Comparative Pharmacokinetics of Hydrophilic Components in Salvia miltiorrhiza Bge. and Carthamus tinctorius L. in Rats That Underwent Cerebral Ischemia Reperfusion Using an HPLC-DAD Method

Zhao, Xixi; Yu, Li; Chen, Yulin; Wang, Yu; Wan, Haitong; Yang, Jiehong

doi:10.3389/fphar.2019.01598

Cited by 14 publications

(10 citation statements)

References 45 publications

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“…With its anti-apoptosis and anti-in ammatory properties, SDSS offers a promising therapeutic candidate for CIRI [24][25][26]. Our study proved that SDSS prevented CIRI both in vivo and in vitro by inhibiting NLRP3mediated endothelial cells pyroptosis.…”

Section: Discussionsupporting

confidence: 57%

SDSS ameliorates cerebral ischemia/reperfusion injury by inhibiting CLIC4/NLRP3 inflammasome-mediated endothelial cell pyroptosis

Zhang

Yang

Guo

et al. 2022

Preprint

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Background: Endothelial pyroptosis promotes cerebral ischemic-reperfusion injury (CIRI). Sodium Danshensu (SDSS) has been shown to attenuate CIRI and have anti-inflammatory properties in endothelial cells. Nevertheless, the mechanism of SDSS on endothelial pyroptosis after CIRI remains unclear. Objective: We aimed to investigate the efficacy and mechanism of SDSS for reducing endothelial pyroptosis. Methods: In vitro, the effect of SDSS alleviating CIRI was first confirmed by detecting pyroptosis and NLRP3 inflammasome related indicators in oxygen-glucose deprivation/reoxygen (OGD/R) treated bEnd3 cells. Further, CLIC4 was identified as a potential target of SDSS through protein microarray, molecular docking, and cellular thermal shift assay (CETSA). Following this, the translocation and expression of CLIC4, and chloride outflow were detected. Finally, CLIC4 was further tested, either overexpressed or knocked down, to determine whether it is a target of SDSS to inhibit endothelial pyroptosis. In vivo, neurological deficit scores and infarct volume were served to evaluate the effect of SDSS in middle cerebral artery occlusion/reperfusion (MCAO/R) rats. Further investigation of pyroptosis was conducted using the CLIC4/NLRP3/GSDMD pathway. Results: SDSS administration inhibited NLRP3 inflammasome mediated pyroptosis in vitro and vivo. As demonstrated by protein microarray, molecular docking and CETSA, SDSS bound strongly to CLIC4 and decreased its protein level, and inhibited its translocation from cytoplasm to cell membrane. Further, SDSS effectiveness was weakened by CLIC4 overexpression but not knockdown. Conclusion: The present study indicated that a beneficial effect of SDSS against CIRI was ascribed to block endothelial pyroptosis via binding to CLIC4, and then inhibiting chloride efflux-dependent NLRP3 inflammasome activation.

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Section: Discussionsupporting

confidence: 57%

SDSS ameliorates cerebral ischemia/reperfusion injury by inhibiting CLIC4/NLRP3 inflammasome-mediated endothelial cell pyroptosis

Zhang

Yang

Guo

et al. 2022

Preprint

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“…Acute ischemic stroke (IS) accounts for >80% of all strokes ( Cheng et al, 2020 ). The global burden of ISs is approximately fourfold higher than hemorrhagic strokes ( Zhao et al, 2019 ). Tissue plasminogen activator (tPA) is the only Food and Drug Administration- (FDA-) approved treatment for acute IS ( Chan et al, 2010 ).…”

Section: Introductionmentioning

confidence: 99%

S1PR3, as a Core Protein Related to Ischemic Stroke, is Involved in the Regulation of Blood–Brain Barrier Damage

Fan

Chen

et al. 2022

Front. Pharmacol.

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Background: Ischemic stroke is the most common stroke incident. Sphingosine-1-phosphate (S1P) receptor 3 (S1PR3) is a member of the downstream G protein-coupled receptor family of S1P. The effect of S1PR3 on ischemic stroke remains elusive.Methods: We downloaded two middle cerebral artery occlusion (MCAO) microarray datasets from the Gene Expression Omnibus (GEO) database and screened differentially expressed genes (DEGs). Then, we performed a weighted gene coexpression network analysis (WGCNA) and identified the core module genes related to ischemic stroke. We constructed a protein–protein interaction (PPI) network for the core genes in which DEGs and WGCNA intersected. Finally, we discovered that S1PR3 was involved as the main member of the red proteome. Then, we explored the mechanism of S1PR3 in the mouse tMCAO model. The S1PR3-specific inhibitor CAY10444 was injected into the abdominal cavity of mice after cerebral ischemia/reperfusion (I/R) injury, and changes in the expression of blood–brain barrier-related molecules were measured using PCR, western blotting, and immunofluorescence staining.Results: Both GEO datasets showed that S1PR3 was upregulated during cerebral I/R in mice. WGCNA revealed that the light yellow module had the strongest correlation with the occurrence of IS. We determined the overlap with DEGs, identified 146 core genes that are potentially related to IS, and constructed a PPI network. Finally, S1PR3 was found to be the main member of the red proteome. In the mouse cerebral I/R model, S1PR3 expression increased 24 h after ischemia. After the administration of CAY10444, brain edema and neurological deficits in mice were ameliorated. CAY10444 rescued the decreased expression of the tight junction (TJ) proteins zonula occludens 1 (ZO1) and occludin after ischemia induced by transient MCAO (tMCAO) and reduced the increase in aquaporin 4 (AQP4) levels after tMCAO, preserving the integrity of the BBB. Finally, we found that S1PR3 is involved in regulating the mitogen-activated protein kinase (MAPK) and (phosphatidylinositol-3 kinase/serine-threonine kinase) PI3K-Akt signaling pathways.Conclusion: S1PR3 participates in the regulation of blood–brain barrier damage after cerebral I/R. S1PR3 is expected to be an indicator and predictor of cerebral ischemia, and drugs targeting S1PR3 may also provide new ideas for clinical medications.

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“…4,26 Adequate evidence have demonstrated the higher morbidity and mortality rate in older adults with cerebrovascular disease. [27][28][29] Furthermore, the physical deterioration, prevalent comorbidities, and the potential psychological effects generally lead to a worse outcome in such population after a fracture. After multivariate logistic regression on total patients involved in this study, our data demonstrated that age≥80 and the number of comorbidities≥3 are independently associated with perioperative complications in fall-related fractured patients with the cerebrovascular disease while the type of cerebrovascular disease, fracture location, and comorbidities of prior fragility fracture and respiratory disease were not…”

Section: Discussionmentioning

confidence: 99%

Characteristics of Fall-Related Fractures in Older Adults with Cerebrovascular Disease: A Cross-Sectional Study

Guo

Zhao

et al. 2021

CIA

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Limited information exists on fall-related fractures in older adults with cerebrovascular disease. This study aimed to determine the characteristics of older adults with cerebrovascular disease who sustained fall-related fractures and identify the associated risk factors for perioperative complications. Patients and Methods: This was a cross-sectional study, which included patients with cerebrovascular disease who sustained fractures between Jan. 2017 and Dec. 2019. The collected data included demographics (age and gender), time and place of fracture occurrence, mechanism of injury, fracture location, type of cerebrovascular disease, complications, and comorbidities. Results: A total of 768 patients with 815 fractures were included; there were 253 males and 515 females, with an average age of 78.3 years. For either males or females, 80-84 years was the most commonly involved age group. Most (61.0%) patients had their fractures occurring at home and most fractures (70.7%) occurred during the daytime. Most were hip fractures and limb weakness; instability-related falls were the most common cause of fracture, making a proportion of 34.5%. Patients who suffered falls were mainly combining ischemic cerebrovascular disease. Most (85.9%) patients presented with at least one comorbid disease and the perioperative complication rate was 76.9% in total cases. Age≥80 (OR: 1.772, 95% CI: 1.236-2.540) and the number of comorbidities≥3 (OR: 1.606, 95% CI: 1.035-2.494) were found independently associated with complications, while the type of cerebrovascular disease, fracture location, and comorbidities of prior fragility fracture and respiratory disease were not significantly correlated with complications. Conclusion: Our findings highlighted that more focus on improved physical function explored in intervention setting and the importance of primary home prevention measures seems justified in China and maybe other countries as well. It is the first study that presented the epidemiological characteristics of older adults with cerebrovascular disease who later experienced a fracture.

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Comparative Pharmacokinetics of Hydrophilic Components in Salvia miltiorrhiza Bge. and Carthamus tinctorius L. in Rats That Underwent Cerebral Ischemia Reperfusion Using an HPLC-DAD Method

Cited by 14 publications

References 45 publications

SDSS ameliorates cerebral ischemia/reperfusion injury by inhibiting CLIC4/NLRP3 inflammasome-mediated endothelial cell pyroptosis

SDSS ameliorates cerebral ischemia/reperfusion injury by inhibiting CLIC4/NLRP3 inflammasome-mediated endothelial cell pyroptosis

S1PR3, as a Core Protein Related to Ischemic Stroke, is Involved in the Regulation of Blood–Brain Barrier Damage

Characteristics of Fall-Related Fractures in Older Adults with Cerebrovascular Disease: A Cross-Sectional Study

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