Melatonin protects H9c2 cardiomyoblasts from oxygen glucose deprivation and reperfusion‐induced injury by inhibiting Rac1/JNK/Foxo3a/Bim signaling pathway

2021 ◽  
Author(s):  
Yulin Wang ◽  
Ying Jian ◽  
Xiaofu Zhang ◽  
Bin Ni ◽  
Mingwei Wang ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
H9c2 Cardiomyoblasts

Expression changes of the notch signaling pathway of PC12 cells after oxygen glucose deprivation

2018 ◽  
Vol 118 ◽  
pp. 1984-1988 ◽  
Author(s):  
Zhong-Xin Xu ◽  
Lei Xu ◽  
Jiao-Qi Wang ◽  
Jing Mang ◽  
Le Yang ◽  
...  
Keyword(s):  
Notch Signaling ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Glucose Deprivation ◽  
Notch Signaling Pathway ◽  
Oxygen Glucose Deprivation

scholarly journals Troxerutin attenuates oxygen‑glucose deprivation and reoxygenation‑induced oxidative stress and inflammation by enhancing the PI3K/AKT/HIF‑1α signaling pathway in H9C2 cardiomyocytes

2020 ◽  
Vol 22 (2) ◽  
pp. 1351-1361
Author(s):  
Zhang‑Ping Yu ◽  
Han‑Qiao Yu ◽  
Jun Li ◽  
Chao Li ◽  
Xian Hua ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation ◽  
H9c2 Cardiomyocytes

Che-1 inhibits oxygen–glucose deprivation/reoxygenation-induced neuronal apoptosis associated with inhibition of the p53-mediated proapoptotic signaling pathway

Neuroreport ◽  
2018 ◽  
Vol 29 (14) ◽  
pp. 1193-1200 ◽  
Author(s):  
Shenglong Guo ◽  
Ruili Chen ◽  
Xiaoli Chen ◽  
Zhen Xie ◽  
Fangfang Huo ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Neuronal Apoptosis ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation

scholarly journals HMG-CoA Reductase Inhibitors Attenuate Neuronal Damage by Suppressing Oxygen Glucose Deprivation-Induced Activated Microglial Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Dan Lu ◽  
Lingling Shen ◽  
Hongcheng Mai ◽  
Jiankun Zang ◽  
Yanfang Liu ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Neuronal Damage ◽  
Glucose Deprivation ◽  
Inflammatory Factors ◽  
Oxygen Glucose Deprivation ◽  
Hmg Coa Reductase ◽  
Reductase Inhibitors ◽  
Bv2 Microglia ◽  
Hmg Coa Reductase Inhibitors ◽  
Coa Reductase

Ischemic stroke is usually followed by inflammatory responses mediated by microglia. However, the effect of statins on directly preventing posthypoxia microglia inflammatory factors to prevent injury to surrounding healthy neurons is unclear. Atorvastatin and rosuvastatin, which have different physical properties regarding their lipid and water solubility, are the most common HMG-CoA reductase inhibitors (statins) and might directly block posthypoxia microglia inflammatory factors to prevent injury to surrounding neurons. Neuronal damage and microglial activation of the peri-infarct areas were investigated by Western blotting and immunofluorescence after 24 hours in a middle cerebral artery occlusion (MCAO) rat model. The decrease in neurons was in accordance with the increase in microglia, which could be reversed by both atorvastatin and rosuvastatin. The effects of statins on blocking secretions from posthypoxia microglia and reducing the secondary damage to surrounding normal neurons were studied in a coculture system in vitro. BV2 microglia were cultured under oxygen glucose deprivation (OGD) for 3 hours and then cocultured following reperfusion for 24 hours in the upper wells of transwell plates with primary neurons being cultured in the bottom wells. Inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and cyclooxygenase-2 (COX2), which are activated by the nuclear factor-kappa B (NF-κB) signaling pathway in OGD-induced BV2 microglia, promoted decreased release of the anti-inflammatory cytokine IL-10 and apoptosis of neurons in the coculture systems according to ELISA and Western blotting. However, pretreatment with atorvastatin or rosuvastatin significantly reduced neuronal death, synaptic injury, and amyloid-beta (Aβ) accumulation, which might lead to increased low-density lipoprotein receptors (LDLRs) in BV2 microglia. We concluded that the proinflammatory mediators released from postischemia damage could cause damage to surrounding normal neurons, while HMG-CoA reductase inhibitors prevented neuronal apoptosis and synaptic injury by inactivating microglia through blocking the NF-κB signaling pathway.

Downregulation of TRIM8 protects neurons from oxygen–glucose deprivation/re-oxygenation-induced injury through reinforcement of the AMPK/Nrf2/ARE antioxidant signaling pathway

2020 ◽  
Vol 1728 ◽  
pp. 146590 ◽  
Author(s):  
Wei Zhao ◽  
Xiajing Zhang ◽  
Yan Chen ◽  
Yongping Shao ◽  
Yan Feng
Keyword(s):  
Signaling Pathway ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation

scholarly journals Neuroprotective Effect of Modified Xijiao Dihuang Decoction against Oxygen-Glucose Deprivation and Reoxygenation-Induced Injury in PC12 Cells: Involvement of TLR4-MyD88/NF-κB Signaling Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Xu Zhang ◽  
Xiaojun Fei ◽  
Weiwei Tao ◽  
Jingbo Li ◽  
Hao Shen ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Pc12 Cells ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Glucose Deprivation ◽  
Treated Group ◽  
Chinese Herbs ◽  
Oxygen Glucose Deprivation ◽  
Control Group ◽  
Stroke Treatment

Modified Xijiao Dihuang (XJDH) decoction has been shown to exert powerful neuroprotective properties in clinical ischemic stroke treatment. It consists of 4 Chinese herbs: Buffalo Horn, Paeonia suffruticosa Andrews, Rehmannia glutinosa (Gaertn.) DC, and Paeonia lactiflora Pall. In the present study, the neuroprotective effect and specific mechanisms of XJDH in protecting PC12 cells from oxygen-glucose deprivation-induced injury were investigated. It was found that OGD/R significantly decreased the cell viability and lactate dehydrogenase (LDH) activity and increased the release of IL-1β, IL-6, and TNF-α in PC12 cells, and these effects were suppressed by XJDH and one of its major active constituents, paeoniflorin. Additionally, XJDH inhibited caspase-3 activity and reduced cleaved caspase-3 level. Mechanistic studies showed that the expressions of TLR4, MyD88, TRAF6, and NF-κB p65 and phosphorylation of IκBα and p65 were significantly lower in the XJDH-treated group than in the OGD/R control group. Additionally, XJDH reversed the OGD/R-induced increases in p-JNK and p-ERK1/2 expression. These results suggest that XJDH protects PC12 cells from oxygen-glucose deprivation-induced injury, which may be associated with the inhibition of the TLR4-MyD88/NF-κB signaling pathway. As an anti-inflammation factor, XJDH might be used as a neuronal protection strategy for the ischemia injury and related diseases.

Daucosterol protects neurons against oxygen–glucose deprivation/reperfusion-mediated injury by activating IGF1 signaling pathway

2015 ◽  
Vol 152 ◽  
pp. 45-52 ◽  
Author(s):  
Li-hua Jiang ◽  
Xiao-lin Yuan ◽  
Nian-yun Yang ◽  
Li Ren ◽  
Feng-ming Zhao ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Glucose Deprivation ◽  
Oxygen Glucose Deprivation
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