Moxibustion Exerts a Neuroprotective Effect through Antiferroptosis in Parkinson’s Disease

Lü, Juan; Liu, Xuelei; Tian, Ye; Li, Hang; Ren, Zhenxing; Liang, Shuang; Zhang, Guiyu; Zhao, Caiping; Li, Xinrong; Wang, Tingting; Chen, Dongfeng; Kuang, Weihong; Zhu, Meiling

doi:10.1155/2019/2735492

Cited by 23 publications

(24 citation statements)

References 46 publications

(46 reference statements)

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“…TFR1 transports iron from the extracellular environment into cells, facilitating the cellular iron pool essential for ferroptosis ( 14 ). FTH1 is a major iron storage protein responsible for maintaining the iron balance in cells ( 15 ). Ferroptosis is implicated in ischemic stroke ( 4 , 16 ).…”

Section: Introductionmentioning

confidence: 99%

Carthamin yellow improves cerebral ischemia‑reperfusion injury by attenuating inflammation and ferroptosis in rats

et al. 2021

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Carthamin yellow (CY), a flavonoid compound extracted from safflower, has been reported to attenuate cardiac ischemia and reperfusion injury. However, whether CY could ameliorate ischemic stroke is not completely understood. In the present study, the preventive effects of CY on experimental ischemic stroke were investigated using middle cerebral artery occlusion (MCAO) model rats. Neurological scores, brain edema, infarct area and microtubule-associated protein 2 (MAP-2) immunoreactivity were assessed to evaluate the effects of CY on ischemic brain injury. The involvement of inflammation and ferroptosis were examined to investigate the mechanism underlying the effects of CY. The results demonstrated that 2-week CY treatment attenuated the neurological deficit score, brain water content and infarct area, and increased MAP-2 immunoreactivity in the cortex in MCAO model rats. CY administration also deactivated the cortex NF-κB/NLR family pyrin domain containing 3 inflammasome signaling pathway, and decreased serum TNF-α, IL-1β and IL-6 concentrations. Moreover, CY treatment inhibited Fe 2+ and reactive oxygen species accumulation, and reversed acyl-CoA synthetase long-chain family member 4, transferrin receptor 1, glutathione peroxidase 4 and ferritin heavy chain 1 protein expression levels in the brain. The levels of glutathione, superoxide dismutase and malondialdehyde in the serum were also reversed by CY treatment. Collectively, the results of the present study demonstrated that CY protected rats against ischemic stroke, which was associated with mitigation of inflammation and ferroptosis.

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Section: Introductionmentioning

confidence: 99%

Carthamin yellow improves cerebral ischemia‑reperfusion injury by attenuating inflammation and ferroptosis in rats

et al. 2021

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“…PD was established in the rats as previously described ( 15 ). Briefly, the rats were anesthetized (100 mg/kg ketamine and 10 mg/kg xylazine, intraperitoneal injection) and placed in a stereotaxic apparatus with the skull flat.…”

Section: Methodsmentioning

confidence: 99%

“…Fe 2+ release and ferritin degradation are associated with cell dysfunction through the process of ferritinophagy, causing ROS formation and lipid peroxidation by releasing iron at sufficient levels, triggering ferroptosis ( 13 ). In previous studies, the authors demonstrated that was involved in ferroptosis in in vivo and in vitro models of Parkinson's disease (PD) ( 14 , 15 ). Therefore, it is of considerable interest to explore the upstream molecules targeting FTH1.…”

Section: Introductionmentioning

confidence: 99%

“…Ferroptosis, an iron-dependent cell death pathway, has recently been identified to play a role in the early stages of PD ( 15 , 18 ). Fe 2+ is a potent reducing agent that can generate hydroxyl radicals and cause dopamine oxidation, which can act to further increase the oxidative environment of the SN and contribute to dopaminergic neuron loss ( 19 ).…”

Section: Introductionmentioning

confidence: 99%

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miR‑335 promotes ferroptosis by targeting ferritin heavy chain 1 in in vivo and in vitro models of Parkinson's disease

et al. 2021

Int J Mol Med

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Parkinson's disease (PD) is a neurodegenerative disease characterized by the selective loss of dopaminergic neurons in the substantia nigra (SN). In a previous study, the authors demonstrated that ferritin heavy chain 1 (FTH1) inhibited ferroptosis in a model of 6-hydroxydopamine (6-OHDA)-induced PD. However, whether and how microRNAs (miRNAs/miRs) modulate FTH1 in PD ferroptosis is not yet well understood. In the present study, in vivo and in vitro models of PD induced by 6-OHDA were established. The results in vivo and in vitro revealed that the levels of the ferroptosis marker protein, glutathione peroxidase 4 (GPX4), and the PD marker protein, tyrosine hydroxylase (TH), were decreased in the model group, associated with a decreased FTH1 expression and the upregulation of miR-335. In both the in vivo and in vitro models, miR-335 mimic led to a lower FTH1 expression, exacerbated ferroptosis and an enhanced PD pathology. The luciferase 3′-untranslated region reporter results identified FTH1 as the direct target of miR-335. The silencing of FTH1 in 6-OHDA-stimulated cells enhanced the effects of miR-335 on ferroptosis and promoted PD pathology. Mechanistically, miR-335 enhanced ferroptosis through the degradation of FTH1 to increase iron release, lipid peroxidation and reactive oxygen species (ROS) accumulation, and to decrease mitochondrial membrane potential (MMP). On the whole, the findings of the present study reveal that miR-335 promotes ferroptosis by targeting FTH1 in in vitro and in vivo models of PD, providing a potential therapeutic target for the treatment of PD.

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“…TFR1 transported iron from extracellular environment into cells, facilitating the cellular iron pool essential for ferroptosis [13]. FTH1 is a major iron storage protein responsible for maintaining the iron balance in cells [14]. Ferroptosis has been reported to influence NF-κB/NLRP3 inflammasome signaling, and is implicated in ischemic stroke [15,16].…”

Section: Introductionmentioning

confidence: 99%

Carthamin yellow protected rats from cerebral ischemia–reperfusion injury by improving neuronal dendritic plasticity via antiferroptosis mediated NF-κB/NLRP3 inflammasome pathway deactivation

Guo

Zhu

Tang

et al. 2020

Preprint

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Background: Carthamin yellow (CY), a flavonoid compound extracted from safflower, has been reported to attenuate cardiac ischemia and reperfusion injury. It is unclear whether CY could ameliorate ischemic stroke. Methods: We examined the preventive effects of CY in experimental ischemic stroke using middle cerebral artery occlusion (MCAO) rats model. Neurological function, brain edema and infarct area were assessed to elucidate the effects of CY on neurological function and ischemic brain injury. MAP-2 Immunofluorescence activity, expressions in NF-κB/NLRP3 inflammasome pathway and ferroptosis were determined to reveal its underlying mechanism. Results: A 2-week CY treatment attenuated the neurological deficit score, brain water content and infarct area in MCAO rats. Meanwhile, CY intervention increased the MAP-2 Immunofluorescence activity and deactivated NF-κB/NLRP3 inflammasome pathway in the cortex. Declined serum TNF-α, IL-1β and IL-6 concentrations were detected following CY administration. Furthermore, CY treatment inhibited Fe2+ and ROS accumulation, and restored the protein expressions of ACSL4, TFR1, GPX4 and FTH1 in the brain. The levels of GSH, SOD and MDA in the serum were reversed by CY intervention. Conclusion: CY protected rats from ischemic stroke, which was associated with the improvement of neuronal dendritic plasticity through antiferroptosis mediated NF-κB/NLRP3 inflammasome pathway deactivation.

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Moxibustion Exerts a Neuroprotective Effect through Antiferroptosis in Parkinson’s Disease

Cited by 23 publications

References 46 publications

Carthamin yellow improves cerebral ischemia‑reperfusion injury by attenuating inflammation and ferroptosis in rats

Carthamin yellow improves cerebral ischemia‑reperfusion injury by attenuating inflammation and ferroptosis in rats

miR‑335 promotes ferroptosis by targeting ferritin heavy chain 1 in in vivo and in vitro models of Parkinson's disease

Carthamin yellow protected rats from cerebral ischemia–reperfusion injury by improving neuronal dendritic plasticity via antiferroptosis mediated NF-κB/NLRP3 inflammasome pathway deactivation

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