Animal models of cerebral ischemia: A review

Ma, Rong; Xie, Qian; Li, Yong; Chen, Zhuoping; Ren, Mihong; Chen, Hai; Li, Hongyan; Li, Jinxiu; Wang, Jian

doi:10.1016/j.biopha.2020.110686

Cited by 72 publications

(54 citation statements)

References 120 publications

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“…It is undeniable that only few patients receive thrombolysis within 6–8 h in the treatment of cerebral ischemia, which results in most patients developing permanent cerebral ischemia ( Chalela et al, 2007 ). Regrettably, most experimental studies being focused on transient ischemic stroke ( Mcbride and Zhang, 2017 ; Ma et al, 2020 ). This phenomenon can also be seen in Table 1 .…”

Section: Discussionmentioning

confidence: 99%

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Progress in Borneol Intervention for Ischemic Stroke: A Systematic Review

Ren

Wang

et al. 2021

Front. Pharmacol.

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Background: Borneol is a terpene and bicyclic organic compound that can be extracted from plants or chemically synthesized. As an important component of proprietary Chinese medicine for the treatment of stroke, its neuroprotective effects have been confirmed in many experiments. Unfortunately, there is no systematic review of these studies. This study aimed to systematically examine the neuroprotective effects of borneol in the cascade reaction of experimental ischemic stroke at different periods.Methods: Articles on animal experiments and cell-based research on the actions of borneol against ischemic stroke in the past 20°years were collected from Google Scholar, Web of Science, PubMed, ScienceDirect, China National Knowledge Infrastructure (CNKI), and other biomedical databases. Meta-analysis was performed on key indicators in vivo experiments. After sorting the articles, we focused on the neuroprotective effects and mechanism of action of borneol at different stages of cerebral ischemia.Results: Borneol is effective in the prevention and treatment of nerve injury in ischemic stroke. Its mechanisms of action include improvement of cerebral blood flow, inhibition of neuronal excitotoxicity, blocking of Ca2+ overload, and resistance to reactive oxygen species injury in the acute ischemic stage. In the subacute ischemic stage, borneol may antagonize blood-brain barrier injury, intervene in inflammatory reactions, and prevent neuron excessive death. In the late stage, borneol promotes neurogenesis and angiogenesis in the treatment of ischemic stroke.Conclusion: Borneol prevents neuronal injury after cerebral ischemia via multiple action mechanisms, and it can mobilize endogenous nutritional factors to hasten repair and regeneration of brain tissue. Because the neuroprotective effects of borneol are mediated by various therapeutic factors, deficiency caused by a single-target drug is avoided. Besides, borneol promotes other drugs to pass through the blood-brain barrier to exert synergistic therapeutic effects.

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Section: Discussionmentioning

confidence: 99%

“…(Chalela et al, 2007). Regrettably, most experimental studies being focused on transient ischemic stroke (Mcbride and Zhang, 2017;Ma et al, 2020). This phenomenon can also be seen in Table 1.…”

Section: Outlooksmentioning

confidence: 95%

Progress in Borneol Intervention for Ischemic Stroke: A Systematic Review

Ren

Wang

et al. 2021

Front. Pharmacol.

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“…Conversely, the drug has proven effective in mice which underwent transient models of middle cerebral artery occlusion (tMCAO) [7]. Some evidence suggests a cerebral ischemia-reperfusion model such as tMCAO should be preferentially used for testing anti-inflammatory drugs [52]. This is particularly true in cases where the drug candidate may be used as an adjunct to thrombolysis [53].…”

Section: Discussionmentioning

confidence: 99%

The effect of fingolimod on regulatory T cells in a mouse model of brain ischaemia

Malone

Díaz

Shearer

et al. 2021

J Neuroinflammation

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Background The role of the immune system in stroke is well-recognised. Fingolimod, an immunomodulatory agent licensed for the management of relapsing-remitting multiple sclerosis, has been shown to provide benefit in rodent models of stroke. Its mechanism of action, however, remains unclear. We hypothesised fingolimod increases the number and/or function of regulatory T cells (Treg), a lymphocyte population which promotes stroke recovery. The primary aim of this study was to rigorously investigate the effect of fingolimod on Tregs in a mouse model of brain ischaemia. The effect of fingolimod in mice with common stroke-related comorbidities (ageing and hypercholesteremia) was also investigated. Methods Young (15–17 weeks), aged C57BL/6 mice (72–73 weeks), and ApoE−/− mice fed a high-fat diet (20–21 weeks) underwent permanent electrocoagulation of the left middle cerebral artery. Mice received either saline or fingolimod (0.5 mg/kg or 1 mg/kg) at 2, 24, and 48 h post-ischaemia via intraperitoneal injection. Another cohort of young mice (8–9, 17–19 weeks) received short-term (5 days) or long-term (10 days) fingolimod (0.5 mg/kg) treatment. Flow cytometry was used to quantify Tregs in blood, spleen, and lymph nodes. Immunohistochemistry was used to quantify FoxP3+ cell infiltration into the ischaemic brain. Results Fingolimod significantly increased the frequency of Tregs within the CD4+ T cell population in blood and spleen post-ischaemia in all three mouse cohorts compared to untreated ischemic mice. The highest splenic Treg frequency in fingolimod-treated mice was observed in ApoE−/− mice (9.32 ± 1.73% vs. 7.8 ± 3.01% in young, 6.09 ± 1.64% in aged mice). The highest circulating Treg frequency was also noted in ApoE−/− mice (8.39 ± 3.26% vs. 5.43 ± 2.74% in young, 4.56 ± 1.60% in aged mice). Fingolimod significantly increased the number of FoxP3+ cells in the infarct core of all mice. The most pronounced effects were seen when mice were treated for 10 days post-ischaemia. Conclusions Fingolimod increases Treg frequency in spleen and blood post-ischaemia and enhances the number of FoxP3+ cells in the ischaemic brain. The effect of fingolimod on this regulatory cell population may underlie its neuroprotective activity and could be exploited as part of future stroke therapy.

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“…Neurogenesis under physiological and pathological conditions was found in hippocampal and motor cortex (Chamaa et al, 2018;Lv et al, 2019;Wu et al, 2020), but different results were reported (Sorrells et al, 2018). MCAO model leads to the injury of cortex, basal ganglia (Longa et al, 1989;Ma et al, 2020), and motor deficit induced by MCAO is partially related to motor cortex. Rodent motor cortex plays an important role in motor control (Peters et al, 2017;Bundy et al, 2019;Veuthey et al, 2020).…”

Section: Introductionmentioning

confidence: 92%

Cerebral Ischemia-Reperfusion Is Associated With Upregulation of Cofilin-1 in the Motor Cortex

Yin

Cheng

et al. 2021

Front. Cell Dev. Biol.

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Cerebral ischemia is one of the leading causes of death. Reperfusion is a critical stage after thrombolysis or thrombectomy, accompanied by oxidative stress, excitotoxicity, neuroinflammation, and defects in synapse structure. The process is closely related to the dephosphorylation of actin-binding proteins (e.g., cofilin-1) by specific phosphatases. Although studies of the molecular mechanisms of the actin cytoskeleton have been ongoing for decades, limited studies have directly investigated reperfusion-induced reorganization of actin-binding protein, and little is known about the gene expression of actin-binding proteins. The exact mechanism is still uncertain. The motor cortex is very important to save nerve function; therefore, we chose the penumbra to study the relationship between cerebral ischemia-reperfusion and actin-binding protein. After transient middle cerebral artery occlusion (MCAO) and reperfusion, we confirmed reperfusion and motor function deficit by cerebral blood flow and gait analysis. PCR was used to screen the high expression mRNAs in penumbra of the motor cortex. The high expression of cofilin in this region was confirmed by immunohistochemistry (IHC) and Western blot (WB). The change in cofilin-1 expression appears at the same time as gait imbalance, especially maximum variation and left front swing. It is suggested that cofilin-1 may partially affect motor cortex function. This result provides a potential mechanism for understanding cerebral ischemia-reperfusion.

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Animal models of cerebral ischemia: A review

Cited by 72 publications

References 120 publications

Progress in Borneol Intervention for Ischemic Stroke: A Systematic Review

Progress in Borneol Intervention for Ischemic Stroke: A Systematic Review

The effect of fingolimod on regulatory T cells in a mouse model of brain ischaemia

Cerebral Ischemia-Reperfusion Is Associated With Upregulation of Cofilin-1 in the Motor Cortex

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