Buyang Huanwu decoction facilitates neurorehabilitation through an improvement of synaptic plasticity in cerebral ischemic rats

Pan, Ruihuan; Cai, Jun; Zhan, Lechang; Guo, Youhua; Huang, Run‐Yue; Xiong, Lize; Zhou, Mingchao; Xu, Dandan; Zhan, Jie; Chen, Hongxia

doi:10.1186/s12906-017-1680-9

Cited by 55 publications

(35 citation statements)

References 54 publications

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“…MAP-2, a protein that was enriched in neuronal dendrites, regulates microtubule dynamics in dendrites and is important for dendritic plasticity. MAP-2 loss has been documented after cerebral ischemic, and therapies that enhanced MAP-2 expression decreased the mortality and neurological impairments of MCAO rats [26]. In our study, declined MAP-2 Immunofluorescence activity was noticed in rats subjected to MCAO modeling, while CY inhibited this decrease and improved the neurological outcomes and pathological changes in MCAO animals, reflecting the essential role of MAP-2 in experimental ischemic stroke and CY-generated therapeutic efficacy.…”

Section: Discussionsupporting

confidence: 58%

Carthamin yellow protected rats from cerebral ischemia–reperfusion injury by improving neuronal dendritic plasticity via antiferroptosis mediated NF-κB/NLRP3 inflammasome pathway deactivation

Guo

Zhu

Tang

et al. 2020

Preprint

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Background: Carthamin yellow (CY), a flavonoid compound extracted from safflower, has been reported to attenuate cardiac ischemia and reperfusion injury. It is unclear whether CY could ameliorate ischemic stroke. Methods: We examined the preventive effects of CY in experimental ischemic stroke using middle cerebral artery occlusion (MCAO) rats model. Neurological function, brain edema and infarct area were assessed to elucidate the effects of CY on neurological function and ischemic brain injury. MAP-2 Immunofluorescence activity, expressions in NF-κB/NLRP3 inflammasome pathway and ferroptosis were determined to reveal its underlying mechanism. Results: A 2-week CY treatment attenuated the neurological deficit score, brain water content and infarct area in MCAO rats. Meanwhile, CY intervention increased the MAP-2 Immunofluorescence activity and deactivated NF-κB/NLRP3 inflammasome pathway in the cortex. Declined serum TNF-α, IL-1β and IL-6 concentrations were detected following CY administration. Furthermore, CY treatment inhibited Fe2+ and ROS accumulation, and restored the protein expressions of ACSL4, TFR1, GPX4 and FTH1 in the brain. The levels of GSH, SOD and MDA in the serum were reversed by CY intervention. Conclusion: CY protected rats from ischemic stroke, which was associated with the improvement of neuronal dendritic plasticity through antiferroptosis mediated NF-κB/NLRP3 inflammasome pathway deactivation.

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Section: Discussionsupporting

confidence: 58%

Carthamin yellow protected rats from cerebral ischemia–reperfusion injury by improving neuronal dendritic plasticity via antiferroptosis mediated NF-κB/NLRP3 inflammasome pathway deactivation

Guo

Zhu

Tang

et al. 2020

Preprint

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“…Taken together, the NF-κB signaling pathway is crucial for the regulation of inflammation following ischemic stroke. It means that suppression of the NF-κB signaling pathway could downregulate inflammation and alleviate I/R injury [49][50][51]. is study has shown that LSZ contribute to the inhibition of proinflammatory cascades following ischemic stroke by suppressing the NF-κB signaling pathway.…”

Section: Evidence-based Complementary and Alternative Medicinementioning

confidence: 99%

Longshengzhi Capsules Improve Ischemic Stroke Outcomes and Reperfusion Injury via the Promotion of Anti‐Inflammatory and Neuroprotective Effects in MCAO/R Rats

Yang

Zhang

Chen

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Stroke is the leading cause of death in the elderly. Traditional Chinese medicine provides an exciting strategy for treating stroke. Previous reports indicated that Longshengzhi capsules (LSZ), a modified Chinese formula, reduced formed thrombi and oxidative stress and were promising in the clinical treatment of ischemic stroke. However, the specific therapeutic effect and mechanism of LSZ are still ambiguous. This study aimed to define the effects of LSZ on proinflammatory mediators and neuroprotective effects on middle cerebral artery occlusion and refusion (MCAO/R) rats. Rats were treated with different doses of LSZ (0.54, 1.62, and 4.32 g/(kg·d)) in a week after model building. LSZ could improve the survival rate, ischemic stroke outcome, and infarct volume. In addition, significant decrease was observed in reactive oxygen species (ROS) levels and inflammatory factor levels in LSZ-treated groups, concomitant with increase in activities of superoxide dismutase (SOD), neurosynaptic remodeling, and decrease in brain edema. It is proposed that LSZ has anti-inflammatory and neuroprotective effects resulting in downregulating matrix metalloproteinase 2/9 (MMP-2/9) and vascular endothelial growth factor (VEGF) and nuclear factor kappa-B (NF-κB) and upregulating microtubule-associated protein-2 (Map-2) and growth-associated protein-43 (GAP-43) via p38 MAPK and HIF-1α signaling pathways in MCAO/R rats. This study provides potential evidences that p38 MAPK and HIF-1α/VEGF signaling pathways play significant roles in the anti-inflammatory and neuroprotective effects of LSZ.

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“…BHD has been reported to improve ischemic brain injury by reducing glutamate-mediated excitatory amino acid toxicity, resulting in enhanced ATP supply and weakened apoptosis (Wang et al, 2011). At the same time, the improved synaptic ultrastructure by BHD also contributed to the recovery of cerebral ischemia sequelae (Pan et al, 2017). Similarly, ShenGui SanSheng san could also improve the efficiency of citric acid cycle to improve the brain energy deficit after ischemia (Luo et al, 2019).…”

Section: Prescription and Molecular Mechanisms In Regulating Mptp Opementioning

confidence: 99%

Mitochondrial MPTP: A Novel Target of Ethnomedicine for Stroke Treatment by Apoptosis Inhibition

Sun

et al. 2020

Front. Pharmacol.

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Mammalian mitochondrial permeability transition pore (MPTP), across the inner and outer membranes of mitochondria, is a nonspecific channel for signal transduction or material transfer between mitochondrial matrix and cytoplasm such as maintenance of Ca 2+ homeostasis, regulation of oxidative stress signals, and protein translocation evoked by some of stimuli. Continuous MPTP opening has been proved to stimulate neuronal apoptosis in ischemic stroke. Meanwhile, inhibition of MPTP overopening-induced apoptosis has shown excellent efficacy in the treatment of ischemic stroke. Among of which, the potential molecular mechanisms of drug therapy for stroke has also been gradually revealed by researchers. The characteristics of multi-components or multitargets for ethnic drugs also provide the possibility to treat stroke from the perspective of mitochondrial MPTP. The advantages mentioned above make it necessary for us to explore and clarify the new perspective of ethnic medicine in treating stroke and to determine the specific molecular mechanisms through advanced technologies as much as possible. In this review, we attempt to uncover the relationship between abnormal MPTP opening and neuronal apoptosis in ischemic stroke. We further summarized currently authorized drugs, ethnic medicine prescriptions, herbs, and identified monomer compounds for inhibition of MPTP overopening-induced ischemic neuron apoptosis. Finally, we strive to provide a new perspective and enlightenment for ethnic medicine in the prevention and treatment of stroke by inhibition of MPTP overopeninginduced neuronal apoptosis.

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Buyang Huanwu decoction facilitates neurorehabilitation through an improvement of synaptic plasticity in cerebral ischemic rats

Cited by 55 publications

References 54 publications

Carthamin yellow protected rats from cerebral ischemia–reperfusion injury by improving neuronal dendritic plasticity via antiferroptosis mediated NF-κB/NLRP3 inflammasome pathway deactivation

Carthamin yellow protected rats from cerebral ischemia–reperfusion injury by improving neuronal dendritic plasticity via antiferroptosis mediated NF-κB/NLRP3 inflammasome pathway deactivation

Longshengzhi Capsules Improve Ischemic Stroke Outcomes and Reperfusion Injury via the Promotion of Anti‐Inflammatory and Neuroprotective Effects in MCAO/R Rats

Mitochondrial MPTP: A Novel Target of Ethnomedicine for Stroke Treatment by Apoptosis Inhibition

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