Endoplasmic reticulum stress regulates oxygen‐glucose deprivation‐induced parthanatos in human SH‐SY5Y cells via improvement of intracellular ROS

Wang, Haifeng; Wang, Zongqi; Ding, Ye; Piao, Meihua; Feng, Chong; Chi, Guangfan; Luo, Yan; Ge, Pengfei

doi:10.1111/cns.12771

Cited by 53 publications

(45 citation statements)

References 40 publications

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“…N‐acetylcysteine, a classical antioxidant drug used in chronic obstructive pulmonary disease and contrast‐induced nephropathy, was involved in the metabolism of glutamate, cysteine, and glutathione . NAC was reported to protect cells from oxidative stress, inflammation, and apoptosis in many issues including neuronal cells . In the present study, we demonstrated that NAC treatment could also prevent activation of ER stress via blocking the PI3K/Akt and ERK pathways and consistently ameliorate apoptosis of AVP neurons in acute phase after PEL surgery.…”

Section: Discussionsupporting

confidence: 61%

“…40 NAC was reported to protect cells from oxidative stress, inflammation, and apoptosis in many issues including neuronal cells. 40,41 In the present study, we demonstrated that NAC treatment could also prevent activation of ER stress via blocking the PI3K/Akt and ERK pathways and consistently ameliorate apoptosis of AVP neurons in acute phase after PEL surgery. However, at the late stage of CDI, NAC treatment did not make a difference in deactivation of ER stress or apoptosis pattern.…”

Section: Therapeutic Target For Er Stress and Apoptosis In CDIsupporting

confidence: 55%

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Endoplasmic reticulum stress induces apoptosis of arginine vasopressin neurons in central diabetes insipidus via PI3K/Akt pathway

Zhou

Feng

et al. 2019

CNS Neurosci Ther

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Aims Central diabetes insipidus (CDI), a typical complication caused by pituitary stalk injury, often occurs after surgery, trauma, or tumor compression around hypothalamic structures such as the pituitary stalk and optic chiasma. CDI is linked to decreased arginine vasopressin (AVP) neurons in the hypothalamic supraoptic nucleus and paraventricular nucleus, along with a deficit in circulating AVP and oxytocin. However, little has been elucidated about the changes in AVP neurons in CDI. Hence, our study was designed to understand the role of several pathophysiologic changes such as endoplasmic reticulum (ER) stress and apoptosis of AVP neurons in CDI. Methods In a novel pituitary stalk electric lesion (PEL) model to mimic CDI, immunofluorescence and immunoblotting were used to understand the underlying regulatory mechanisms. Results We reported that in CDI condition, generated by PEL, ER stress induced apoptosis of AVP neurons via activation of the PI3K/Akt and ERK pathways. Furthermore, application of N‐acetylcysteine protected hypothalamic AVP neurons from ER stress‐induced apoptosis through blocking the PI3K/Akt and ERK pathways. Conclusion Our findings showed that AVP neurons underwent apoptosis induced by ER stress, and ER stress might play a vital role in CDI condition through the PI3K/Akt and ERK pathways.

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Section: Discussionsupporting

confidence: 61%

Section: Therapeutic Target For Er Stress and Apoptosis In CDIsupporting

confidence: 55%

Endoplasmic reticulum stress induces apoptosis of arginine vasopressin neurons in central diabetes insipidus via PI3K/Akt pathway

Zhou

Feng

et al. 2019

CNS Neurosci Ther

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“…In ERS, disorganized disulfide bond formation and disruption may lead to ROS accumulation and oxidative stress [44]. At the same time, ERS can cause mitochondrial damage and increase mitochondrial ROS production [45]. In addition, some UPR components such as CHOP may cause oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Acetaldehyde Induces Neurotoxicity In Vitro via Oxidative Stress- and Ca²⁺ Imbalance-Mediated Endoplasmic Reticulum Stress

Cui

Liu

Chang

et al. 2019

Oxidative Medicine and Cellular Longevity

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Excessive drinking can damage brain tissue and cause cognitive dysfunction. Studies have found that the early stage of neurodegenerative disease is closely related to heavy drinking. Acetaldehyde (ADE) is the main toxic metabolite of alcohol. However, the exact mechanisms of ADE-induced neurotoxicity are not fully clear. In this article, we studied the cytotoxic effect of ADE in HT22 cells and primary cultured cortical neuronal cells. We found that ADE exhibited cytotoxicities against HT22 cells and primary cultured cortical neuronal cells in dose-dependent manners. Furthermore, ADE induced apoptosis of HT22 cells by upregulating the expression of caspase family proapoptotic proteins. Moreover, ADE treatment could significantly increase the intracellular Ca2+ and reactive oxygen species (ROS) levels and activate endoplasmic reticulum stress (ERS) in HT22 cells. ADE upregulated ERS-related CHOP expression dose-dependently in primary cultured cortical neuronal cells. In addition, inhibition of ROS with antioxidant N-acetyl-L-cysteine (NAC) reduced the accumulation of ROS and reversed ADE-induced increase of ERS-related protein and apoptosis-related protein levels. Mitigation of ERS with ERS inhibitor 4-PBA obviously suppressed ADE-induced apoptosis and the expression of ERS-related proteins. Therefore, ADE induces neurotoxicity of HT22 cells via oxidative stress- and Ca2+ imbalance-mediated ERS.

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“…Antioxidant activity is characterized by oxygen‐glucose deprivation (OGD)‐induced injury model of human neuroblastoma SH‐SY5Y cells . Then, in order to evaluate neuroprotective activity of all derivatives, the cytotoxicity was determined by MTT assay to make sure all the compounds were within the testable range and could be tested for subsequent bioactivity.…”

Section: Resultsmentioning

confidence: 99%

Synthesis and Structure Activity Relationships of Novel Dehydroepiandrosterone Derivatives as Potent Neuroprotective Agents and Nitric Oxide Production Inhibitors

Gan

Jiang

et al. 2019

ChemistrySelect

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In this study, a series of dehydroepiandrosterone (DHEA) derivatives were synthesized by linking DHEA with active fragments such as carbamate, phthalimide and indoleacetic acid. In addition, the in vitro neuroprotective effects, via the oxidative stress mechanism, and nitric oxide (NO) production inhibitory activities of each compound were tested. The preliminary structure‐activity relationships of them indicated that DHEA with carbamate structure had a certain neuroprotective and anti‐inflammatory effect such as 3β‐(Cyclohexylamine‐1‐carboxylate)‐5‐androsten‐17‐one (A2) and 3β‐(3‐Chlorobenzylamine‐1‐carboxylate)‐5‐androsten‐17‐one (A6). And the ester derivatives with indoleacetic acid like 17β–(Heteroauxin‐1‐carboxylate)‐androst‐4‐en‐3‐one (A12) also exhibited both significant neuroprotective activity and NO inhibitory activity. According to these results, compound A6 is considered as a potential agent for the treatment of Alzheimer′s disease (AD) and deserve for further investigations.

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Endoplasmic reticulum stress regulates oxygen‐glucose deprivation‐induced parthanatos in human SH‐SY5Y cells via improvement of intracellular ROS

Abstract: Endoplasmic reticulum stress regulates OGD-induced parthanatos in human SH-SY5Y cells via improvement of intracellular ROS.

Cited by 53 publications

References 40 publications

Endoplasmic reticulum stress induces apoptosis of arginine vasopressin neurons in central diabetes insipidus via PI3K/Akt pathway

Endoplasmic reticulum stress induces apoptosis of arginine vasopressin neurons in central diabetes insipidus via PI3K/Akt pathway

Acetaldehyde Induces Neurotoxicity In Vitro via Oxidative Stress- and Ca²⁺ Imbalance-Mediated Endoplasmic Reticulum Stress

Synthesis and Structure Activity Relationships of Novel Dehydroepiandrosterone Derivatives as Potent Neuroprotective Agents and Nitric Oxide Production Inhibitors

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Endoplasmic reticulum stress regulates oxygen‐glucose deprivation‐induced parthanatos in human SH‐SY5Y cells via improvement of intracellular ROS

Abstract: Endoplasmic reticulum stress regulates OGD-induced parthanatos in human SH-SY5Y cells via improvement of intracellular ROS.

Cited by 53 publications

References 40 publications

Endoplasmic reticulum stress induces apoptosis of arginine vasopressin neurons in central diabetes insipidus via PI3K/Akt pathway

Endoplasmic reticulum stress induces apoptosis of arginine vasopressin neurons in central diabetes insipidus via PI3K/Akt pathway

Acetaldehyde Induces Neurotoxicity In Vitro via Oxidative Stress- and Ca2+ Imbalance-Mediated Endoplasmic Reticulum Stress

Synthesis and Structure Activity Relationships of Novel Dehydroepiandrosterone Derivatives as Potent Neuroprotective Agents and Nitric Oxide Production Inhibitors

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Product

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Acetaldehyde Induces Neurotoxicity In Vitro via Oxidative Stress- and Ca²⁺ Imbalance-Mediated Endoplasmic Reticulum Stress