmacological mechanism of baicalin and gardenin in focal cerebral ischemia in rats with high-density cDNA microarray.
METHODS
Rat left middle cerebral arteries were occluded and treated with either baicalin or gardenin. The
Poly-dimensional network comparative analysis reveals the pure pharmacological mechanism of baicalin in the targeted network of mouse cerebral ischemia.
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This study aimed to investigate the pure pharmacological mechanisms of baicalin/baicalein (BA) in the targeted network of mouse cerebral ischemia using a poly-dimensional network comparative analysis.
Eighty mice with induced focal cerebral ischemia were randomly divided into four groups: BA, Concha
Baicalin can scavenge peroxynitrite and ameliorate endogenous peroxynitrite-mediated neurotoxicity in cerebral ischemia-reperfusion injury.
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BACKGROUND
Baicalin is one of the principal flavonoids isolated from the dried root of Scutellaria baicalensis Georgi that has long been used to treat ischemic stroke. However, its neuroprotective mechanisms against cerebral ischemia injury are poorly understood.
OBJECTIVE
To explore the
Neuroprotective effect of baicalin in a rat model of permanent focal cerebral ischemia.
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This investigation was performed to determine the neuroprotective effect of baicalin on permanent cerebral ischemia injury in rats and the potential mechanisms in this process. Adult male Sprague-Dawley rats underwent permanent middle cerebral artery occlusion (pMCAO). The rats were then received
Baicalin inhibits TLR2/4 signaling pathway in rat brain following permanent cerebral ischemia.
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Recent work from our laboratory demonstrated that baicalin attenuates inflammatory reaction and cerebral ischemia injury in rats. Toll-like receptor 2 and 4 (TLR2/4) and the downstream nuclear factor-kappa B (NF-κB) signaling pathway, which mediate the inflammatory reaction, are involved in the
Baicalin attenuates focal cerebral ischemic reperfusion injury through inhibition of nuclear factor κB p65 activation.
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Baicalin is a flavonoid compound purified from plant Scutellaria baicalensis Georgi. We aimed to evaluate the neuroprotective effects of baicalin against cerebral ischemic reperfusion injury. Male Wistar rats were subjected to middle cerebral artery occlusion (MCAO) for 2 h followed by reperfusion
Baicalin attenuates myocardial ischemia-reperfusion injury through Akt/NF-κB pathway.
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BACKGROUND
Baicalin can attenuate myocardial ischemia-reperfusion (I/R) on damage. However, the mechanisms are still not fully understood. The study aimed to investigate the antiapoptosis and anti-inflammatory effects of baicalin on myocardial I/R-induced injury.
METHODS
We established male rats I/R
Promoting effect of baicalin on nitric oxide production in CMECs via activating the PI3K-AKT-eNOS pathway attenuates myocardial ischemia-reperfusion injury.
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Neuroprotective effect of baicalin on focal cerebral ischemia in rats.
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Baicalin, a flavonoid compound from the root of the herb Scutellaria baicalensis Georgi, has been widely used to treat patients with inflammatory disease. The aim of this study was to assess the efficacy of baicalin in a rat model of focal cerebral ischemia. Adult male Sprague-Dawley rat models of
Pure mechanistic analysis of additive neuroprotective effects between baicalin and jasminoidin in ischemic stroke mice.
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Both baicalin (BA) and jasminoidin (JA) are active ingredients in Chinese herb medicine Scutellaria baicalensis and Fructus gardeniae, respectively. They have been shown to exert additive neuroprotective action in ischemic stroke models. In this study we used transcriptome analysis to explore the
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