Edaravone protects rat astrocytes from oxidative or neurotoxic inflammatory insults by restoring Akt/Bcl-2/Caspase-3 signaling axis

Guo, Zhe; Wu, Huantong; Li, Xixi; Yu, Yun; Gu, Run-Ze; Lan, Rongfeng; Qin, Xiao-Yan

doi:10.1016/j.ibror.2020.04.003

Cited by 20 publications

(15 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Edaravone protects astrocytes through the PI3K/Akt pathway against H 2 O 2 -induced oxidative stress and LPS-induced pro-inflammatory responses. 31 Edaravone reduces oxidative stress by up-regulating the Nrf2/ARE pathway and also inhibiting inflammation by inhibiting the activation of NF-κB. 32 The antioxidant capacity of edaravone has been confirmed in many disease models.…”

Section: Discussionmentioning

confidence: 99%

Edaravone Alleviated Propofol-Induced Neurotoxicity in Developing Hippocampus by mBDNF/TrkB/PI3K Pathway

Yang¹,

Yi²,

Pan³

et al. 2021

DDDT

View full text Add to dashboard Cite

Background: To investigate the neuroprotective effect of edaravone on excessive-dose propofol-induced neurotoxicity in the hippocampus of newborn rats and HT22 cells.Methods: Cell proliferation was investigated by assessing ki67 expression in the neural stem of the hippocampus of newborn rats and by cell counting kit-8 (CCK8) assay in HT22 cells. Cell apoptosis was assessed in vivo by caspase 3 detection in Western blots and measurement of apoptosis in neurons and glial cells by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Apoptosis was analyzed by flow cytometry in HT22 cells. The Morris water maze was used to evaluate the long-term learning and memory ability of rats. Inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA). The expression of mBDNF/TrkB/PI3K pathway-related proteins was detected by Western blot and quantitative reverse transcription-polymerase chain reaction (q-RT PCR). Results: In neonatal rat hippocampus and HT22 cells, edaravone increased cell proliferation and decreased cell apoptosis after excessive propofol-induced neurotoxicity. In addition, the levels of proinflammatory factors interleukin (IL)-6 and tumor necrosis factor (TNF)-α were reduced by edaravone pretreatment. The use of the tropomyosin receptor kinase B (TrkB) antagonist ANA-12 and TrkB agonist 7,8DHF with propofol groups showed that edaravone mitigated excessive propofol-induced neurotoxicity through the mature brain-derived neurotrophic factor (mBDNF)/TrkB/phosphoinositide 3-kinase (PI3K) pathway. However, the current dose of propofol did not significantly affect long-term learning and memory in rats. Conclusion: Edaravone pretreatment ameliorated propofol-induced proliferation inhibition, neuroapoptosis, and neural inflammation by activating the mBDNF/TrkB/PI3K pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Edaravone Alleviated Propofol-Induced Neurotoxicity in Developing Hippocampus by mBDNF/TrkB/PI3K Pathway

Yang¹,

Yi²,

Pan³

et al. 2021

DDDT

View full text Add to dashboard Cite

show abstract

“…Tajima et al found that EDA prevented lung injury and attenuated inflammatory cell activation and the release of inflammatory cytokines (IL-6 and TNF- α ) in the BALF of the LPS-induced ALI mouse model [ 29 ]. It was also reported that EDA attenuated LPS-mediated inflammatory response in astrocytes [ 30 ]. Thus, EDA might be a powerful drug for inhibiting inflammatory responses.…”

Section: Discussionmentioning

confidence: 99%

Edaravone Attenuated Particulate Matter-Induced Lung Inflammation by Inhibiting ROS-NF-κB Signaling Pathway

Zeng

Zhu

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Background. Particulate matter (PM) exposure is related to mitochondria dysfunction and airway inflammation. Antioxidant drug edaravone (EDA) is reported to improve the occurrence and development of oxidative stress-related diseases. At present, there is no data on whether EDA can alleviate lung inflammation caused by PM. Methods. The anti-inflammatory effects of EDA were investigated in urban PM-induced human bronchial epithelial cells (HBECs) and C57/BL6J mouse models. In vitro, its effects on the production of intracellular reactive oxygen species (ROS), mitochondrial membrane potential (MMP), and inflammatory cytokines were assessed by DCFH-DA staining, JC-1 assay, and real-time PCR, respectively. In vivo, the oxidant stress in lung tissues was assessed by dihydroethidium (DHE) staining and malondialdehyde (MDA) activity, and inflammatory cytokines in bronchoalveolar lavage fluid (BALF) were assessed by ELISA, respectively. Furthermore, the potential signaling pathways were studied by siRNA transfection and western blot. Results. PM increased the expression of inflammatory cytokines and protein, including IL-6, IL-1α, IL-1β, and COX-2, while these alternations were significantly alleviated following EDA treatment in a dose-dependent manner. EDA treatment also alleviated the inflammatory responses in lung tissues of PM-exposed mice. We further showed mitochondrial dysfunction in PM-exposed HBECs and mice, which were reversed by EDA treatment. Moreover, the phosphorylation of NF-κB p65 in PM-exposed HBECs and mice was weakened by EDA. Transfection with NF-κB p65 siRNA further inhibited PM-induced inflammation in HBECs. Conclusion. We demonstrated that EDA treatment had a protective role in PM-induced lung inflammation through maintaining mitochondrial balance and regulating the ROS-NF-κB p65 signaling pathway. This provided a new therapeutic method for PM-induced lung inflammation in the future.

show abstract

“…is study also analyzed the two groups of patients before and after treatment of serum SOD, MDA levels, and Bcl-2, Bax, and Caspase-3 protein levels. SOD can indirectly reflect the body's ability to scavenge oxygen free radicals, MDA belongs to an oxygen free radical, Bax is a proapoptotic gene, Caspase-3 is a multiple apoptotic pathway related factor, and Bcl-2 is mainly distributed in the mitochondrial membrane, and it not only can maintain the normal function of mitochondria and inhibit the spillover of apoptotic factors but also inhibit the release of calcium ions, playing a good role in antioxidant [18][19][20]. According to the above, the higher the levels of SOD and Bcl-2 are, the lower the levels of MDA, Bax, and Caspase-3 proteins are, indicating that the free radicals scavenging is better.…”

Section: Discussionmentioning

confidence: 99%

Deep Learning Reconstruction Algorithm‐Based MRI Image Evaluation of Edaravone in the Treatment of Lower Limb Ischemia‐Reperfusion Injury

Liu

Duan

et al. 2022

Contrast Media & Molecular Imaging

View full text Add to dashboard Cite

This research aimed to evaluate the therapeutic effect of edaravone on lower limb ischemia-reperfusion injury by MRI images of graph patch-based directional curvelet transform (GPBDCT), compression reconstruction algorithm. 200 patients with lower limb ischemia-reperfusion injury after replantation of severed limb were randomly divided into the observation group (edaravone treatment) and control group (Mailuoning injection treatment), with 100 cases in each group. MRI scanning and image processing using the GPBDCT algorithm were used to evaluate the therapeutic effect of the two groups of patients. The results showed that the signal noise ratio (SNR) (22.01), relative l 2 norm error (RLNE) (0.0792), and matching degree γ (0.9997) of the compression and reconstruction algorithm based on GPBDCT were superior to those of the conventional compression and reconstruction algorithm ( P < 0.05 ). MRI examination showed that the decrease of bleeding signal after treatment in the observation group was superior to that in the control group. The levels of superoxide dismutase (SOD) (15 ± 2.02), malondialdehyde (MDA) (2.27 ± 1.02), B cell lymphoma-2 (Bcl-2) (8.5 ± 1.02), Bcl-2-associated X (Bax) (3.7 ± 0.42), and Caspase-3 protein (35.9 ± 5.42) in the observation group before and after treatment were significantly higher than those in the control group ( P < 0.05 ). In conclusion, the GPBDCT-based compression reconstruction algorithm has a better effect on MRI image processing, and edaravone can better remove free radicals and alleviate apoptosis.

show abstract

Edaravone protects rat astrocytes from oxidative or neurotoxic inflammatory insults by restoring Akt/Bcl-2/Caspase-3 signaling axis

Cited by 20 publications

References 27 publications

Edaravone Alleviated Propofol-Induced Neurotoxicity in Developing Hippocampus by mBDNF/TrkB/PI3K Pathway

Edaravone Alleviated Propofol-Induced Neurotoxicity in Developing Hippocampus by mBDNF/TrkB/PI3K Pathway

Edaravone Attenuated Particulate Matter-Induced Lung Inflammation by Inhibiting ROS-NF-κB Signaling Pathway

Deep Learning Reconstruction Algorithm‐Based MRI Image Evaluation of Edaravone in the Treatment of Lower Limb Ischemia‐Reperfusion Injury

Contact Info

Product

Resources

About