Intermittent fasting ameliorates neuronal ferroptosis and cognitive impairment in mice after traumatic brain injury

Yang, Qixiang; Li, Manrui; Liu, Jinyuan; Zhang, Lingxuan; Yuan, Ruixuan; Yang, Xu; Zheng, Jingwen; Cao, Shuqiang; Dai, Hao; Liao, Miao; Lv, Meili; Chen, Xiaogang; Guo, Yadong; Xie, Xiaoqi; Zhang, Lin; Chen, Xiameng; Liang, Weibo

doi:10.1016/j.nut.2023.111992

Cited by 9 publications

(4 citation statements)

References 17 publications

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“…(continued) 67 Juvenile rat (#) Post-TBI KD for 7 days Reduced cerebral glucose metabolism and contusion volume at PND35, but not PND70 CCI 62 Rat (#) Post-TBI fasting for 1 day Increased tissue sparing; improved cognition; better mitochondrial function CCI 59 Mouse (# & $) Pre-TBI alternate day fasting for 30 days Enhanced hippocampal neurogenesis; improved cognition mediated by NPY CCI 63 Mouse (# & $) Pre-TBI alternate day fasting for 30 days Elevated Gpx4 and Hspb1 gene expression; attenuated ferroptosis; improved recognition memory Weight-drop 61 Mouse (#) Post-TBI 30% CR Improved cognition; Decreased mTOR expression; increased autophagy Weight-drop 60 Mouse (#) Alternate day IF or 10-40% CR Improved visual memory; prevented post-TBI SIRT1 reduction Weight-drop 64 Mouse (#) Post-TBI KD for 3, 7, or 30 days Improved cognition; SIRT1 preserved; reduced neuronal loss and astrogliosis Weight-drop 58 Juvenile rat (#) Post-TBI KD for 3 days Downregulated Bax expression; reduced edema and apoptosis Weight projectile 68 Juvenile rat (# & $) 17 days pre-or 20 days post-TBI KD Pre-TBI KD improved motor function; Post-TBI KD reduced anxiety-and depression-like behaviors Exercise FPI 71 Rat (#) Post-TBI voluntary running wheel (days 0-6 or 14-20)…”

Section: Hyperbaric Oxygenmentioning

confidence: 99%

“…59 The above regimen of IF was also shown to attenuate TBI-induced ferroptosis leading to beneficial outcomes. 63 Studies involving dietary adaptations need frequent monitoring of the health conditions of the study participants as there is risk of malnutrition.…”

Section: Dietary Adaptationsmentioning

confidence: 99%

“…27,32,38,95 Other molecular mechanisms targeted by non-pharmacological interventions in TBI include ferroptosis (in IF), autophagy via mTOR (in IF and CR), and metabolism via SIRT1 (in IF, CR, and KD). 60,61,63,64 Stem cells transplanted at the site of injury secrete factors such as neurotrophic factors, cytokines, and chemokines and regulate the function of surrounding cells. 140,154 Furthermore, part of the neuroprotection by probiotics is through the short-chain fatty acids produced by the beneficial microorganisms that colonize the gut.…”

Section: Pharmacological Aspects Of Non-pharmacological Interventionsmentioning

confidence: 99%

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Non-pharmacological interventions for traumatic brain injury

Davis,

Arruri,

Joshi

et al. 2024

J Cereb Blood Flow Metab

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Heterogeneity and variability of symptoms due to the type, site, age, sex, and severity of injury make each case of traumatic brain injury (TBI) unique. Considering this, a universal treatment strategy may not be fruitful in managing outcomes after TBI. Most of the pharmacological therapies for TBI aim at modifying a particular pathway or molecular process in the sequelae of secondary injury rather than a holistic approach. On the other hand, non-pharmacological interventions such as hypothermia, hyperbaric oxygen, preconditioning with dietary adaptations, exercise, environmental enrichment, deep brain stimulation, decompressive craniectomy, probiotic use, gene therapy, music therapy, and stem cell therapy can promote healing by modulating multiple neuroprotective mechanisms. In this review, we discussed the major non-pharmacological interventions that are being tested in animal models of TBI as well as in clinical trials. We evaluated the functional outcomes of various interventions with an emphasis on the links between molecular mechanisms and outcomes after TBI.

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Section: Hyperbaric Oxygenmentioning

confidence: 99%

Section: Dietary Adaptationsmentioning

confidence: 99%

Section: Pharmacological Aspects Of Non-pharmacological Interventionsmentioning

confidence: 99%

See 1 more Smart Citation

Non-pharmacological interventions for traumatic brain injury

Davis,

Arruri,

Joshi

et al. 2024

J Cereb Blood Flow Metab

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“…Addressing this, the clearance of ROS through medication to protect brain neurons is emerging as a promising strategy for PND management. [12][13][14] In this context, plant-derived drugs, particularly flavonoids like Kaempferol (KAE), are gaining attention for their antiinflammatory and antioxidant properties. 15,16 KAE, a natural flavonoid, is effective in scavenging ROS and maintaining antioxidant enzyme activity.…”

Section: Introductionmentioning

confidence: 99%

Polydopamine-Coated Kaempferol-Loaded MOF Nanoparticles: A Novel Therapeutic Strategy for Postoperative Neurocognitive Disorder

Huang,

Li,

Han

et al. 2024

IJN

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The primary objective of this study was to develop an innovative nanomedicine-based therapeutic strategy to alleviate Postoperative Neurocognitive Disorder (PND) in patients undergoing surgery. Patients and Methods: To achieve this goal, polydopamine-coated Kaempferol-loaded Metal-Organic Framework nanoparticles (pDA/ KAE@ZIF-8) were synthesized and evaluated. The study involved encapsulating Kaempferol (KAE) within ZIF-8 nanoparticles, followed by coating with polydopamine (PDA) to enhance biocompatibility and targeted delivery. The characterization of these nanoparticles (NPs) was conducted using various techniques including Scanning Electron Microscopy, Fourier-Transform Infrared Spectroscopy, X-ray Diffraction, and Ultraviolet-Visible spectroscopy. The efficacy of pDA/KAE@ZIF-8 NPs was tested in both in vitro and in vivo models, specifically focusing on their ability to penetrate the blood-brain barrier and protect neuronal cells against oxidative stress. Results: The study found that pDA/KAE@ZIF-8 NPs efficiently penetrated the blood-brain barrier and were significantly taken up by neuronal cells. These nanoparticles demonstrated remarkable Reactive Oxygen Species (ROS) scavenging capabilities and stability under physiological conditions. In vitro studies showed that pDA/KAE@ZIF-8 NPs provided protection to HT-22 neuronal cells against H 2 O 2 -induced oxidative stress, reduced the levels of pro-inflammatory cytokines, and decreased apoptosis rates. In a PND mouse model, the treatment with pDA/KAE@ZIF-8 NPs significantly improved cognitive functions, surpassing the effects of KAE alone. This improvement was substantiated through behavioral tests and a noted reduction in hippocampal inflammation. Conclusion:The findings from this study underscore the potential of pDA/KAE@ZIF-8 NPs as an effective nanotherapeutic agent for PND. This approach offers a novel direction in the postoperative care of elderly patients, with the potential to transform the therapeutic landscape for neurocognitive disorders following surgery. The application of nanotechnology in this context opens new avenues for more effective and targeted treatments, thereby improving the quality of life for patients suffering from PND.

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Cellular Adaptations to Intermittent Fasting with Emphasis on the Brain

Mattson

2024

Intermittent and Periodic Fasting, Aging and Disease

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Intermittent fasting ameliorates neuronal ferroptosis and cognitive impairment in mice after traumatic brain injury

Cited by 9 publications

References 17 publications

Non-pharmacological interventions for traumatic brain injury

Non-pharmacological interventions for traumatic brain injury

Polydopamine-Coated Kaempferol-Loaded MOF Nanoparticles: A Novel Therapeutic Strategy for Postoperative Neurocognitive Disorder

Cellular Adaptations to Intermittent Fasting with Emphasis on the Brain

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