Abstract
Background and purposeThrombolysis 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 ischemia-reperfusion (CI/R) injury.MethodsTo observe the antagonistic effect of picroside II on CI/R damage, the neurological deficit score and the infarct volume were measured. To detect the protective effect of picroside II on nerve cells and the BBB, the morphology and structure of cortical brain tissue were observed, respectively. To investigate the antioxidant effect and mechanism of picroside II, reactive oxygen species (ROS) content, the activity of Nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase), and the protein levels of Nox2 and Rac-1 were detected. To investigate the protective mechanism of picroside II on the BBB, the levels of ROCK, MLCK, MMP-2 and claudin-5 were tested.ResultsA higher neurological score, bigger cortex infarction, more damaged neuron structure and injured BBB, increased content of ROS and activity of NADPH oxidase, higher protein levels of Nox2, Rac-1, ROCK, MLCK and MMP-2 and lower levels of claudin-5 were observed in the model group. In the picroside group, the neurological score, neuronal damage, BBB injury, ROS content and NADPH oxidase activity were reduced (P<0.05), and the protein levels of Rac-1, Nox2, ROCK, MLCK and MMP-2 were down-regulated (P<0.05), while the expression of claudin-5 was up-regulated (P<0.05).ConclusionsPicroside II could protect the nervous system possibly through reducing the content of ROS by down-regulating the expression of Rac-1 and Nox2 and could protect the BBB through reducing the expression of ROCK, MLCK, and MMP-2, while enhancing the expression of claudin-5.
Highlights
Stroke is a common cerebrovascular emergency, including ischemic stroke and hemorrhagic stroke
A higher neurological score, bigger cortex infarction, more damaged neuron structure and injured blood-brain barrier (BBB), increased content of reactive oxygen species (ROS) and activity of NADPH oxidase, higher protein levels of Nox2, Rac-1, ROCK, myosin light chain kinase (MLCK) and matrix metalloproteinase (MMP)-2 and lower levels of claudin-5 were observed in the model group
In order to improve the neurological function of cerebral apoplexy patients, the Guidelines for Diagnosis and Treatment of Acute Ischemic Stroke have noted that neuroprotective drugs that resist ROS must be used in conjunction with thrombolysis therapy
Summary
Stroke is a common cerebrovascular emergency, including ischemic stroke and hemorrhagic stroke. In the pathological process of cerebral ischemia/reperfusion (CI/R), the restitution of cerebral blood flow re-offers oxygen and glucose, and, at the same time, a series of oxygen-producing enzymes are activated, which leads to the release of a large amount of ROS (O2-, H2O2 and its derivatives)[7,8]. In order to improve the neurological function of cerebral apoplexy patients, the Guidelines for Diagnosis and Treatment of Acute Ischemic Stroke have noted that neuroprotective drugs that resist ROS must be used in conjunction with thrombolysis therapy. Thrombolysis is used to improve cerebral circulation; at the same time, neuroprotective drugs such as antioxidants should 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 ischemia-reperfusion (CI/R) injury
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