picroside/ischemia

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Protective effect of picroside II on myocardial ischemia reperfusion injury in rats.

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The aim of this study was to determine the effect of picroside II on myocardial ischemia reperfusion injury in rats and to explore its underlying mechanism. Isolated rat hearts underwent 30 minutes of global ischemia followed by 120 minutes of reperfusion. Different doses of picroside II (1 μM, 10

Picroside II decreases the development of fibrosis induced by ischemia/reperfusion injury in rats.

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In kidney transplantation, renal ischemia and reperfusion injury was one of the leading factors to the development of renal fibrosis, which was the main cause of graft loss. The fibrogenic changes were associated with the long term inflammation elicited by ischemia and reperfusion injury. In the

Effect of picroside II on erythrocyte deformability and lipid peroxidation in rats subjected to hind limb ischemia reperfusion injury.

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BACKGROUND Ischemia reperfusion injury (I/R) in hind limb is a frequent and important clinical phenomenon. Many structural and functional damages are observed in cells and tissues in these kinds of injuries. In this study, we aimed to evaluate the effect of picroside II on lipid peroxidation and

The neuroprotective effect of picroside II via regulating the expression of myelin basic protein after cerebral ischemia injury in rats.

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BACKGROUND To explore the neuroprotective effect and optimize the therapeutic dose and time window of picroside II by orthogonal test and the expression of myelin basic protein (MBP) in cerebral ischemic injury in rats. Bilateral common carotid artery occlusion (BCCAO) was used to establish

Picroside II attenuates ischemia/reperfusion testicular injury by alleviating oxidative stress and apoptosis through reducing nitric oxide synthesis.

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To investigate the effect of Picroside II on testicular ischemia and reperfusion (l/R) injury and the underlying mechanism.Sprague-Dawley rats were randomly divided into 4 groups: sham operated group (Sham), Sham with Picroside II treatment group (Sham+ Pic

Neuroprotective properties of picroside II in a rat model of focal cerebral ischemia.

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The aim of this study was to explore the effect of picroside II on neuronal apoptosis and the expression of caspase-3 and poly ADP-ribose polymerase (PARP) following middle cerebral artery occlusion/reperfusion in male Wistar rats. Picroside II (10 mg/kg) was administered intravenously into the tail

Picroside II Exerts a Neuroprotective Effect by Inhibiting mPTP Permeability and EndoG Release after Cerebral Ischemia/Reperfusion Injury in Rats.

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Mitochondrial membrane permeability is closely related to cerebral ischemia/reperfusion (I/R) injury. This paper explored the neuroprotective effect of picroside II (Picr), which inhibits the permeability of mitochondrial permeability transition pore (mPTP) and endonuclease G (EndoG) release from

Picroside II Exerts a Neuroprotective Effect by Inhibiting the Mitochondria Cytochrome C Signal Pathway Following Ischemia Reperfusion Injury in Rats.

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Stroke is a common neurodegenerative disease in the wide world, and mitochondrial defects underlie the pathogenesis of ischemia, especially during reperfusion. Picroside II, the principal active component of Picrorhiza, is a traditional Chinese medicine. Our previous study demonstrated that the best

Effect of picroside II on apoptosis induced by renal ischemia/reperfusion injury in rats.

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Renal ischemia and reperfusion (I/R) injury, which commonly occurs in kidney transplantation, is the leading cause of acute kidney injury. Picroside II possesses a wide range of pharmacological effects, including anti-apoptosis effects. In the present study, the ability of picroside II to attenuate

Picroside II protects the blood-brain barrier by inhibiting the oxidative signaling pathway in cerebral ischemia-reperfusion injury.

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OBJECTIVE Thrombolysis is used to improve cerebral circulation; at the same time, neuroprotective drugs such as antioxidants should also be used. The aim of these experiments was to explore the protective mechanism of an antioxidant, picroside II, on the blood-brain barrier (BBB) after cerebral

Picroside II protects rat kidney against ischemia/reperfusion-induced oxidative stress and inflammation by the TLR4/NF-κB pathway.

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Picroside II possesses a wide range of pharmacological effects and has been demonstrated to ameliorate cerebral ischemia and reperfusion (I/R) injury. However, its effects on renal I/R injury remain unclear. In the present study, the role of picroside II in attenuating oxidative stress and the

Effect of picroside II on hind limb ischemia reperfusion injury in rats.

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BACKGROUND Many structural and functional damages are observed in cells and tissues after reperfusion of previously viable ischemic tissues. Acute ischemia reperfusion (I/R) injury of lower extremities occurs especially when a temporary cross-clamp is applied to the abdominal aorta during aortic

Picroside II protects myocardium from ischemia/reperfusion-induced injury through inhibition of the inflammatory response.

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The inflammatory response is important in the pathogenesis of myocardial ischemia/reperfusion (I/R) injury. Picroside II, the primary active constituent of Picrorhizae, has been reported to protect the myocardium from I/R-induced injury, however, the exact mechanism underlying these protective

[Effect of picroside II on expressions of TLR4 and NFkappaB in rats with cerebral ischemia reperfusion injury].

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OBJECTIVE To explore the effects of picrodide II on the expressions of Toll-like receptor 4 (TLR4) and nuclear transcription factor kappaB (NFkappaB) in brain tissue of rat after cerebral ischemic reperfusion (I/R) injury. METHODS Ten rats from 60 adult healthy female Wistar rats received

[Effect of picroside Ⅱ on the expression of mitochondrial VDAC1 after cerebral ischemia/reperfusion in rats].

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Objective: To explore the effect of picroside Ⅱ on the expression of mitochondrial voltage-dependent anion channel 1 (VDAC1) in rats after cerebral ischemiareperfusion. Methods: A total of 70 Wistar rats models with middle cerebral artery occlusionreperfusion (MCAO/R) were randomly divided into the

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