Hydrogen attenuates radiation-induced intestinal damage by reducing oxidative stress and inflammatory response

Qiu, Xiaochen; Dong, Kaisheng; Guan, Jian-Long; He, JianMiao

doi:10.1016/j.intimp.2020.106517

Cited by 41 publications

(36 citation statements)

References 32 publications

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“…However, it is also necessary to consider the indirect mechanisms of •OH. In cellular and animal models in which radioprotective effects were examined, H 2 showed not only antioxidant but also anti-inflammatory, anti-apoptotic, and gene expression regulating effects [36][37][38][39][40][41][42][43][44][45][46][47][48][49][50][51][52][53][54]. It is possible that H 2 may also indirectly exert its antioxidant effects by regulating gene expression through intracellular responses.…”

Section: Prospects Of H 2 As a Radioprotective Agentmentioning

confidence: 99%

“…Qiu et al investigated the radioprotective effects of H 2 in animal experiments using mice and in cellular experiments using the intestinal crypt epithelial cell (IEC-6) line [ 45 ]. H 2 -rich saline (1.2 ppm) improved mouse survival and intestinal mucosal damage and function, as well as oxidative stress and inflammatory response.…”

Section: Radioprotective Effects Of H 2 In Animal Modelsmentioning

confidence: 99%

“…H 2 inhibited mitochondrial depolarization, cytochrome c release, and the activities of caspase-3, caspase-9, and polymerase (PARP). In addition, H 2 recovered from the decreased expression of B cell lymphoma-extra-large (Bcl-xl) and B cell lymphoma-2 (Bcl-2), proteins that suppress apoptosis, and suppressed the increased expression of BCL2-associated X protein (Bax), a protein that promotes apoptosis [ 45 ]. They suggested that the protective effects of H 2 against radiation damage may involve the blockage of the mitochondrial apoptotic pathway.…”

Section: Radioprotective Effects Of H 2 In Animal Modelsmentioning

confidence: 99%

“…H 2 , on the other hand, is an inert substance, but it can protect living organisms from radiation-induced oxidative damage by selectively scavenging the large amounts of •OH generated in the living body. Although the radioprotective effects of H 2 have been confirmed in the past literature, there are few that report the detailed mechanisms of H 2 [ 36 , 37 , 38 , 39 , 40 , 41 , 42 , 43 , 44 , 45 , 46 , 47 , 48 , 49 , 50 , 51 , 52 , 53 , 54 ]. In this section, we will discuss the possible mechanisms of the radioprotective effects of H 2 from these reports.…”

Section: Mechanism Of the Radioprotective Effects Of Hmentioning

confidence: 99%

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Molecular Hydrogen as a Potential Clinically Applicable Radioprotective Agent

Hirano¹,

Ichikawa²,

Sato³

et al. 2021

IJMS

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Although ionizing radiation (radiation) is commonly used for medical diagnosis and cancer treatment, radiation-induced damages cannot be avoided. Such damages can be classified into direct and indirect damages, caused by the direct absorption of radiation energy into DNA and by free radicals, such as hydroxyl radicals (•OH), generated in the process of water radiolysis. More specifically, radiation damage concerns not only direct damages to DNA, but also secondary damages to non-DNA targets, because low-dose radiation damage is mainly caused by these indirect effects. Molecular hydrogen (H2) has the potential to be a radioprotective agent because it can selectively scavenge •OH, a reactive oxygen species with strong oxidizing power. Animal experiments and clinical trials have reported that H2 exhibits a highly safe radioprotective effect. This paper reviews previously reported radioprotective effects of H2 and discusses the mechanisms of H2, not only as an antioxidant, but also in intracellular responses including anti-inflammation, anti-apoptosis, and the regulation of gene expression. In doing so, we demonstrate the prospects of H2 as a novel and clinically applicable radioprotective agent.

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Section: Prospects Of H 2 As a Radioprotective Agentmentioning

confidence: 99%

Section: Radioprotective Effects Of H 2 In Animal Modelsmentioning

confidence: 99%

Section: Radioprotective Effects Of H 2 In Animal Modelsmentioning

confidence: 99%

Section: Mechanism Of the Radioprotective Effects Of Hmentioning

confidence: 99%

See 2 more Smart Citations

Molecular Hydrogen as a Potential Clinically Applicable Radioprotective Agent

Hirano¹,

Ichikawa²,

Sato³

et al. 2021

IJMS

View full text Add to dashboard Cite

show abstract

“…OS occur when the generation of ROS exceeds the capacity of the antioxidant clearance systems, which is considered as an important pathological factor leading to aging and disease [ 7 ]. Previous studies suggested that ROS induced apoptosis by increasing p53 and cytochrome c release, reducing Bcl2, and activating caspase-9 and caspase-3 [ 8 , 9 ]. After ischemic brain injury, the overproduction of ROS not only directly damaged neurons and resulted in neuronal apoptosis but also indirectly caused neuronal degeneration by regulating mitochondrial pathways, DNA repair enzymes, and transcription factors [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Rh-CSF1 Attenuates Oxidative Stress and Neuronal Apoptosis via the CSF1R/PLCG2/PKA/UCP2 Signaling Pathway in a Rat Model of Neonatal HIE

Xiao

Liu

Doycheva

et al. 2020

Oxidative Medicine and Cellular Longevity

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Oxidative stress (OS) and neuronal apoptosis are major pathological processes after hypoxic-ischemic encephalopathy (HIE). Colony stimulating factor 1 (CSF1), binding to CSF1 receptor (CSF1R), has been shown to reduce neuronal loss after hypoxic-ischemia- (HI-) induced brain injury. In the present study, we hypothesized that CSF1 could alleviate OS-induced neuronal degeneration and apoptosis through the CSF1R/PLCG2/PKA/UCP2 signaling pathway in a rat model of HI. A total of 127 ten-day old Sprague Dawley rat pups were used. HI was induced by right common carotid artery ligation with subsequent exposure to hypoxia for 2.5 h. Exogenous recombinant human CSF1 (rh-CSF1) was administered intranasally at 1 h and 24 h after HI. The CSF1R inhibitor, BLZ945, or phospholipase C-gamma 2 (PLCG2) inhibitor, U73122, was injected intraperitoneally at 1 h before HI induction. Brain infarct volume measurement, cliff avoidance test, righting reflex test, double immunofluorescence staining, western blot assessment, 8-OHdG and MitoSOX staining, Fluoro-Jade C staining, and TUNEL staining were used. Our results indicated that the expressions of endogenous CSF1, CSF1R, p-CSF1R, p-PLCG2, p-PKA, and uncoupling protein2 (UCP2) were increased after HI. CSF1 and CSF1R were expressed in neurons and astrocytes. Rh-CSF1 treatment significantly attenuated neurological deficits, infarct volume, OS, neuronal apoptosis, and degeneration at 48 h after HI. Moreover, activation of CSF1R by rh-CSF1 significantly increased the brain tissue expressions of p-PLCG2, p-PKA, UCP2, and Bcl2/Bax ratio, but reduced the expression of cleaved caspase-3. The neuroprotective effects of rh-CSF1 were abolished by BLZ945 or U73122. These results suggested that rh-CSF1 treatment attenuated OS-induced neuronal degeneration and apoptosis after HI, at least in part, through the CSF1R/PLCG2/PKA/UCP2 signaling pathway. Rh-CSF1 may serve as therapeutic strategy against brain damage in patients with HIE.

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Transition Metal Oxide‐Decorated MXenes as Drugless Nanoarchitectonics for Enriched Nanocatalytic Chemodynamic Treatment

Xia,

Li,

et al. 2024

Adv Healthcare Materials

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Despite their unique characteristics, the recently emerged two‐dimensional (2D) MXenes with sole photothermal conversion ability are required to explore their superfluous abilities in biomedicine. To this end, small‐molecule‐based chemotherapeutics suffer from various shortcomings of time‐consuming and expensiveness in terms of molecular docking and subsequent mechanistic (preclinical/clinical) performance checks, hampering their full potential of precisely eradicating diseases. This study demonstrates the fabrication of Ti3C2 MXene nanosheets (TC‐MX NSs) and decoration with transition metal oxides, i.e., copper oxide (Cu2O/MX, shortly denoted as CO‐MX NCs) as drugless nanoarchitectonics for synergistic photothermal (PTT)‐chemodynamic therapeutic (CDT) efficacies. Initially, the monolayer/few‐layered TC‐MX NSs are prepared using the chemical etching‐assisted ultrasonic exfoliation method and then deposited with Cu2O nanoconstructs using the in situ reduction method. Further, the photothermal ablation under near‐infrared (NIR)‐II laser irradiation evidently showed mild PTT effects of CO‐MX NCs. The deposited Cu2O on TC‐MX NSs facilitated the release of copper (Cu+) ions in the acidic microenvironment intracellularly for Fenton‐like reaction‐assisted CDT effects and enriched PTT effects synergistically. Mechanistically, these deadly free radicals intracellularly imbalanced the glutathione (GSH) levels and subsequently resulted in mitochondrial dysfunction, inducing apoptosis of 4T1 cells. Finally, the in vivo investigations in BALB/c mice confirmed the substantial therapeutic effects of ablating breast carcinoma. Together, these findings demonstrated the potential synergistic photothermal‐chemodynamic therapeutic effects of the designed CO‐MX NCs as drugless nanoarchitectonics against breast carcinoma.This article is protected by copyright. All rights reserved

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Hydrogen attenuates radiation-induced intestinal damage by reducing oxidative stress and inflammatory response

Cited by 41 publications

References 32 publications

Molecular Hydrogen as a Potential Clinically Applicable Radioprotective Agent

Molecular Hydrogen as a Potential Clinically Applicable Radioprotective Agent

Rh-CSF1 Attenuates Oxidative Stress and Neuronal Apoptosis via the CSF1R/PLCG2/PKA/UCP2 Signaling Pathway in a Rat Model of Neonatal HIE

Transition Metal Oxide‐Decorated MXenes as Drugless Nanoarchitectonics for Enriched Nanocatalytic Chemodynamic Treatment

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