scholarly journals MicroRNA-668-3p Protects Against Oxygen-Glucose Deprivation in a Rat H9c2 Cardiomyocyte Model of Ischemia-Reperfusion Injury by Targeting the Stromal Cell-Derived Factor-1 (SDF-1)/CXCR4 Signaling Pathway

2020 ◽  
Vol 26 ◽  
Author(s):  
Zhan Gao ◽  
Qiang Gao ◽  
Xiaodong Lv
Keyword(s):  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Stromal Cell ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Cxcr4 Signaling ◽  
Stromal Cell Derived Factor

scholarly journals Anthocyanin attenuates oxygen-glucose deprivation/reperfusion-induced apoptosis of PC12 cells via inactivation of ASK1/JNK/p38 signaling pathway

2021 ◽  
Vol 18 (10) ◽  
pp. 2037-2043
Author(s):  
Hong Zhu ◽  
Dan Ren ◽  
Lan Xiao ◽  
Ting Zhang ◽  
Ruomeng Li ◽  
...  
Keyword(s):  
Cell Viability ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Induced Apoptosis

Purpose: To investigate whether the cytoprotective effect of anthocyanin (Anc) on oxygen-glucose deprivation/reperfusion (OGD/R)-induced cell injury is related to apoptosis signal-regulating kinase 1 (ASK1)/c-Jun N-terminal kinase (JNK)/p38 signaling pathway. Methods: PC12 cells were pre-treated with various concentrations of Anc (10, 50, and 100 μg/mL) in OGD/R-induced cell injury model. The 3-(4, 5)-dimethylthiahiazo (-z-y1)-3, 5-di-phenytetrazoliumromide (MTT) assay was used to assess cell viability. Cell apoptosis was measured by lactic acid dehydrogenase (LDH) release assay and flow cytometry. Western blot was employed to determine the protein expressions of BCL-2, BAX, caspase-3, p-ASK1 (Thr845), p-JNK, and p-p38. Results: The results indicate that Anc increased the viability of PC12 cells after OGD/R exposure (p < 0.05), and also efficiently rescued OGD/R-induced apoptosis (p < 0.05). Mechanistic studies showed that these protective roles of Anc are related to the inhibition of ASK1/JNK/p38 signaling pathway. Conclusion: The results indicate Anc protects against OGD/R-induced cell injury by enhancing cell viability and inhibiting cell apoptosis. The underlying mechanism of action is partly via inactivation of ASK1/JNK/p38 signaling pathway. Thus, Anc has promise as a potential natural agent to prevent and treat cerebral ischemia-reperfusion injury.

scholarly journals Combination of Paeoniflorin and Calycosin-7-glucoside Promotes Ischemic Stroke Recovery via the PI3K/AKT Signaling Pathway

2020 ◽  
Author(s):  
shengxin Wang ◽  
Xiangli Yan ◽  
Yingying He ◽  
Haozhen Zheng ◽  
PengCheng Wang ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Therapeutic Effect ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Gsk 3Β

Abstract Background Paeoniflorin (PF) and calycosin-7-glucoside (CG) play a role in protecting against brain damage following cerebral ischemia. However, the mechanism of action of PF in combination with CG (PF + CG) against ischemia/reperfusion injury remains unclear. Methods The aim of this study was to investigate the protective role of PF + CG on ischemia/reperfusion injury in vivo and in vitro, as well as its potential mechanism of action indicating that PF + CG attenuates middle cerebral artery occlusion (MCAO) /oxygen-glucose deprivation reperfusion (OGD/R) injury via the PI3K/AKT pathway. MCAO rat model was prepared by modified suture method, and behavioral scoring, cerebral infarction area, brain tissue water content measurement, using PI3K, p-PI3K, AKT, p-AKT, Bcl-2, Bax, GSK-3β protein expression as indicators, observe the effect of PI3K / AKT signaling pathway inhibitor LY294002 on the anti-ischemia-reperfusion effect of PF + CG. Oxygen deprivation method was used to prepare the OGD/R model, CCK-8 was used to determine the survival rate of HT22 cells, the contents of SOR, ROS, MDA, and LHD were determined, and apoptosis was detected by flow cytometry and mitochondrial membrane potential, using PI3K, p-PI3K, AKT, p-AKT, Bcl-2, Bax, GSK-3β protein expression as indicators, observe the effect of PI3K/AKT signaling pathway inhibitor LY294002 on the anti- oxidative and glucose deprivation effect of PF + CG. Results The animal studies showed that PF + CG significantly decreased neurobehavioral deficits, cerebral infarct volume, and brain edema; ameliorated histopathological damage in model rats; increased levels of PI3K, AKT, p-PI3K, p-AKT, and Bcl-2; and reduced BAX and GSK-3β expression. After treatment with PF + CG, the morphology and number of cells in brain tissue were restored to normal, demonstrating a therapeutic effect in cerebral ischemia-reperfusion injury. Results of further studies revealed that, in vitro, PF + CG has a therapeutic effect to enhance cell vitality; elevate levels of superoxide dismutase (SOD); reduce levels of reactive oxygen species (ROS), lactate dehydrogenase (LDH), and malondialdehyde (MDA); decrease apoptosis rate; increase levels of PI3K, AKT, p-PI3K, p-AKT, and Bcl-2; and reduce BAX and GSK-3β expression. Conclusion These results demonstrate that PF + CG has a positive therapeutic effect on ischemia/reperfusion and OGD/R injury, and the mechanism is attributed to activation of the PI3K/AKT signaling pathway.

scholarly journals Hsp20 Protects against Oxygen-Glucose Deprivation/Reperfusion-Induced Golgi Fragmentation and Apoptosis through Fas/FasL Pathway

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Bingwu Zhong ◽  
Zhiping Hu ◽  
Jieqiong Tan ◽  
Tonglin Lu ◽  
Qiang Lei ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Cerebral Ischemia Reperfusion ◽  
N2a Cells ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Golgi Fragmentation

Cerebral ischemia-reperfusion injury plays an important role in the development of tissue injury after acute ischemic stroke. Finding effective neuroprotective agents has become a priority in the treatment of ischemic stroke. The Golgi apparatus (GA) is a pivotal organelle and its protection is an attractive target in the treatment of cerebral ischemia-reperfusion injury. Protective effects of Hsp20, a potential cytoprotective agent due to its chaperone-like activity and involvement in regulation of many vital processes, on GA were assessed in an ischemia-reperfusion injury model. Mouse neuroblastoma Neuro2a (N2a) cells were subjected to oxygen-glucose deprivation/reperfusion (OGDR) insult. OGDR induces Golgi fragmentation, apoptosis, and p115 cleavage in N2a cells. However, transfection with Hsp20 significantly attenuates OGDR-induced Golgi fragmentation and apoptosis. Hsp20 interacts with Bax, decreases FasL and Bax expression, and inhibits caspases 3 and p115 cleavage in N2a cells exposed to OGDR. Our data demonstrate that increased Hsp20 expression protects against OGDR-induced Golgi fragmentation and apoptosis, likely through interaction with Bax and subsequent amelioration of the OGDR-induced elevation in p115 cleavage via the Fas/FasL signaling pathway. This neuroprotective potential of Hsp20 against OGDR insult and the underlying mechanism will pave the way for its potential clinical application for cerebral ischemia-reperfusion related disorders.

scholarly journals Cardioprotective Effect of Propofol against Oxygen Glucose Deprivation and Reperfusion Injury in H9c2 Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Dandan Zhao ◽  
Qing Li ◽  
Qiuping Huang ◽  
Xuguang Li ◽  
Min Yin ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Glucose Deprivation ◽  
Underlying Mechanism ◽  
Oxygen Glucose Deprivation ◽  
H9c2 Cell ◽  
Dependent Manner ◽  
H9c2 Cells

Background. The intravenous anesthetic propofol is reported to be a cardioprotective agent against ischemic-reperfusion injury in the heart. However, the regulatory mechanism still remains unclear.Methods. In this study, we used H9c2 cell line under condition of oxygen glucose deprivation (OGD) followed by reperfusion (OGD/R) to inducein vitrocardiomyocytes ischemia-reperfusion injury. Propofol (5, 10, and 20 μM) was added to the cell cultures before and during the OGD/R phases to investigate the underlying mechanism.Results. Our data showed that OGD/R decreased cell viability, and increased lactate dehydrogenase leakage, and reactive oxygen species and malondialdehyde production in H9c2 cells, all of which were significantly reversed by propofol. Moreover, we found that propofol increased both the activities and protein expressions of superoxide dismutase and catalase. In addition, propofol increased FoxO1 expression in a dose-dependent manner and inhibited p-AMPK formation significantly.Conclusions. These results indicate that the propofol might exert its antioxidative effect through FoxO1 in H9c2 cells, and it has a potential therapeutic effect on cardiac disorders involved in oxidative stress.

scholarly journals LncRNA MALAT1 aggravates oxygen‐glucose deprivation/reoxygenation-induced neuronal endoplasmic reticulum stress and apoptosis via the miR-195a-5p/HMGA1 axis

2021 ◽  
Vol 54 (1) ◽  
Author(s):  
Ying Jia ◽  
Lian Yi ◽  
Qianqian Li ◽  
Tingjiao Liu ◽  
Shanshan Yang
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Cell Model ◽  
Ischemia Reperfusion ◽  
High Mobility ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Abstract Background This study aimed to investigate the potential role and molecular mechanism of lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) in cerebral ischemia/reperfusion injury. Results Using an oxygen-glucose deprivation/reoxygenation (OGD/R) cell model, we determined that the expression of MALAT1 was significantly increased during OGD/R. MALAT1 knockdown reversed OGD/R-induced apoptosis and ER stress. Mechanistically, MALAT1 promoted OGD/R-induced neuronal injury through sponging miR-195a-5p to upregulating high mobility group AT-hook1 (HMGA1). Conclusions Collectively, these data demonstrate the mechanism underlying the invovlvement of MALAT1 in cerebral ischemia/reperfusion injury, thus providing translational evidence that MALAT1 may serve as a novel biomarker and therapeutic target for ischemic stroke.

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