Cerebrolysin alleviates cognitive deficits induced by chronic cerebral hypoperfusion by increasing the levels of plasticity-related proteins and decreasing the levels of apoptosis-related proteins in the rat hippocampus

Liu, Zhijuan; Hu, Ming; Lu, Peiyuan; Wang, Hebo; Qi, Qianqian; Xu, Jing; Xiao, Yining; Fan, Mingyue; Jia, Yanqiu; Zhang, Dandan

doi:10.1016/j.neulet.2017.04.022

Cited by 32 publications

(22 citation statements)

References 32 publications

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“…It is characterized by cytoplasmic condensation, pyknotic nuclei and DNA fragmentation, which can be labeled by TUNEL staining of single or double strands break in DNA. Research have reported chronic cerebral hypoperfusion could promote apoptosis [35]. Our results observed that a large number of apoptotic neurons in VD model rats, while SalB prevented apoptosis of hippocampal neurons in CA1 region in VD model rats.…”

Section: Discussionsupporting

confidence: 60%

Salvianolic Acid B Ameliorates Cognitive Deficits Through IGF-1/Akt Pathway in Rats with Vascular Dementia

Zhang

et al. 2017

Cell Physiol Biochem

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BackgroundAims: Salvianolic acid B (SalB) is a natural polyphenolic compound enriched in Salvia miltiorrhiza Bunge. Our study was designed to explore the role of Sal B on cognitive impairment in vascular dementia (VD) model rats, as well as its possible molecular mechanisms. Methods: Rats were randomly divided into four groups (n = 15 for each group): Control group, Sal B group (normal Sprague Dawley rats treated with Sal B), VD group and VD + Sal B group. The VD group rats were established by permanent bilateral common carotid artery occlusion (BCCAO). Animals in the Control and Sal B group received the same operation without bilateral common carotid arteries occlusion. The animals in Sal B group and VD + Sal B group received Sal B (20 mg/kg) orally once a day for consecutive 6 weeks. We investigated the effects of SalB on BCCAO-induced cognitive deficits rats models via the Morris water maze experiment. To explore the mechanisms of Sal B on cognitive function, we detected the expression of IGF-1, Akt and p-Akt, and the rate of cell apoptosis in CA1 region. Results: Our results observed that hippocampal IGF-1 was decreased in VD model rats, while SalB reversed the alteration of IGF-1 levels. The expression of hippocampal Akt showed no significant difference between control and VD group, however, p-Akt level was significantly decreased in VD group. After 6 weeks of SalB treatment, p-Akt level was significantly increased. A large number of apoptotic neurons were found in VD model rats, while SalB prevented apoptosis of hippocampal neurons in CA1 region in VD model rats. Conclusion: SalB significantly ameliorated cognitive deficits in BCCAO-induced VD model rats. The potential mechanism underlying the protective effects may be mediated through IGF-1/Akt pathway.

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Section: Discussionsupporting

confidence: 60%

Salvianolic Acid B Ameliorates Cognitive Deficits Through IGF-1/Akt Pathway in Rats with Vascular Dementia

Zhang

et al. 2017

Cell Physiol Biochem

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“…10 min before pilocarpine injection. The present study used this cerebrolysin concentration since several works have demonstrated a significant neuroprotective effect after brain insult (Zhang Y. et al, 2013;Liu et al, 2017;Zhang et al, 2019).…”

Section: Cerebrolysin Administrationmentioning

confidence: 99%

Effects of Cerebrolysin on Hippocampal Neuronal Death After Pilocarpine-Induced Seizure

et al. 2020

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Epilepsy is one of the most common and severe brain diseases. The exact cause of epilepsy is unclear. Epilepsy often occurs following brain damage, such as traumatic brain injury (TBI) and ischemia. Cerebrolysin is a porcine brain peptide that is a unique neurotropic and neuroprotective agent. Cerebrolysin has been reported to increase neuroprotective effects after TBI, ischemia, and other CNS diseases. However, the effects of cerebrolysin on seizures are not known. Therefore, this study aimed to investigate the effects of neuropeptide cerebrolysin on neuronal death in the hippocampus after a seizure. To confirm the effects of cerebrolysin, we used a pilocarpine-induced seizure animal model. Cerebrolysin (2.5 ml/kg, i.p., once per day for 7 days) was immediately injected after a seizure induction. After 1 week, we obtained brain tissues and performed staining to histologically evaluate the potentially protective effects of cerebrolysin on seizure-induced neuronal death in the hippocampus. We found that cerebrolysin decreased hippocampal neuronal death after a seizure. In addition, an increase in brain-derived neurotrophic factor (BDNF) was confirmed through Western blot analysis to further support our hypothesis. Therefore, the present study suggests that the administration of cerebrolysin can be a useful therapeutic tool for preventing neuronal death after a seizure.

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“…Chronic cerebral hypoperfusion (CCH), a common consequence of various cerebral vascular disorders, has been identified as a key etiological factor in VCI 2 . CCH can induce neuroplasticity damage, cerebral circulation abnormality, and hypoperfusion-related metabolic changes in various regions of the brain, including hippocampus, leading to an irreversible dysfunction in cognition 3 , 4 . Currently, many neuroprotective agents are commonly used to control the neuronal degenerative processes in patients with CCH 5 .…”

Section: Introductionmentioning

confidence: 99%

Xiaoshuan enteric-coated capsule alleviates cognitive impairment by enhancing hippocampal glucose metabolism, hemodynamics and neuroplasticity of rat with chronic cerebral hypoperfusion

Zhang

Zou

et al. 2018

Sci Rep

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Chronic cerebral hypoperfusion (CCH) is identified as a critical risk factor of dementia in patients with cerebrovascular disease. Xiaoshuan enteric-coated capsule (XSECC) is a compound Chinese medicine approved by Chinese State Food and Drug Administration for promoting brain remodeling and plasticity after stroke. The present study aimed to explore the potential of XSECC to improve cognitive function after CCH and further investigate the underlying mechanisms. CCH was induced by bilateral common carotid artery occlusion (BCCAO) in rats. XSECC (420 or 140 mg/kg) treatment remarkably reversed BCCAO-induced cognitive deficits. Notably, after XSECC treatment, magnetic resonance angiography combined with arterial spin labeling noninvasively demonstrated significantly improved hippocampal hemodynamics, and 18F-FDG PET/CT showed enhanced hippocampal glucose metabolism. In addition, XSECC treatment markedly alleviated neuropathologies and improved neuroplasticity in the hippocampus. More importantly, XSECC treatment facilitated axonal remodeling by regulating the phosphorylation of axonal growth related proteins including protein kinase B (AKT), glycogen synthase kinase-3β (GSK-3β) and collapsin response mediator protein-2 (CRMP2) in the hippocampus. Taken together, the present study demonstrated the beneficial role of XSECC in alleviating BCCAO-induced cognitive deficits by enhancing hippocampal glucose metabolism, hemodynamics and neuroplasticity, suggesting that XSECC could be a useful strategy in cerebral hypoperfusion state and dementia.

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Cerebrolysin alleviates cognitive deficits induced by chronic cerebral hypoperfusion by increasing the levels of plasticity-related proteins and decreasing the levels of apoptosis-related proteins in the rat hippocampus

Cited by 32 publications

References 32 publications

Salvianolic Acid B Ameliorates Cognitive Deficits Through IGF-1/Akt Pathway in Rats with Vascular Dementia

Salvianolic Acid B Ameliorates Cognitive Deficits Through IGF-1/Akt Pathway in Rats with Vascular Dementia

Effects of Cerebrolysin on Hippocampal Neuronal Death After Pilocarpine-Induced Seizure

Xiaoshuan enteric-coated capsule alleviates cognitive impairment by enhancing hippocampal glucose metabolism, hemodynamics and neuroplasticity of rat with chronic cerebral hypoperfusion

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