scholarly journals Taohong Siwu Decoction Ameliorates Ischemic Stroke Injury Via Suppressing Pyroptosis

2020 ◽  
Vol 11 ◽  
Author(s):  
Mengmeng Wang ◽  
Zhuqing Liu ◽  
Shoushan Hu ◽  
Xianchun Duan ◽  
Yanyan Zhang ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Blood Stasis ◽  
Mapk Signaling ◽  
Artery Occlusion ◽  
Inflammatory Factors ◽  
Intragastric Administration ◽  
Therapeutic Effects ◽  
Treatment Groups ◽  
Caspase 1 ◽  
Taohong Siwu Decoction

Objective: Taohong Siwu decoction (THSWD) is one of the classic prescriptions for promoting blood circulation and removing blood stasis, and it has a good therapeutic effect on ischemic stroke. We sought to explore the therapeutic effects of THSWD on pyroptosis in rats with middle cerebral artery occlusion-reperfusion (MCAO/R).Methods: MCAO/R model of rats were established by suture-occluded method. MCAO/R rats were randomly divided into five groups, which were model group, nimodipine group, THSWD high, medium and low dose group (18, 9, and 4.5 g/kg, respectively), rats of sham group without thread embolus. All rats were treated by intragastric administration for 7 days. We detected the level of inflammatory factors. NLRP3 and Caspase-1 were detected by immunofluorescence. Western blot was used to detect NLRP3, Caspase-1, ASC, and GSDMD in penumbra. Also, the expression of TXNIP, HMGB1, toll-like receptors (TLR4), NF-κB, and MAPK were detected.Results: THSWD treatment improved the behavioral function and brain pathological damage. These results showed that the levels of TNF-α, TGF-β, IL-2, IL-6, IL-1β, and IL-18 were significantly reduced in THSWD treatment groups. THSWD could significantly decrease the expression levels of NLRP3, Caspase-1, Caspase-1 p10, ASC, TXNIP, GSDMD, HMGB1, TLR4/NFκB, p38 MAPK, and JNK in penumbra.Conclusion: Our results showed that THSWD could reduce the activation level of NLRP3 inflammatory corpuscle, down-regulate GSDMD, and inhibit pyroptosis in MCAO/R rats. These may be affected by inhibiting HMGB1/TLR4/NFκB, MAPK signaling pathways.

scholarly journals Cerebral endothelial cell-derived small extracellular vesicles enhance neurovascular function and neurological recovery in rat acute ischemic stroke models of mechanical thrombectomy and embolic stroke treatment with tPA

2021 ◽  
pp. 0271678X2199298
Author(s):  
Chao Li ◽  
Chunyang Wang ◽  
Yi Zhang ◽  
Owais K Alsrouji ◽  
Alex B Chebl ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Extracellular Vesicles ◽  
Mechanical Thrombectomy ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Therapeutic Effects ◽  
Vessel Occlusion ◽  
Healthy Human ◽  
Stroke Treatment

Treatment of patients with cerebral large vessel occlusion with thrombectomy and tissue plasminogen activator (tPA) leads to incomplete reperfusion. Using rat models of embolic and transient middle cerebral artery occlusion (eMCAO and tMCAO), we investigated the effect on stroke outcomes of small extracellular vesicles (sEVs) derived from rat cerebral endothelial cells (CEC-sEVs) in combination with tPA (CEC-sEVs/tPA) as a treatment of eMCAO and tMCAO in rat. The effect of sEVs derived from clots acquired from patients who had undergone mechanical thrombectomy on healthy human CEC permeability was also evaluated. CEC-sEVs/tPA administered 4 h after eMCAO reduced infarct volume by ∼36%, increased recanalization of the occluded MCA, enhanced cerebral blood flow (CBF), and reduced blood-brain barrier (BBB) leakage. Treatment with CEC-sEVs given upon reperfusion after 2 h tMCAO significantly reduced infarct volume by ∼43%, and neurological outcomes were improved in both CEC-sEVs treated models. CEC-sEVs/tPA reduced a network of microRNAs (miRs) and proteins that mediate thrombosis, coagulation, and inflammation. Patient-clot derived sEVs increased CEC permeability, which was reduced by CEC-sEVs. CEC-sEV mediated suppression of a network of pro-thrombotic, -coagulant, and -inflammatory miRs and proteins likely contribute to therapeutic effects. Thus, CEC-sEVs have a therapeutic effect on acute ischemic stroke by reducing neurovascular damage.

scholarly journals Nanobody-Mediated Inhibition of P2X7 on Microglia Improves Stroke Outcome

2021 ◽  
Author(s):  
Maximilian Wilmes ◽  
Carolina Pinto Espinoza ◽  
Peter Ludewig ◽  
Arthur Liesz ◽  
Annette Nicke ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Transgenic Mice ◽  
Tissue Damage ◽  
Calcium Influx ◽  
Atp Release ◽  
Artery Occlusion ◽  
Membrane Pores ◽  
Caspase 1 ◽  
Ischemic Tissue

Abstract BackgroundPrevious studies have demonstrated that purinergic receptors could be therapeutic targets to modulate the inflammatory response in multiple brain disease models. However, tools for the selective and efficient targeting of these receptors are scarce. The new development of P2X7-specific nanobodies (nbs) enables us to effectively block the P2X7-channel.MethodsTemporary middle cerebral artery occlusion (tMCAO) in wildtype and P2X7-transgenic mice was used as a model for ischemic stroke. ATP release was assessed in transgenic ATP sensor mice. Stroke size was measured without treatment and after injection of P2X7-specific nbs i.v. and i.c.v. directly before tMCAO-surgery. P2X7-GFP expressing transgenic mice were used to show immunhistochemically P2X7 distribution in the brain. In vitro cultured microglia were used to investigate calcium-influx, pore-formation via DAPI uptake, caspase 1 activation and IL-1b release after incubation with P2X7-specific nbs. ResultsATP sensor mice showed an increase of ATP-release in the ischemic hemisphere compared to the contralateral hemisphere or sham mice up to 24 h after stroke. We could further verify the role of the ATP-P2X7 axis in P2X7-overexpressing mice, which showed significantly greater stroke volumes after 24 h. In vitro experiments with primary microglia cells showed that P2X7-specific nanobodies were capable of dampening the ATP-trigged calcium-influx and formation of membrane pores measured by Fluo4 fluorescence or DAPI uptake. We found a lower caspase 1 activity and a subsequently lower IL-1b release. However, the intravenous (i.v.) injection of P2X7-specific nanobodies compared to isotype controls before the tMCAO-surgery did not result in smaller stroke size compared to isotype controls. As demonstrated by FACS, nbs had only reached brain infiltrating macrophages but not microglia. To reach microglia, we injected the P2X7-spezific nbs or the isotype directly intraventricularly (icv). 30 mg of P2X7-specific nbs proved efficient for microglial targeting, reducing post-stroke microglia activation and stroke size significantly.ConclusionHere, we demonstrate the importance of locally produced ATP for the tissue damage observed in ischemic stroke and we show the potential of icv injected P2X7-specific nbs to reduce ischemic tissue damage.

The therapeutic effect and mechanism of Qishen Yiqi dripping pills on cardiovascular and cerebrovascular diseases and diabetic complications

2021 ◽  
Vol 14 ◽  
Author(s):  
Chunlai Zhao ◽  
Wenjia Wang ◽  
Kaijing Yan ◽  
He Sun ◽  
Jihong Han ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Diabetic Nephropathy ◽  
Heart Disease ◽  
Ischemic Stroke ◽  
Diabetic Complications ◽  
Blood Stasis ◽  
Blood Stasis Syndrome ◽  
Syndrome Differentiation ◽  
Therapeutic Effects ◽  
The Common

: The alterations in vascular homeostasis is deeply involved in the development of numerous diseases, such as coronary heart disease, stroke, and diabetic complications. Changes in blood flow and endothelial permeability caused by vascular dysfunction are the common mechanisms for these three types of diseases. The disorders of glucose and lipid metabolism can result in changes of the energy production patterns in endothelium and surrounding cells which may consequently cause local energy metabolic disorders, oxidative stress and inflammatory responses. Traditional Chinese medicine (TCM) follows the principle of the “treatment by the syndrome differentiation”. TCM considers of that coronary heart disease, stroke and diabetes complications all as the type of “Qi deficiency and Blood stasis” syndrome, which mainly happens to the vascular system. Therefore, the common pathogenesis of these three types of diseases suggests the treatment strategy by TCM should be in a close manner and named as “treating different diseases by the same treatment”. Qishen Yiqi dripping pills is a modern Chinese herbal medicine which has been widely used for treatment of patients with coronary heart disease characterized as “Qi deficiency and blood stasis” in China. Recently, many clinical reports have demonstrated the potent therapeutic effects of Qishen Yiqi dripping pills on ischemic stroke and diabetic nephropathy. Based on these reports, we will summarize the clinical applications of Qishen Yiqi dripping pills on coronary heart disease, ischemic stroke and diabetic nephropathy, including the involved mechanisms with basic researches.

scholarly journals Temporal and Spatial Dynamics of Inflammasome Activation After Ischemic Stroke

2021 ◽  
Vol 12 ◽  
Author(s):  
Danli Lu ◽  
Mengyan Hu ◽  
Bingjun Zhang ◽  
Yinyao Lin ◽  
Qiang Zhu ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Spatial Dynamics ◽  
Size Control ◽  
Inflammasome Activation ◽  
Therapeutic Effects ◽  
Ischemic Lesion ◽  
Stroke Outcomes ◽  
Post Stroke ◽  
Caspase 1 ◽  
The Impact

Background: The inflammasome represents a highly pro-inflammatory mechanism. It has been identified that inflammasome was activated after ischemic stroke. However, the impact of inflammasomes on stroke outcomes remains contradictory. The participating molecules and the functioning arena of post-stroke inflammasome activation are still elusive.Methods: In the present study, blood samples from stroke patients were collected and analyzed with flow cytometry to evaluate the correlation of inflammasome activation and stroke outcomes. A stroke model was established using male C57/Bl6 mice with transient middle cerebral artery occlusion (tMCAO, 1 h). The dynamics of inflammasome components, cell type, and location of inflammasome activation and the therapeutic effects of inhibiting post-stroke inflammasome executors were evaluated.Results: We found that a high level of inflammasome activation might indicate detrimental stroke outcomes in patients and mice models. Post-stroke inflammasome activation, especially NLRP3, cleaved Caspase-1, cleaved Caspase-11, IL-1β, IL-18, and GSDMD, peaked at 3–5 days and declined at 7 days with the participation of multiple components in mice. Macrophage that infiltrated into the ischemic lesion was the main arena for post-stroke inflammasome activation among myeloid cells according to the data of mice. Among all the members of the Caspase family, Caspase-1 and −11 served as the main executing enzymes. Inhibiting Caspase-1/−11 signaling efficiently suppressed DAMPs-induced macrophage inflammasome activation and displayed neuroprotection to stroke models including infarct size (Control: 48.05 ± 14.98; Cas1.i: 19.34 ± 12.21; Cas11.i: 21.43 ± 14.67, P < 0.001) and neurological deficit score (0 d-Control: 2.20 ± 0.63; 0 d-Cas1.i: 2.20 ± 0.63; 0 d-Cas11.i: 2.20 ± 0.63; 1 d-Control: 2.50 ± 0.53; 1 d-Cas1.i: 1.50 ± 0.71; 1 d-Cas11.i: 2.00 ± 0.67; 2 d-Control: 2.30 ± 0.48; 2 d-Cas1.i: 1.30 ± 0.48; 2 d-Cas11.i: 1.50 ± 0.53; 3 d-Control: 2.00 ± 0.67; 3 d-Cas1.i: 1.20 ± 0.42; 3 d-Cas11.i: 1.30 ± 0.48, P < 0.001).Conclusions: Taken together, inflammasome activation played a detrimental role in stroke pathology. Targeting post-stroke inflammasome executing enzymes fitting in the dynamics of macrophages might obtain potential and efficient therapeutic effects.

Abstract WP307: Molecular Mechanisms, Temporal and Spatial Dynamics of Inflammasome Activation in Ischemic Stroke

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Wei Cai ◽  
Mengyan Hu ◽  
Zhengqi Lu
Keyword(s):  
Ischemic Stroke ◽  
Molecular Mechanisms ◽  
Spatial Dynamics ◽  
Inflammasome Activation ◽  
Therapeutic Effects ◽  
Stroke Patients ◽  
Stroke Outcomes ◽  
Post Stroke ◽  
Caspase 1 ◽  
Temporal And Spatial

Background: Multiple sensors, executors and products are involved in inflammasome activation. Inflammasome activation has been found in several immune cells after stroke. However, the molecular mechanisms, the temporal and spatial dynamics of inflammasome activation in stroke remain elusive. Therapeutic value of modifying inflammasome activation in stroke is still debatable. Methods: Inflammasome markers of NLRP3 and IL-1β in stroke patients and healthy control were evaluated with flow cytometry. Correlation of NLRP3/IL-1β expression with stroke outcomes of patients was assessed. Ischemic stroke was induced in mice with transient middle cerebral artery occlusion (tMCAO, 1h). Expression dynamics of inflammasome components, location and cellular target of inflammasome activation in tMCAO models were analyzed. Therapeutic effects of inhibiting inflammasome activation on stroke outcomes were evaluated. Results: Rapid increase of inflammasome markers NLRP3 and IL-1β was detected at 1d after disease onset in stroke patients, which was positively correlated with patients’ infarct volume and NIHSS score. The sensors of NLRP3 and NLRC4 were involved in post stroke inflammasome activation, which increased at 1-3d after stroke and peaked at 3-5d in tMCAO models. Similar dynamics of the executors cleaved Caspase-1/11, as well as the products IL-1β, IL-18 and GSDMD were detected. AIM2 and Caspase-8 seemed not to take any part in post-stroke inflammasome activation. Macrophage was demonstrated as the main cell in which inflammasome was formed in both patients and mice, while microglia, dendritic cells and neutrophil also had inflammasome formation. Inflammasome activation of macrophage was mostly detected in stroke lesion. The executors of Caspase-1 and -11 were the key factors in inflammasome activation in stroke. Preventing inflammasome activation by inhibiting Caspase-1/11 signalings showed promising therapeutic efficacy. Conclusion: The impact of inflammasome activation is detrimental to ischemic stroke. Inhibiting Caspase-1/11 signalings is a promising therapeutic strategy for stroke.

scholarly journals Long Course Hyperbaric Oxygen Stimulates Neurogenesis and Attenuates Inflammation after Ischemic Stroke

2013 ◽  
Vol 2013 ◽  
pp. 1-13 ◽  
Author(s):  
Ying-Sheng Lee ◽  
Chung-Ching Chio ◽  
Ching-Ping Chang ◽  
Liang-Chao Wang ◽  
Po-Min Chiang ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Hyperbaric Oxygen ◽  
Artery Occlusion ◽  
Trophic Factors ◽  
Therapeutic Effects ◽  
Ischemic Brain ◽  
Neurological Severity Score ◽  
Group Mobilization ◽  
Long Course ◽  
Cerebral Artery Occlusion

Several studies have provided evidence with regard to the neuroprotection benefits of hyperbaric oxygen (HBO) therapy in cases of stroke, and HBO also promotes bone marrow stem cells (BMSCs) proliferation and mobilization. This study investigates the influence of HBO therapy on the migration of BMSCs, neurogenesis, gliosis, and inflammation after stroke. Rats that sustained transient middle cerebral artery occlusion (MCAO) were treated with HBO three weeks or two days. The results were examined using a behavior test (modified neurological severity score, mNSS) and immunostaining to evaluate the effects of HBO therapy on migration of BMSCs, neurogenesis, and gliosis, and expression of neurotrophic factors was also evaluated. There was a lower mNSS score in the three-week HBO group when compared with the two-day HBO group. Mobilization of BMSCs to an ischemic area was more improved in long course HBO treatments, suggesting the duration of therapy is crucial for promoting the homing of BMSCs to ischemic brain by HBO therapies. HBO also can stimulate expression of trophic factors and improve neurogenesis and gliosis. These effects may help in neuronal repair after ischemic stroke, and increasing the course of HBO therapy might enhance therapeutic effects on ischemic stroke.

scholarly journals Taohong Siwu Decoction Regulates Cell Necrosis and Neuroinflammation in the Rat Middle Cerebral Artery Occlusion Model

2021 ◽  
Vol 12 ◽  
Author(s):  
Ni Wang ◽  
Changyi Fei ◽  
Furui Chu ◽  
Shi Huang ◽  
Lingyu Pan ◽  
...  
Keyword(s):  
Rat Brain ◽  
Artery Occlusion ◽  
Inflammatory Factors ◽  
Sham Operation ◽  
Cell Necrosis ◽  
Expression Levels ◽  
Sham Operation Group ◽  
Taohong Siwu Decoction ◽  
Tnf Α ◽  
Cerebral Artery Occlusion

Cell necrosis and neuroinflammation play an important role in brain injury induced by ischemic stroke. Previous studies reported that Taohong Siwu decoction (THSWD)can reduce heart muscle cell necrosis and has anti-inflammatory properties. In this study, we investigated the effects of THSWD on cell necrosis and neuroinflammation in a rat model of middle cerebral artery occlusion (MCAO). Thirty-six male Sprague-Dawley (SD) rats were randomly divided into three groups with 12 rats in each group. They were the sham operation group, MCAO model group, and MCAO + THSWD group. We used ELISA to determine the levels of TNF-α, Mcp-1, and IL-1β inflammatory factors in rat serum, qRT‐PCR to detect the expression of TNF‐α, Mcp‐1 and IL‐1β mRNA in rat brain, and immunohistochemistry to detect the number of microglia and neutrophils in rat brain. qRT-PCR and Western blot were used to detect the mRNA and protein expression levels of IBA-1 and MPO inflammatory factors and the TNF-α/RIP1/RIP3/MLKL pathway in the rat brain and protein expression levels. Compared with the sham operation group, the expression of MCP-1, IL-1β, IBA-1, and MPO inflammatory factors and the TNF-α/RIP1/RIP3/MLKL pathway were significantly upregulated in the MCAO group. Compared with the MCAO group, the expressions of MCP-1, IL-1β, IBA-1, and MPO inflammatory factors and the TNF-α/RIP1/RIP3/MLKL pathway were significantly downregulated in the MCAO + THSWD group. THSWD can reduce the expression levels of MCP-1, IL-1β, IBA-1, and MPO inflammatory factors as well as the TNF-α/RIP1/RIP3/MLKL pathway. Meanwhile, it can reduce the necrosis and inflammation of brain cells after cerebral ischemia, so as to protect the brain tissue of rats.

scholarly journals Thousand and one kinase 1 protects MCAO-induced cerebral ischemic stroke in rats by decreasing apoptosis and pro-inflammatory factors

2019 ◽  
Vol 39 (10) ◽  
Author(s):  
Jiahui Li ◽  
Zhijie Liu ◽  
Liling Wang ◽  
Haiyan Xu ◽  
Yulin Wang
Keyword(s):  
Animal Model ◽  
Ischemic Stroke ◽  
Signaling Pathways ◽  
Mapk Signaling ◽  
Immunofluorescent Staining ◽  
Inflammatory Factors ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Mapk Signaling Pathways

Abstract Background: Birth hypoxia causes neonatal mortality and morbidity. Hypoxia/ischemia can facilitate brain damage, causing various kinds of diseases, such as ischemic stroke. It is necessary to understand the potential underlying mechanisms of ischemic stroke. Previous studies revealed the involvement of thousand and one kinase 1 (TAOK1) in many cellular processes. Methods: Herein, middle cerebral artery (MCA) occlusion (MCAO) was performed in rats to establish ischemic stroke in the animal model, and cortical neural stem cells from rats were treated with oxygen-glucose deprivation (OGD) to induce ischemic stroke cell model. The animal model of ischemic stroke was validated by Bederson and Zea-Longa neurological deficit scores and rotarod test. TAOK1 expression was examined by quantitative real-time PCR (qRT-PCR), Western blot, and immunofluorescent staining both in vivo and in vitro. Result: Compared with sham animals, the MCAO rats showed a significant increase in the neurological scores, and obvious motor behavioral deficits. Meanwhile, there was increased apoptosis and inflammatory response in the model group. TAOK1 overexpression reversed the OGD-induced cell injury, while TAOK1 knockdown exhibited the opposing effects. On the mechanism, the OGD-induced suppression of PI3K/AKT, and activation of mitogen-activated protein kinase (MAPK) signaling pathways were abolished by TAOK1 overexpression, and aggravated by TAOK1 knockdown in vitro. Moreover, we proved that the inhibitory effect of TAOK1 on OGD-induced apoptosis was dependent on the intracellular kinase activity. Conclusion: TAOK1 protected MCAO-induced cerebral ischemic stroke by decreasing the pro-inflammatory factors and apoptosis via PI3K/AKT and MAPK signaling pathways.

scholarly journals GC-MS-Based Metabolomics to Reveal the Protective Effect of Gross Saponins of Tribulus terrestris Fruit against Ischemic Stroke in Rat

Molecules ◽  
2019 ◽  
Vol 24 (4) ◽  
pp. 793 ◽  
Author(s):  
Yang Wang ◽  
Hongyu Zhao ◽  
Yue Liu ◽  
Wenjun Guo ◽  
Yanru Bao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Protective Effect ◽  
Human Life ◽  
Artery Occlusion ◽  
Tribulus Terrestris ◽  
Therapeutic Effects ◽  
Triphenyltetrazolium Chloride ◽  
Fatty Acids Metabolism ◽  
Neuroprotective Treatment ◽  
Cerebral Artery Occlusion

Stroke is one of the most common neurological disorders and seriously threatens human life. Gross saponins of Tribulus terrestris fruit (GSTTF) are used for neuroprotective treatment on convalescents of ischemic stroke. However, the therapeutic effects and mechanisms have not yet well understood, especially from the metabolic perspective. In this study, the protective effect of GSTTF on ischemic stroke in a middle cerebral artery occlusion (MCAO) rat model was investigated by the GC-MS-based metabolomics approach. 2,3,5-triphenyltetrazolium chloride (TTC) staining of brain tissues showed that GSTTF significantly reduced the infarct area after MCAO surgery. Metabolomic profiling showed a series of metabolic perturbation occurs in ischemic stroke compared with sham group. GSTTF can reverse the MCAO-induced serum metabolic deviations by regulating multiple metabolic pathways including fatty acids metabolism, amino acids metabolism, and carbohydrates metabolism. The current study provided a useful approach for understanding the mechanism of MCAO-induced ischemic stroke and a reliable basis for evaluating the efficacy of GSTTF in the treatment of ischemic stroke.

scholarly journals Antineuroinflammatory effects of dl-3-n-butylphthalide conferred by stimulation of Foxp3 and Ki-67 in an ischemic stroke model

2020 ◽  
Author(s):  
Xi Liu ◽  
Runzhe Liu ◽  
Dongxu Fu ◽  
Hao Wu ◽  
Xin Zhao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Artery Occlusion ◽  
Neurological Deficits ◽  
Stroke Model ◽  
Ki 67 ◽  
Ischemic Brain ◽  
Caspase 1 ◽  
And Function ◽  
Cerebral Artery Occlusion ◽  
First Time

Abstract Background Dl-3-n-butylphthalide (NBP) has been widely used for the treatment of ischemic stroke in China. However, its mechanisms of action have not been fully elucidated. Methods We established a permanent middle cerebral artery occlusion (pMCAO) rat model and administered 4 mg/kg/d NBP by tail vein injection for 9 days. Changes in some molecules related to neuroinflammation, neovascularization and nerve regeneration were observed, such as MALDI-TOF MSI to study the distribution of phospholipids in the brain, LA-ICP MSI to observe the changes of Foxp3, Ki-67 and pCREB, immunohistochemistry to investigate NLRP3 and its downstream inflammatory products Caspase-1 and IL-1β. Results These results showed that NBP attenuated ischemic damage in pMCAO rats, accompanied by improving neurological deficits. It was revealed for the first time in an animal stroke model that NBP decreased the levels of PE (18:0), NLRP3, Caspase-1 and IL-1β, while increasing the levels of several phospholipids, such as PA (16:0/18:1), PA (18:0/22:6), PE (16:0/22:6), PE (P-18:0/22:6), PE (18:0/22:6), PS (18:0/22:6), PI (18:0/20:4), Foxp3, Ki-67 and pCREB, in the ischemic brain region. Conclusion These results provide evidence that NBP can reduce neuroinflammation in brain tissue and promote the regeneration of nerves and blood vessels, thus exerting a protective effect on neuromorphology and function.

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