Carnosic acid protects against ferroptosis in PC12 cells exposed to erastin through activation of Nrf2 pathway

Cheng, Jie; Xu, Tao; Xun, Chuanhui; Guo, Hailong; Cao, Rui; Gao, Shutao; Sheng, Weibin

doi:10.1016/j.lfs.2020.118905

Cited by 52 publications

(22 citation statements)

References 52 publications

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“…NRF2 translocates to the nucleus and interacts with ARE, leading to the transcriptional induction of some cell defense genes, such as phase II detoxification enzymes HO-1, NQO1, and direct ROS scavenging proteins (GPx, SOD, CAT) [ 49 , 50 ]. Many studies have confirmed that activation of NRF2 can prevent damage caused by ferroptosis [ 14 , 24 , 51 ]. Here, our data demonstrated that trehalose treatment activated the NRF2/HO-1 pathway in the occurrence of neuronal ferroptosis, and inhibition of the NRF2 pathway significantly reversed the inhibition of trehalose on ferroptosis, indicating that trehalose alleviated ferroptosis after SCI by inhibiting the NRF2 pathway.…”

Section: Discussionmentioning

confidence: 99%

“…Zhang et al used the ferroptosis specific inhibitor SRS 16–86 to treat rats with SCI and found that it can reverse the changes in mitochondria, reduce lipid peroxidation products, and enhance endogenous antioxidant capacity, thereby inhibiting the occurrence of ferroptosis and promoting recovery of nerve function in rats [ 13 ]. In addition, studies have shown that carnosic acid can inhibit the ferroptosis of PC12 cells induced by Erastin by activating the NRF2 pathway, suggesting that carnosic acid can play a neuroprotective effect in the inhibition of ferroptosis occurrence [ 14 ]. The latest research findings indicate that both zinc and proanthocyanidin can inhibit ferroptosis, thereby promoting functional recovery after SCI [ 15 , 16 ].…”

Section: Introductionmentioning

confidence: 99%

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Trehalose inhibits ferroptosis via NRF2/HO-1 pathway and promotes functional recovery in mice with spinal cord injury

Gong

Liu

et al. 2022

Aging

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Spinal cord injury (SCI) is the main cause of severe damage to the central nervous system and leads to irreversible tissue loss and neurological dysfunction. Ferroptosis is a cell death pattern, newly discovered in recent years. Ferroptosis is an oxidizing cell death induced by small molecules, and is an iron-dependent process caused by the imbalance between the generation and degradation of lipid reactive oxygen species (ROS) in cells. As an antioxidant, trehalose can effectively prevent lipid peroxidation. Studies have reported that trehalose can improve the prognosis of SCI. However, it is unclear whether these benefits are related to ferroptosis. In this study, we demonstrated for the first time that trehalose reduces the degeneration and iron accumulation of neurons by inhibiting the production of ROS and ferroptosis caused by lipid peroxides after SCI, thus promoting the survival of neurons and improving the recovery of motor function. More specifically, we found that trehalose inhibited the expansion of cavities in the nerve tissue of mice with SCI, inhibited neuron loss, and improved functional recovery. In terms of mechanism, our results indicate that the neuroprotective effect of trehalose is due to the activation of the NRF2/HO-1 pathway, which in turn inhibits ferroptosis and ferroptosis-related inflammation. Our findings provide important insights into the previously unknown role of trehalose in SCI, as well as new evidence supporting the hypothesis that suppression of ferroptosis plays a key neuroprotective role in SCI.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Trehalose inhibits ferroptosis via NRF2/HO-1 pathway and promotes functional recovery in mice with spinal cord injury

Gong

Liu

et al. 2022

Aging

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“…The p62-Keap1-Nrf2 signaling pathway was examined to further explore the pathological mechanisms by which the cellular ischemia-reperfusion process induces ferroptosis. 47,50 Western blotting assay shown in Fig. 5g-k indicated that the p62-Keap1-Nrf2 signaling pathway was activated in the OGD/R cells, while GPX4 expression was signicantly downregulated.…”

Section: Imaging Of Ferroptosis During Ogd/rmentioning

confidence: 92%

Near-infrared fluorescent probe for hydrogen sulfide: high-fidelity ferroptosis evaluation in vivo during stroke

et al. 2022

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“…By stimulating the AKT/Nrf2/HO-1 signaling pathway, the anti-inflammatory mediator lipoxin A4 can reduce ferroptosis in spinal cord neurons [ 77 ]. Similarly, syringic acid [ 75 ], proanthocyanidins [ 73 ], and zinc [ 74 ] all reversed ferroptosis to varying degrees by activating the Nrf2/HO-1 pathway. It is worth mentioning that Nrf2 is oxidative stress in cells and is regulated by a crucial transcription factor and regulates hundreds of antioxidant genes.…”

Section: Research Progress Of Ferroptosis In Scimentioning

confidence: 99%

Ferroptosis: A Novel Therapeutic Direction of Spinal Cord Injury

Zhao

Liu

Zhou

et al. 2022

Computational and Mathematical Methods in Medicine

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An injury to the spinal cord results in a crucial central nervous system event that further causes irreversible impairment or loss of motor, autonomic, and sensory functions. A progressive pathophysiological cascade following spinal cord injury (SCI) includes ischemia/reperfusion injury, oxidative stress, proapoptotic signaling, peripheral inflammatory cell infiltration, and glutamate-mediated excitotoxicity, and regulated cell death. These complex pathological and physiological changes continue to cause cell injury over the long-term and severely limit the efficacy of clinical treatment strategies in restoring the injured nervous system. Ferroptosis is a nonapoptotic, iron-regulated kind of cell death that has recently been discovered. It is distinguished by iron overload-induced toxic lipid peroxidation associated with mitochondrial morphological changes during the cell death process. For example, after SCI, iron overload activates the reactive oxygen species generation, dysregulation of glutathione/glutathione peroxidase 4 (GSH/GPX4) metabolism, and accumulation of lipid peroxides, which cause lipid membrane deterioration and ferroptosis. Conversely, knockout or differential expression of key genes and application of lipid peroxidation inhibitors and iron chelators (e.g., deferoxamine) (e.g., SRS-16-86) can block ferroptosis and promote neuronal repair for functional recovery after SCI. Although the findings of numerous investigations have been confirmed the importance of ferroptosis in several human neurologic sicknesses and its potential in SCI, the mechanism of ferroptosis and its application in SCI has not been elucidated. This review highlights current ferroptosis research and its impact on SCI, as well as the key molecular mechanism of ferroptosis in promoting the recovery from SCI. Understanding ferroptosis’ process and function in SCI could provide useful insight into the treatment and avoidance of such a destructive injury.

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Carnosic acid protects against ferroptosis in PC12 cells exposed to erastin through activation of Nrf2 pathway

Cited by 52 publications

References 52 publications

Trehalose inhibits ferroptosis via NRF2/HO-1 pathway and promotes functional recovery in mice with spinal cord injury

Trehalose inhibits ferroptosis via NRF2/HO-1 pathway and promotes functional recovery in mice with spinal cord injury

Near-infrared fluorescent probe for hydrogen sulfide: high-fidelity ferroptosis evaluation in vivo during stroke

Ferroptosis: A Novel Therapeutic Direction of Spinal Cord Injury

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