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[Protective effect of picroside Ⅱ on the brain tissue through antioxidation in stroke rats].
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Objective: To investigate the effect and mechanisms of picroside Ⅱ on the brain tissue after cerebral ischemia reperfusion(I/R) in rats. Methods: The middle cerebral artery occlusion(MCAO) rat model was established by inserting a monofilament into middle cerebral artery. The
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
Primary study for the therapeutic dose and time window of picroside II in treating cerebral ischemic injury in rats.
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The aim of this study was to explore the optimal therapeutic dose and time window of picroside II for treating cerebral ischemic injury in rats according to the orthogonal test. The middle cerebral artery occlusion (MCAO) models were established by intraluminally inserting a thread into middle
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
Anti-inflammation effects of picroside 2 in cerebral ischemic injury rats.
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BACKGROUND
Excitatory amino acid toxicity, oxidative stress, intracellular calcium overload, as well as inflammation and apoptosis are involved in the pathological process after cerebral ischemic reperfusion injury. Picrodide 2 could inhibit neuronal apoptosis and play anti-oxidant and
Picroside II Inhibits Neuronal Apoptosis and Improves the Morphology and Structure of Brain Tissue following Cerebral Ischemic Injury in Rats.
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This paper aimed to explore the protective effects of picroside II against the neuronal apoptosis and changes in morphology and structure that follow cerebral ischemic injury in rats. A focal cerebral ischemic model was established by inserting a monofilament thread to achieve middle cerebral artery
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
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 has a neuroprotective effect by inhibiting ERK1/2 activation after cerebral ischemic injury in rats.
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In the study, the neuroprotective effect and underlying mechanism of picroside II were explored, and its involvement in the ERK1/2 signal pathway after cerebral ischemia injury in rats. A monofilament thread was inserted to generate middle cerebral artery occlusion (MCAO) in 100 Wistar rats that
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