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Neuroprotective effects of LBP on brain ischemic reperfusion neurodegeneration
1Department of Pharmacology, Ningxia Medical University, Yinchuan, China. yujq910315@163.com.
Aim:
The present study was conducted to investigate whether LBP had a protective effect on cerebral ischemic reperfusion injury and to determine the possible mechanisms.
Materials And Methods:
Male Kunming (KM) mice were used to make the model cerebral artery occlusion/reperfusion (MCAO/R). The behavioral test was used to measure neurological deficit scores for evaluation of ischemic reperfusion damage of brain. The change of electroencephalograph (EEG) was monitored by Model SMUP-E Bio-electric Signals Processing System. The infarction area of brain was assessed in brain slices with 2% solution of 2,3,5-triphenyl tetrazolium chloride (TTC). Spectrophotometric assay was used to determine the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and lactate dehydrogenase (LDH), contents of malondialdehyde (MDA) and adenosine triphosphate (ATP) of the brain.
Results:
The results showed that LBP at doses of 20 and 40 mg/kg markedly decreased the neurological deficit scores and the infarction area in MCAO/R mice. At the same time, LBP significantly decreased MDA content, and increased SOD, GSH-Px, CAT, LDH activities in ischemic reperfusion brain.
Conclusions:
These suggest that LBP might act as a potential neuroprotective agent against the cerebral reperfusion-induced injury in the brain through reducing lipid peroxides, scavenging free radicals, and improving the energy metabolism.
Insights
This study shows that LBP protects the brain from ischemic reperfusion injury by reducing oxidative stress and improving energy metabolism. LBP significantly decreased neurological deficits and brain infarction areas in mice.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Cerebral ischemic reperfusion injury is a significant cause of brain damage.
- Understanding protective mechanisms against this injury is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the neuroprotective effects of LBP on cerebral ischemic reperfusion injury.
- To elucidate the underlying mechanisms of LBP's protective action.
Main Methods:
- A mouse model of middle cerebral artery occlusion/reperfusion (MCAO/R) was established.
- Neurological deficit scores, electroencephalograph (EEG) changes, and brain infarction areas were assessed.
- Biochemical assays were performed to measure antioxidant enzyme activities (SOD, GSH-Px, CAT), lactate dehydrogenase (LDH), malondialdehyde (MDA), and adenosine triphosphate (ATP) levels.
Main Results:
- LBP administration (20 and 40 mg/kg) significantly reduced neurological deficit scores and brain infarction areas in MCAO/R mice.
- LBP treatment decreased malondialdehyde (MDA) content, indicating reduced lipid peroxidation.
- LBP increased the activities of key antioxidant enzymes (superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT)) and lactate dehydrogenase (LDH) in the ischemic reperfusion brain.
Conclusions:
- LBP exhibits significant neuroprotective effects against cerebral ischemic reperfusion injury.
- LBP's mechanism involves reducing lipid peroxides and scavenging free radicals.
- LBP improves energy metabolism, suggesting its potential as a therapeutic agent for brain injury.
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