Protective effects of Brownea grandiceps (Jacq.) against ϒ-radiation-induced enteritis in rats in relation to its secondary metabolome fingerprint

: Radiation-induced lung injury is characterized by an acute pneumonia phase followed by a fibrotic phase. At the time of irradiation, a rapid, short-lived burst of reactive oxygen species (ROS) such as hydroxyl radicals (•OH) occurs, but chronic radiation-induced lung injury may occur due to excess ROS such as H2O2 , O2•− , ONOO− , and •OH. Molecular hydrogen (H2 ) is an efficient antioxidant that quickly diffuses cell membranes, reduces ROS such as •OH and ONOO− , and suppresses damage caused by oxidative stress in various organs. In 2011, through the evaluation of electron-spin resonance and fluorescent indicator signals, we had reported that H2 can eliminate •OH and can protect against oxidative stress-related apoptotic damage induced by irradiation of cultured lung epithelial cells. We had explored for the first time the radioprotective effects of H2 treatment on acute and chronic radiation-induced lung damage in mice by inhaled H2 gas (for acute) and imbibed H2 -enriched water (for chronic). Thus, we had proposed that H2 be considered a potential radioprotective agent. Recent publications have shown that H2 directly neutralizes highly reactive oxidants and indirectly reduces oxidative stress by regulating the expression of various genes. By regulating gene expression, H2 functions as an anti-inflammatory and anti-apoptotic molecule and promotes energy metabolism. The increased evidence obtained from cultured cells or animal experiments reveal a putative place for H2 treatment and its radioprotective effect clinically. This review focuses on major scientific advances of in the treatment of H2 as a new class of radioprotective agents.

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Protective Activity of C-Geranylflavonoid Analogs from Paulownia tomentosa against DNA Damage in 137Cs Irradiated AHH-1Cells

Natural Product Communications ◽

10.1177/1934578x1400900919 ◽

2014 ◽

Vol 9 (9) ◽

pp. 1934578X1400900

Author(s):

Hyung-In Moon ◽

Min Ho Jeong ◽

Wol Soon Jo

Keyword(s):

Dna Damage ◽

Protective Effects ◽

Strand Breaks ◽

Human Lymphoblastoid Cell ◽

Wide Range ◽

Radiation Induced ◽

Anti Oxidant ◽

Dna Strand ◽

Cellular Dna

Radiotherapy is an important form of treatment for a wide range of cancers, but it can damage DNA and cause adverse effects. We investigated if the diplacone analogs of P. tomentosa were radio-protective in a human lymphoblastoid cell line (AHH-1). Four geranylated flavonoids, diplacone, 3′- O-methyl-5′-hydroxydiplacone, 3′- O-methyl-5′- O-methyldiplacone and 3′- O-methyldiplacol, were tested for their antioxidant and radio-protective effects. Diplacone analogs effectively scavenged free radicals and inhibited radiation-induced DNA strand breaks in vitro. They significantly decreased levels of reactive oxygen species and cellular DNA damage in 2 Gy-irradiated AHH-1 cells. Glutathione levels and superoxide dismutase activity in irradiated AHH-1 cells increased significantly after treatment with these analogs. The enhanced biological anti-oxidant activity and radioprotective activity of diplacone analogs maintained the survival of irradiated AHH-1 cells in a clonogenic assay. These data suggest that diplacone analogs may protect healthy tissue surrounding tumor cells during radiotherapy to ensure better control of radiotherapy and allow higher doses of radiotherapy to be employed.

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Oligomeric Procyanidin Nanoliposomes Prevent Melanogenesis and UV Radiation-Induced Skin Epithelial Cell (HFF-1) Damage

Molecules ◽

10.3390/molecules25061458 ◽

2020 ◽

Vol 25 (6) ◽

pp. 1458 ◽

Cited By ~ 1

Author(s):

Yashu Chen ◽

Fenghong Huang ◽

David Julian McClements ◽

Bijun Xie ◽

Zhida Sun ◽

...

Keyword(s):

Protective Effect ◽

Fibroblast Cell ◽

Skin Aging ◽

Ultraviolet B ◽

Protective Effects ◽

Protection Mechanism ◽

Uva Irradiation ◽

Culture Model ◽

Radiation Induced ◽

Human Foreskin Fibroblast Cell

The potential protective effect of nanoliposomes loaded with lotus seedpod oligomeric procyanidin (LSOPC) against melanogenesis and skin damaging was investigated. Fluorescence spectroscopy showed that, after encapsulation, the LSOPC-nanoliposomes still possessed strong inhibitory effects against melanogenesis, reducing the activity of both monophenolase and diphenolase. Molecular docking indicated that LSOPC could generate intense interactive configuration with tyrosinase through arene–H, arene–arene, and hydrophobic interaction. An ultraviolet radiated cell-culture model (human foreskin fibroblast cell (HFF-1)) was used to determine the protective effects of the LSOPC-nanoliposomes against skin aging and damage. Results showed that LSOPC-nanoliposomes exerted the highest protective effects against both ultraviolet B (UVB) and ultraviolet A (UVA) irradiation groups compared with non-encapsulated LSOPC and a control (vitamin C). Superoxide dismutase (SOD) and malonaldehyde (MDA) assays demonstrated the protection mechanism may be related to the anti-photooxidation activity of the procyanidin. Furthermore, a hydroxyproline assay suggested that the LSOPC-nanoliposomes had a strong protective effect against collagen degradation and/or synthesis after UVA irradiation.

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Protective effects of systemic dermatan sulfate treatment in a preclinical model of radiation-induced oral mucositis

Strahlentherapie und Onkologie ◽

10.1007/s00066-018-1280-8 ◽

2018 ◽

Vol 194 (7) ◽

pp. 675-685 ◽

Cited By ~ 4

Author(s):

Sylvia Gruber ◽

Katharina Frings ◽

Peter Kuess ◽

Wolfgang Dörr

Keyword(s):

Oral Mucositis ◽

Dermatan Sulfate ◽

Preclinical Model ◽

Protective Effects ◽

Radiation Induced

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Protective Effects of p53 Regulatory Agents Against High-LET Radiation-Induced Injury in Mice

Frontiers in Public Health ◽

10.3389/fpubh.2020.601124 ◽

2020 ◽

Vol 8 ◽

Author(s):

Akinori Morita ◽

Bing Wang ◽

Kaoru Tanaka ◽

Takanori Katsube ◽

Masahiro Murakami ◽

...

Keyword(s):

Cell Death ◽

Radiation Injury ◽

Ion Irradiation ◽

Heavy Ion ◽

Protective Effects ◽

Iron Ion ◽

Normal Tissues ◽

High Let Radiation ◽

High Let ◽

Radiation Induced

Radiation damage to normal tissues is one of the most serious concerns in radiation therapy, and the tolerance dose of the normal tissues limits the therapeutic dose to the patients. p53 is well known as a transcription factor closely associated with radiation-induced cell death. We recently demonstrated the protective effects of several p53 regulatory agents against low-LET X- or γ-ray-induced damage. Although it was reported that high-LET heavy ion radiation (>85 keV/μm) could cause p53-independent cell death in some cancer cell lines, whether there is any radioprotective effect of the p53 regulatory agents against the high-LET radiation injury in vivo is still unclear. In the present study, we verified the efficacy of these agents on bone marrow and intestinal damages induced by high-LET heavy-ion irradiation in mice. We used a carbon-beam (14 keV/μm) that was shown to induce a p53-dependent effect and an iron-beam (189 keV/μm) that was shown to induce a p53-independent effect in a previous study. Vanadate significantly improved 60-day survival rate in mice treated with total-body carbon-ion (p < 0.0001) or iron-ion (p < 0.05) irradiation, indicating its effective protection of the hematopoietic system from radiation injury after high-LET irradiation over 85 keV/μm. 5CHQ also significantly increased the survival rate after abdominal carbon-ion (p < 0.02), but not iron-ion irradiation, suggesting the moderate relief of the intestinal damage. These results demonstrated the effectiveness of p53 regulators on acute radiation syndrome induced by high-LET radiation.

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Neutral Sphingomyelinase Modulation in the Protective/Preventive Role of rMnSOD from Radiation-Induced Damage in the Brain

International Journal of Molecular Sciences ◽

10.3390/ijms20215431 ◽

2019 ◽

Vol 20 (21) ◽

pp. 5431 ◽

Cited By ~ 1

Author(s):

Samuela Cataldi ◽

Antonella Borrelli ◽

Maria Rachele Ceccarini ◽

Irina Nakashidze ◽

Michela Codini ◽

...

Keyword(s):

Superoxide Dismutase ◽

Manganese Superoxide Dismutase ◽

Nuclear Research ◽

Protective Effects ◽

Manganese Superoxide ◽

Additional Group ◽

Gene And Protein Expression ◽

Radiation Induced ◽

The Brain ◽

Preventive Role

Studies on the relationship between reactive oxygen species (ROS)/manganese superoxide dismutase (MnSOD) and sphingomyelinase (SMase) are controversial. It has been demonstrated that SMase increases the intracellular ROS level and induces gene expression for MnSOD protein. On the other hand, some authors showed that ROS modulate the activation of SMase. The human recombinant manganese superoxide dismutase (rMnSOD) exerting a radioprotective effect on normal cells, qualifies as a possible pharmaceutical tool to prevent and/or cure damages derived from accidental exposure to ionizing radiation. This study aimed to identify neutral SMase (nSMase) as novel molecule connecting rMnSOD to its radiation protective effects. We used a new, and to this date, unique, experimental model to assess the effect of both radiation and rMnSOD in the brain of mice, within a collaborative project among Italian research groups and the Joint Institute for Nuclear Research, Dubna (Russia). Mice were exposed to a set of minor γ radiation and neutrons and a spectrum of neutrons, simulating the radiation levels to which cosmonauts will be exposed during deep-space, long-term missions. Groups of mice were treated or not-treated (controls) with daily subcutaneous injections of rMnSOD during a period of 10 days. An additional group of mice was also pretreated with rMnSOD for three days before irradiation, as a model for preventive measures. We demonstrate that rMnSOD significantly protects the midbrain cells from radiation-induced damage, inducing a strong upregulation of nSMase gene and protein expression. Pretreatment with rMnSOD before irradiation protects the brain with a value of very high nSMase activity, indicating that high levels of activity might be sufficient to exert the rMnSOD preventive role. In conclusion, the protective effect of rMnSOD from radiation-induced brain damage may require nSMase enzyme.

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