SET domain containing 7 promotes oxygen-glucose deprivation/reoxygenation-induced PC12 cell inflammation and oxidative stress by regulating Keap1/Nrf2/ARE and NF-κB pathways

Xian-fang, Pan; Fan, Jiulun; Peng, Fang; Li, Xiao; Yang, Zhiyi

doi:10.1080/21655979.2022.2045830

Cited by 7 publications

(4 citation statements)

References 29 publications

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“…Meanwhile, Nrf2 serves as a transcription factor and can regulate the expression of SLC7A11 and GPX4 to inhibit lipid peroxidation and ferroptosis [ 24 ]. Pan et al demonstrate that activating the Nrf2/HO-1 pathway and inhibiting oxidative stress can protect the brain from I/R damage [ 50 ]. Thus, we utilized WB to measure the levels of Nrf2, GPX4, and SLC7A11 and RT‒qPCR to assess Nrf2 mRNA expression.…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture Downregulating Neuronal Ferroptosis in MCAO/R Rats by Activating Nrf2/SLC7A11/GPX4 Axis

Zhu,

Dong,

Han

2024

Neurochem Res

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Ischemic stroke involves various pathological processes, among which ferroptosis is crucial. Previous studies by our group have indicated that electroacupuncture (EA) mitigates ferroptosis after ischemic stroke; however, the precise mechanism underlying this effect remains unclear. In the present study, we developed a rat model of middle cerebral artery occlusion/reperfusion. We chose the main acupoint of the treatment methods of the “Awakening and Opening of the Brain”. Rats’ neurological function and motor coordination were evaluated by neurological function score and the rotarod test, respectively, and the volume of cerebral infarction was analyzed by 2,3,5-triphenyltetrazolium chloride Staining. The cerebrovascular conditions were visualized by time-of-flight magentic resonance angiography. In addition, we detected changes in lipid peroxidation and endogenous antioxidant activity by measuring the malondialdehyde, glutathione, superoxide dismutase activities, glutathione/oxidized glutathione and reduced nicotinamide adenine dinucleotide phosphate/oxidized nicotinamide adenine dinucleotide phosphate ratios. Inductively coupled plasma-mass spectrometry, western blot, reverse transcription-polymerase chain reaction, fluoro-jade B staining, immunofluorescence analysis, and transmission electron microscopy were utilized to examine the influence of EA. The results indicate that EA treatment was effective in reversing neurological impairment, neuronal damage, and protecting mitochondrial morphology and decreasing the cerebral infarct volume in the middle cerebral artery occlusion/reperfusion rat model. EA reduced iron levels, inhibited lipid peroxidation, increased endogenous antioxidant activity, modulated the expression of several ferroptosis-related proteins, and promoted nuclear factor-E2-related factor 2 (Nrf2) nuclear translocation. However, the protective effect of EA was hindered by the Nrf2 inhibitor ML385. These findings suggest that EA can suppress ferroptosis and decrease damage caused by cerebral ischemia/reperfusion by activating Nrf2 and increasing the protein expression of solute carrier family 7 member 11 and glutathione peroxidase 4.

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Section: Discussionmentioning

confidence: 99%

Electroacupuncture Downregulating Neuronal Ferroptosis in MCAO/R Rats by Activating Nrf2/SLC7A11/GPX4 Axis

Zhu,

Dong,

Han

2024

Neurochem Res

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“…HT‐22 cell line were from BeiNa Culture Collection (Beijing, China) and incubated in DMEM (Gibco, 11965092) with 10% FBS (Sigma, 10099141C) and 2 mM glutamine at 37°C, 5% CO 2 . Then, the HT‐22 cells were grown in glucose‐free DMEM (Gibco) with 1 % O 2 , 94 % N 2 , and 5 % CO 2 at 37°C for 1, 2, 4, 8, and 12 h. Subsequently, the HT‐22 cells were placed to normal DMEM with 95% air and 5% CO 2 for 24 h (Pan et al., 2022 ). The HT‐22 cells under normal oxygen conditions were applied as the control.…”

Section: Methodsmentioning

confidence: 99%

Seipin overexpression attenuates cerebral ischemia‐reperfusion injury via preventing apoptosis and autophagy

Zhu,

An,

Chen

et al. 2023

Brain and Behavior

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BackgroundIschemic cerebrovascular disease (ICVD) is one of three fatal diseases in humans, along with heart disease and malignant tumors. Cerebral ischemia/reperfusion injury (CI/RI) is the primary cause of ICVD. Recently, seipin was reported to be crucial for lipid droplet formation, hepatic steatosis, and axonal atrophy. However, the function and mechanism of seipin in CI/RI has not been explicitly stated.MethodsOxygen–glucose deprivation/reoxygenation (OGD/R) hippocampal neuron cell line (HT‐22) and middle cerebral artery occlusion (MCAO) in rats were established. The levels of apoptosis‐ and autophagy‐related proteins and seipin were confirmed by western blot. Cell proliferation was assessed with CCK‐8, and ischemic infarction and pathological structure were monitored by TTC and H&E staining, and tissue apoptosis was assessed through TUNEL assay.ResultsThe proliferative activity was decreased, and apoptosis and autophagy pathways could also be induced in the OGD/R HT‐22 cells. Seipin overexpression accelerated viability and inhibited apoptosis and autophagy in the OGD/R HT‐22 cells. Moreover, the data revealed that seipin overexpression could also attenuate cerebral infarction, apoptosis. Autophagy pathways could be repressed by seipin in the MCAO rats.ConclusionSeipin has a protective role against CI/RI in rats, and its mechanism might be relevant to the suppression of apoptosis and autophagy, suggesting that seipin might be a latent target for CI/RI.

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“…Using an in vitro cell model of cerebral IRI, Pan et al observed increased SETD7 expression in cells, decreased PC12 cell viability, and increased apoptosis. However, SETD7 knockout could reverse the effects of oxygen-glucose deprivation/reoxygenation (OGD/R) on PC12 cell viability and apoptosis by increasing Nrf2 expression and inactivating NF-κB, simultaneously diminishing the inflammatory response and oxidative stress [90].…”

Section: Cerebral Irimentioning

confidence: 99%

“…Another study showed that UA treatment increased SETD7 expression in LNCaP cells and H3K4me1 enrichment at the Nrf2 promoter, enhancing Nrf2 expression and protecting DNA from oxidative damage [160]. In contrast, SETD7 knockdown ameliorated oxidative stress induced by cerebral IRI by increasing Nrf2 transcriptional activity [90]. Furthermore, SETD7 inhibition could reduce Keap1 expression in retinal endothelial cells by preventing H3K4 methylation, thereby increasing Nrf2 expression and reducing apoptosis and oxidative stress damage [105].…”

Section: Ursolic Acidmentioning

confidence: 99%

Comprehensive overview of Nrf2-related epigenetic regulations involved in ischemia-reperfusion injury

et al. 2022

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Ischemic disease is a class of diseases in which an organ is ischemic due to vascular occlusion, a major contributor to death and disability worldwide. However, when the blood flow is restored, more severe damage occurs than ischemia alone and is known as ischemic-reperfusion injury (IRI). During reperfusion, the imbalance between the production of reactive oxygen species (ROS) and buffering capacity of the antioxidant defense system results in cell damage and death. Nuclear factor E2-related factor 2 (Nrf2) significantly affects antioxidant stress damage. The function of Nrf2 in the pathological process of IRI has been widely discussed, but the impact of epigenetic modifications associated with Nrf2 remains unclear. This article provides a comprehensive overview of the role and mechanism of Nrf2-related epigenetic modifications in the IRI of various organs, including the brain, heart, liver, and kidney. In addition, we summarize agonists that may target epigenetic regulation of Nrf2, which may be beneficial in seeking more effective strategies to improve IRI.

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SET domain containing 7 promotes oxygen-glucose deprivation/reoxygenation-induced PC12 cell inflammation and oxidative stress by regulating Keap1/Nrf2/ARE and NF-κB pathways

Cited by 7 publications

References 29 publications

Electroacupuncture Downregulating Neuronal Ferroptosis in MCAO/R Rats by Activating Nrf2/SLC7A11/GPX4 Axis

Electroacupuncture Downregulating Neuronal Ferroptosis in MCAO/R Rats by Activating Nrf2/SLC7A11/GPX4 Axis

Seipin overexpression attenuates cerebral ischemia‐reperfusion injury via preventing apoptosis and autophagy

Comprehensive overview of Nrf2-related epigenetic regulations involved in ischemia-reperfusion injury

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