scholarly journals Protective effect of Ginkgo biloba leaves extract, EGb761, on myocardium injury in ischemia reperfusion rats via regulation of TLR-4/NF-κB signaling pathway

Oncotarget ◽  
2017 ◽  
Vol 8 (49) ◽  
pp. 86671-86680 ◽  
Author(s):  
Yuping Tang ◽  
Guisheng Zhou ◽  
Lijun Yao ◽  
Ping Xue ◽  
Danhong Yu ◽  
...  
Keyword(s):  
Protective Effect ◽  
Signaling Pathway ◽  
Ginkgo Biloba ◽  
Ischemia Reperfusion ◽  
Myocardium Injury

scholarly journals Hydrogen Sulfide Protects Cardiomyocytes against Apoptosis in Ischemia/Reperfusion through MiR-1-Regulated Histone Deacetylase 4 Pathway

2016 ◽  
Vol 41 (1) ◽  
pp. 10-21 ◽  
Author(s):  
Bo Kang ◽  
Wei Li ◽  
Wang Xi ◽  
Yinghong Yi ◽  
Yundan Ciren ◽  
...  
Keyword(s):  
Hydrogen Sulfide ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Tumor Cells ◽  
Histone Deacetylase ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Underlying Mechanism ◽  
Neonatal Rats ◽  
Histone Deacetylase 4

Background/Aims: Hydrogen sulfide (H<Sub>2</Sub>S) is a powerful inhibitor of cardiomyocytes apoptosis following ischemia/reperfusion (IR) injury, but the underlying mechanism remains unclear. Our previous study showed that microRNA-1 (miR-1) was upregulated by 2.21 fold in the IR group compared with that in the H<Sub>2</Sub>S preconditioned group. MiR-206 affected the process of cardiomyocytes hypertrophy by regulating histone deacetylase 4 (HDAC4). HDAC4 is also known to play an anti-apoptotic role in tumor cells, but its role in the myocardium has not been reported. The aim of this study was to test whether H<Sub>2</Sub>S could inhibit apoptosis of cardiomyocytes through HDAC4 regulation by miR-1 in IR. Methods: Cardiomyocytes of neonatal rats were subjected to hypoxia/reoxygenation (HR) injury with or without H<Sub>2</Sub>S pretreatment to simulate IR injury Cardiomyocytes were transfected with miR-1 mimic or HDAC4 siRNA to evaluate whether the miR-1-HDAC4 signaling pathway was involved in the protective effect of H<Sub>2</Sub>S. Results: HR increased cell apoptosis and caspase-3 cleavage, upregulated miR-1, and downregulated HDAC4. H<Sub>2</Sub>S preconditioning attenuated the apoptosis of cardiomyocytes, caspase-3 cleavage and LDH release, and enhanced cell viability In addition, H<Sub>2</Sub>S downregulated miR-1, and preserved HDAC4 expression. HDAC4 protein was down-regulated by miR-1 mimic. Transfection of cardiomyocytes with miR-1 mimic partially reduced the protective effect of H<Sub>2</Sub>S. Meanwhile, transfection of cardiomyocytes with siRNA to HDAC4 partially abrogated the protective effect of H<Sub>2</Sub>S. Conclusions: The miR-1-HDAC4 signaling pathway is involved in the protective effect of H<Sub>2</Sub>S against the apoptosis of cardiomyocytes during the IR injury process.

Possible involvement of PI3K/AKT/mTOR signaling pathway in the protective effect of selegiline (deprenyl) against memory impairment following ischemia reperfusion in rat

Neuropeptides ◽  
2019 ◽  
Vol 77 ◽  
pp. 101942 ◽  
Author(s):  
Hossein Amini-Khoei ◽  
Elham Saghaei ◽  
Gholam-Reza Mobini ◽  
Milad Sabzevary-Ghahfarokhi ◽  
Reza Ahmadi ◽  
...  
Keyword(s):  
Protective Effect ◽  
Signaling Pathway ◽  
Memory Impairment ◽  
Ischemia Reperfusion ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway

scholarly journals Oxymatrine Improves the Integrity of the Blood-Brain Barrier after Cerebral Ischemia-Reperfusion Injury through the Caveolin-1/MMP-9 Signaling Pathway

2020 ◽  
Author(s):  
Jiaoyan Yu ◽  
Qingqing Liu ◽  
Xi Li ◽  
Mei Zhao ◽  
Ting Sun ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Blood Brain Barrier ◽  
Ischemia Reperfusion ◽  
Neurological Function ◽  
Brain Barrier ◽  
High Morbidity ◽  
Cerebral Ischemia Reperfusion ◽  
Blood Brain

Abstract BackgroundIschemic stroke (IS) is a major neurological disease worldwide and is associated with extremely high morbidity and mortality. Oxymatrine (OMT) has neuroprotective properties and protects against IS. However, whether its protective effect involves the blood-brain barrier (BBB) integrity is unknown.MethodsHere, we used in vivo and in vitro models of IS to evaluate the protective effect of OMT and its mechanism with regard to the BBB. We assayed the role of OMT using neurological function scores and triphenyltetrazolium chloride, Nissl, and terminal deoxynucleotidyl transferase dUTP nick end labeling staining.ResultsOMT significantly improved the neurological function and brain state and reduced BBB permeability in a mouse model of cerebral ischemia-reperfusion. Additionally, OMT improved the tight junction of bEend.3 cells under oxygen-glucose deprivation. Moreover, intracranial lentivirus injection-induced Cav-1 knockdown reduced the neuroprotective effects of OMT.ConclusionsOMT could improve I/R injury-induced damage to the BBB, and its effects may be related to the regulation of the Cav-1/MMP-9 signaling pathway. This suggests that OMT may offer effective protection against BBB injury after I/R.

scholarly journals Oxymatrine Improves the Integrity of the Blood-brain Barrier After Cerebral Ischemia-reperfusion Injury Through the Caveolin-1/MMP-9 Signaling Pathway

2020 ◽  
Author(s):  
Jiaoyan Yu ◽  
Qingqing Lu ◽  
Xi Li ◽  
Mei Zhao ◽  
Ting Sun ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Protective Effect ◽  
Signaling Pathway ◽  
Blood Brain Barrier ◽  
Ischemia Reperfusion ◽  
Brain Barrier ◽  
Brain State ◽  
High Morbidity ◽  
Cerebral Ischemia Reperfusion ◽  
Blood Brain

Abstract Ischemic stroke (IS) is a major neurological disease worldwide and is associated with extremely high morbidity and mortality. Oxymatrine (OMT) has neuroprotective properties and protects against IS. However, whether its protective effect involves the blood-brain barrier (BBB) integrity is unknown. In this study, we used in vivo and in vitro models of IS to evaluate the protective effect of OMT and its mechanism with regard to the BBB. Our results showed that OMT significantly improved the neurological function and brain state and reduced BBB permeability in a mouse model of cerebral ischemia-reperfusion. Additionally, OMT improved the tight junction of bEend.3 cells under oxygen-glucose deprivation. Moreover, intracranial lentivirus injection-induced Cav-1 knockdown reduced the neuroprotective effects of OMT. Our results indicated that OMT could improve cI/R injury-induced damage to the BBB, and its effects may be related to the regulation of the Cav-1/MMP-9 signaling pathway. This suggests that OMT may offer effective protection against BBB injury after cI/R.

Protective effect of hydrogen against ischemia-reperfusion induced spinal nerve cell apoptosis

2021 ◽  
Author(s):  
Yanqing Sun ◽  
Wei Shi ◽  
Bo Yuan ◽  
Zhiwei Wang ◽  
Shengyuan Zhou ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Protective Effect ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Pc12 Cell ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Caspase 12

Abstract Background: This study aims to explore the protective effect of hydrogen against oxygen-glucose-serum deprivation/restoration (OGSD/R)-induced PC12 cell apoptosis in vitro and the possible underlying mechanism. Methods: A normal control (NC) group was set where PC12 cells were cultured normal, while a positive control (PC) group, where PC12 cells were exposed to OGSD 12h/R1h without intervention, and a hydrogen intervention (HI) group, where PC12 cells were exposed to OGSD 12h/R1h plus HI, were conducted at the same time. At OGSD 12h/R 1h, cells were DAPI stained to detect viability and changes in the expression of apoptosis-associated proteins caspase-3, caspase-12 and CHOP/GADD153, and the endoplasmic reticulum-related signaling pathway protein PERK-eIF2α-ATF4. At the same time, the effect of HI was observed. Results: The result revealed that compared with NC group, cell apoptosis was more severe and cell viability was reduced significantly in PC group, while cell apoptosis was ameliorated and cell viability was increased significantly in HI as compared with PC group. In addition, the content of caspase-3 and caspase-12 in HI group was decreased significantly as compared with that in PC group. During this process, the endoplasmic reticulum-related signaling pathway protein PERK-eIF2α-ATF4 was activated. In HI group, the expression of this protein was decreased and cell viability was increased significantly as compared with those in PC group. Conclusions: Hydrogen was able to inhibit OGSD/R-induced PC12 cell apoptosis and exert a protective effect against ischemia-repurfusion injury (IRI) to nerve cells, probably through inhibiting the endoplasmic reticulum-related signaling pathway protein.

Renoprotective effect of curcumin labelled on Mesoscale Nanoparticles (MNPs) on Renal Ischemia-Reperfusion Injury (RIRI) via the miR-146a/nNOS/NO/cGMP/PKG signaling pathway

2019 ◽  
Vol 20 ◽  
Author(s):  
Wenjuan Ni ◽  
Songlin Yu ◽  
Fanshu Li ◽  
Jiazhen Zhu ◽  
Ziwei Chen ◽  
...  
Keyword(s):  
Protective Effect ◽  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Renal Ischemia ◽  
Luciferase Assay ◽  
Model Group ◽  
Renal Ischemia Reperfusion Injury

: This study investigated the protective effect of Curcumin on renal ischemia-reperfusion injury (RIRI) as well as the mechanisms underlying the role of Curcumin. Selectivity of Curcumin in kidney in different doses and routes of administration was measured. In addition, the serum levels of β2-MG, UAER, BUN and creatinine were compared among the Sham, the RIRI model and the Curcumin + RIRI model groups. The expression of miR-146a iNOS, eNOS and nNOS, PKG, and caspase-3 among various groups was measured using real-time PCR and Western-blot analysis, while the levels of NO and cGMP in the samples were measured by ELISA. Finally, the effect of Curcumin on the transcriptional efficiencies of miR-146a, nNOS, eNOS and iNOS was studied using luciferase assay. The presence of mesoscale nanoparticles (MNPs) in the kidneys was safe. In addition, the accumulation of MNPs was in a dose-dependent manner and peaked at a dose of 25 mg/kg. The administration of Curcumin reduced the levels of serum β2-MG, UAER, BUN, creatinine as well as the score of renal tubule damage, therefore alleviating the symptoms induced by RIRI. Furthermore, the RIRI model group showed serious congestion and edema in the renal cortex and medulla, whereas the Curcumin + RIRI model group exhibited less renal tissue damage compared with that in the RIRI model group. Moreover, Curcumin enhanced miR-146a expression, while reducing the expression of nNOS, iNOS, cGPM, caspase-3 and PKG as well as the synthesis of NO. Curcumin may exert its effect by reducing the transcriptional efficiency of iNOS promoter, while increasing the transcriptional efficiency of miR-146a promoter. Furthermore, nNOS expression was negatively regulated by miR-146a. The protective effect of Curcumin against RIRI may be mediated by its regulation of cell apoptosis through the miR-146a/nNOS/NO/cGMP/PKG signaling pathway.

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