HO-1 attenuates hippocampal neurons injury via the activation of BDNF–TrkB–PI3K/Akt signaling pathway in stroke

Qi, Dashi; Ouyang, Changjie; Wang, Yulan; Zhang, Shichun; Ma, Xiaohai; Song, Yuanjian; Yu, Hongli; Tang, Jiali; Fu, Wei; Sheng, Lei; Yang, Lihua; Wang, Mei; Zhang, Weihao; Miao, Lei; Li, Tengteng; Huang, Xiaojing; Dong, Hongyan

doi:10.1016/j.brainres.2014.06.031

Cited by 85 publications

(47 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…45,46) Activation of MAPKs or Akt is known to be involved in the upstream signaling pathway for the expression of HO-1 in neuronal and other cell types. 47,48) It has been reported that berberine, an alkaloid derived from Coptis chinensis, induces the stimulation of Akt and p38 MAPK, which is linked to HO-1 expression and neuroprotection in SH-SY5Y cells. 49) Additionally, geniposide, an iridoid glycoside from the fruit of Gardenia jasminoides, has been found to trigger the expression of HO-1 in hippocampal neurons through PI3K/nuclear factor-E2-related factor 2 (Nrf2)-signaling, which largely mediates the anti-oxidant action of this compound.…”

Section: Discussionmentioning

confidence: 99%

Protection of Cultured Cortical Neurons by Luteolin against Oxidative Damage through Inhibition of Apoptosis and Induction of Heme Oxygenase-1

Kim

Chin

Cho

2017

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Protection of Cultured Cortical Neurons by Luteolin against Oxidative Damage through Inhibition of Apoptosis and Induction of Heme Oxygenase-1

Kim

Chin

Cho

2017

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

“…BDNF is a member of the neurotrophin family and the activity of BDNF is mediated by the high-affinity TrkB receptor [64]. Accumulated observations have demonstrated that BDNF induces neuroprotective effects [65][66][67]. Therefore, we focused on the role of BDNF in the protective effect of H 2 S against the corticosterone-induced neurotoxicity.…”

Section: Discussionmentioning

confidence: 99%

H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

Gao

Zou

et al. 2015

ABBS

View full text Add to dashboard Cite

Corticosterone, one of the glucocorticoids, is toxic to neurons and plays an important role in depressive-like behavior and depression. We previously showed that hydrogen sulfide (H 2 S), a novel physiological mediator, plays an inhibitory role in depression. However, the mechanism underlying H 2 S-triggered antidepressant-like role is not clearly known. Brain-derived neurotrophic factor (BDNF), a neurotrophic factor, plays a neuroprotective role that is mediated by its high-affinity tropomysin-related kinase B (TrkB) receptor. In this study, to investigate the underlying mechanism of H 2 S-induced antidepressant-like role, we explored whether H 2 S could protect neurons against corticosterone-mediated cyctotoxicity and whether this protective role of H 2 S was involved in the regulation of BDNF-TrkB pathway. Our data demonstrated that sodium hydrosulfide (NaHS), the donor of H 2 S, could prevent corticosterone-induced cytotoxicity, apoptosis, accumulation of intracellular reactive oxygen species (ROS) and loss of mitochondrial membrane potential (MMP) in PC12 cells. NaHS not only induced the up-regulation of BDNF but also prevented the down-regulation of BDNF by corticosterone. It was also found that blocking BDNF-TrkB pathway by K252a, an inhibitor of TrkB, abolished the protection of H 2 S against corticosterone-induced cytotoxicity, apoptosis, accumulation of ROS, and loss of MMP. These results suggest that H 2 S protects against the neurotoxicity of corticosterone by modulation of the BDNF-TrkB pathway.

show abstract

“…Indeed, low concentrations of free-form bilirubin promote GDNF or BDNF induction through the activation of MEK, Akt and NF-κB pathways [76], and CO increases the expression of neurotrophic factors via sGC-PKG-dependent pathway [75]. More recently, HO-1 role in favoring the release of neurotrophic factors has been confirmed in mice subjected to stroke that show better recovery activating BDNF-PI3K/Akt signaling in HO-1 overexpressing hippocampi [77]. Interestingly, it has been recently demonstrated that resveratrol exerts protective activity against LPS-induced cytotoxicity in oligodendrocytes restoring BDNF, GDNF and TGF-β generation, through the activation of Nrf2 and HO-1, highlighting the existence of a HO-1 dependent glioprotective pathway [78].…”

Section: Ho-1 Protective Effects In Nervous Systemmentioning

confidence: 99%

Heme Oxygenase 1 in the Nervous System: Does It Favor Neuronal Cell Survival or Induce Neurodegeneration?

Nitti

Piras

Brondolo

et al. 2018

IJMS

123

107

View full text Add to dashboard Cite

Heme oxygenase 1 (HO-1) up-regulation is recognized as a pivotal mechanism of cell adaptation to stress. Under control of different transcription factors but with a prominent role played by Nrf2, HO-1 induction is crucial also in nervous system response to damage. However, several lines of evidence have highlighted that HO-1 expression is associated to neuronal damage and neurodegeneration especially in Alzheimer’s and Parkinson’s diseases. In this review, we summarize the current literature regarding the role of HO-1 in nervous system pointing out different molecular mechanisms possibly responsible for HO-1 up-regulation in nervous system homeostasis and neurodegeneration.

show abstract

HO-1 attenuates hippocampal neurons injury via the activation of BDNF–TrkB–PI3K/Akt signaling pathway in stroke

Cited by 85 publications

References 36 publications

Protection of Cultured Cortical Neurons by Luteolin against Oxidative Damage through Inhibition of Apoptosis and Induction of Heme Oxygenase-1

Protection of Cultured Cortical Neurons by Luteolin against Oxidative Damage through Inhibition of Apoptosis and Induction of Heme Oxygenase-1

H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

Heme Oxygenase 1 in the Nervous System: Does It Favor Neuronal Cell Survival or Induce Neurodegeneration?

Contact Info

Product

Resources

About

HO-1 attenuates hippocampal neurons injury via the activation of BDNF–TrkB–PI3K/Akt signaling pathway in stroke

Cited by 85 publications

References 36 publications

Protection of Cultured Cortical Neurons by Luteolin against Oxidative Damage through Inhibition of Apoptosis and Induction of Heme Oxygenase-1

Protection of Cultured Cortical Neurons by Luteolin against Oxidative Damage through Inhibition of Apoptosis and Induction of Heme Oxygenase-1

H&lt;sub&gt;2&lt;/sub&gt;S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway

Heme Oxygenase 1 in the Nervous System: Does It Favor Neuronal Cell Survival or Induce Neurodegeneration?

Contact Info

Product

Resources

About

H<sub>2</sub>S protects PC12 cells against toxicity of corticosterone by modulation of BDNF-TrkB pathway