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Remote Limb Ischemic Preconditioning: A Neuroprotective Technique in Rodents
Published on: June 2, 2015
Picroside II has a neuroprotective effect by inhibiting ERK1/2 activation after cerebral ischemic injury in rats
Tingting Wang1,2, Li Zhai1,2, Yunliang Guo1,2
1Institute of Cerebrovascular Diseases, Affiliated Hospital of Qingdao University, Qingdao, China.
Abstract:
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 were administered an intraperitoneal injection of picroside II (20 mg/kg). The neurobehavioural function of rats was evaluated using a modified neurological severity score (mNSS) test. The cerebral infarct volume (CIV) was measured using tetrazolium chloride (TTC) staining. The morphology and ultra-structure of the nerve cells in the cortex were observed using hematoxylin and eosin (HE) staining and transmission electron microscopy (TEM), respectively. The apoptotic cells were counted using the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expression of extracellular signal-regulated kinase 1/2 (pERK1/2) in the cortex was determined using immunohistochemistry and Western blot analysis. Neurological dysfunction was observed in all rats with MCAO. In both the model and lipopolysaccharide (LPS) groups, the CIV increased, the neuronal damage in the cortex was more severe, and the number of apoptotic cells and the pERK1/2 expression significantly increased compared with the control group (P < 0.05). In treatment and U0126 groups, the neurological function was improved, the CIV decreased, the neuronal damage in the cortex was attenuated, and the number of apoptotic cells and the pERK1/2 expression significantly decreased compared with the model group (P < 0.05). No significant differences in these indices were observed between model and LPS groups or treatment and U0126 groups (P > 0.05). The results suggest that activation of ERK1/2 in cerebral ischaemia induces neuronal apoptosis and picroside II may reduce neuronal apoptosis to confer protection against cerebral ischemic injury by inhibiting ERK1/2 activation.
Insights
Picroside II protects against cerebral ischemic injury by inhibiting ERK1/2 activation, reducing neuronal apoptosis and improving neurological function in rats. This study reveals a key mechanism for neuroprotection against stroke.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Cerebral ischemia injury leads to significant neurological dysfunction.
- The ERK1/2 signaling pathway is implicated in neuronal apoptosis following ischemic events.
- Identifying therapeutic agents that target this pathway is crucial for neuroprotection.
Purpose of the Study:
- To investigate the neuroprotective effects of picroside II after cerebral ischemia.
- To elucidate the underlying mechanism involving the ERK1/2 signaling pathway.
- To evaluate picroside II's impact on neuronal apoptosis and brain injury in a rat model.
Main Methods:
- Middle cerebral artery occlusion (MCAO) model in Wistar rats.
- Administration of picroside II and assessment of neurobehavioral function (mNSS).
- Measurement of cerebral infarct volume (CIV) using TTC staining.
- Histological (HE, TUNEL) and ultrastructural (TEM) analysis of neuronal damage and apoptosis.
- Quantification of pERK1/2 expression via immunohistochemistry and Western blot.
Main Results:
- MCAO induced significant neurological deficits, increased CIV, neuronal damage, apoptosis, and pERK1/2 expression.
- Picroside II treatment significantly improved neurological function, reduced CIV, attenuated neuronal damage, and decreased apoptosis and pERK1/2 levels.
- Inhibition of ERK1/2 activation with U0126 mirrored the protective effects of picroside II.
Conclusions:
- Activation of the ERK1/2 pathway plays a critical role in inducing neuronal apoptosis during cerebral ischemia.
- Picroside II confers neuroprotection against cerebral ischemic injury.
- The neuroprotective mechanism of picroside II involves the inhibition of ERK1/2 activation, thereby reducing neuronal apoptosis.
