Effects of ozone on spinal cord recovery via wnt/ &amp;#946;-catenin pathway following spinal cord injury in rats

Emon, Selin Tural; Uslu, Serap; Aydınlar, Elif Ilgaz; İrban, Arzu; İnce, Ümit; Orakdogen, Metin; Suyen, Guldal Gulec

doi:10.5137/1019-5149.jtn.17508-16.1

Cited by 7 publications

(11 citation statements)

References 14 publications

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“…Interestingly, a study reported the benefit effect of O 3 on Menière’s disease ( Pawlak-Osinska et al, 2004 ). Moreover, as reported for polyphenols and mushrooms ( Hsiao et al, 2016 , Ferreiro et al, 2018 , Oh et al, 2014 , Pan et al, 2018 , Hasanzadeh et al, 2020 , Wang et al, 2019b ), O 3 has been found to be involved in β-catenin system ( Emon et al, 2017 ) as well as in NLRP3 (nitrogen permease regulator-like 3) inflammasome ( Yu et al, 2017 , Wang et al, 2018c ).…”

Section: Molecular Mechanisms Involving Ozone (O 3 mentioning

confidence: 62%

Ozone: a natural bioactive molecule with antioxidant property as potential new strategy in aging and in neurodegenerative disorders

Scassellati

Galoforo

Bonvicini

et al. 2020

Ageing Research Reviews

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Highlights Aging and neurodegenerative diseases are characterized by complex and multifactorial aetiology and challenges regarding treatments efficacy and costs persist. Oxygen-ozone (O 2 -O 3 ) therapy is a non-invasive, non-pharmacological, low cost and no-side effect procedure based on antioxidant capacity of O 3 . A plethora of scientific evidence supports other crucial properties of O 3 in physiopathological processes. Nrf2 is one of the principal molecular signalling on which O 3 exercises its antioxidant/anti-apoptotic/pro-autophagy effects, involved in aging and in neurodegenerative disorders. This review provides a consistent rationale to implement future clinical studies to apply the O 2 -O 3 treatment along with other antioxidants (polyphenols, mushrooms) in aging and in neurodegeneration.

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Section: Molecular Mechanisms Involving Ozone (O 3 mentioning

confidence: 62%

Ozone: a natural bioactive molecule with antioxidant property as potential new strategy in aging and in neurodegenerative disorders

Scassellati

Galoforo

Bonvicini

et al. 2020

Ageing Research Reviews

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“…In recent years, the regulatory effects of Wnt signaling molecule on the proliferation, apoptosis and fate determination of neural tube and neural crest cells in mammalian nervous system have attracted attention (25). It has been found during the embryonic development of Xenopus that inhibiting the Wnt signal pathway can inhibit the formation of the ventral nervous system (25). The deletion of the two signaling proteins Wnt-1 and Wnt-3a will lead to reduced formation of the ventral ganglia (26).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑381/Hes1 is a potential therapeutic target for spinal cord injury

et al. 2018

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The aim of the present study was to investigate whether microRNA‑381 is a potential therapeutic target for spinal cord injury (SCI) and its possible mechanism. Reverse transcription quantitative polymerase chain reaction (qPCR) for mRNA expression was used to analyze the changes of microRNA-381 expression. Cell viability and cell apoptosis were measured using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and ﬂow cytometry. Caspase‑3 activity was measured using caspase‑3 activity kit, and western blot analysis was used to measure the protein expression of neurogenic locus notch homolog protein 1 (Notch1), notch 1 intracellular domain (NICD) and transcription factor HES-1 (Hes1). The data showed that microRNA‑381 expression of model SCI rats was downregulated compared with that of control rats. Overexpression of microRNA‑381 promoted cell proliferation, and inhibited apoptosis and caspase‑3 and apoptosis regulator BAX (Bax) protein expression in neurocytes. Overexpression of microRNA‑381 also increased Wnt and β‑catenin protein expression, and suppressed the protein expression of Notch1, NICD and Hes1 in neurocytes. Wnt inhibitor, Wnt‑C59 (1 µmol/l), inhibited cell proliferation, promoted apoptosis and caspase‑3 and Bax protein expression, suppressed β‑catenin protein expression and induced Hes1 protein expression in neurocytes following microRNA‑381 overexpression. Notch inhibitor, FLI‑06 (1 µmol/l), promoted cell proliferation, inhibited apoptosis and caspase‑3 and Bax protein expression, and suppressed NICD and Hes1 protein expression in neurocytes following microRNA‑381 overexpression. Thus, this study showed that overexpression of microRNA‑381 promotes cell proliferation of neurocytes in SCI via Hes1 expression, which may be a novel important mechanism for SCI in clinical applications.

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“…To elucidate this point, we investigated the effects of low O 3 concentrations currently used in clinical practice on the nuclear activity of cultured cells of neuronal origin. There is, in fact, a growing interest for therapeutic applications of O 3 to the nervous system based on experimental evidence that mild ozonisation induces metabolic stimulation and even regenerative effects in neurons (Molinari et al, 2014;Ozbay et al, 2016;Salem et al, 2016;Tural Emon et al, 2016). The use of an in vitro model ensured controlled experimental conditions, allowing analysis of the direct effects of mild ozonisation on nuclear function without the intermediation of blood/tissue factors as occurs in vivo.…”

Section: Introductionmentioning

confidence: 99%

Effects of mild ozonisation on gene expression and nuclear domains organization in vitro

Scassellati

Costanzo

Cisterna

et al. 2017

Toxicology in Vitro

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In the last two decades, the use of ozone (O) as a complementary medical approach has progressively been increasing; however, its application is still limited due to the numerous doubts about its possible toxicity, despite the low concentrations used in therapy. For an appropriate and safe clinical application of a potentially toxic agent such as O, it is crucial to elucidate the cellular response to its administration. Molecular analyses and transmission electron microscopy were here combined to investigate in vitro the effects of O administration on transcriptional activity and nuclear domains organization of cultured SH-SY5Y neuronal cells; low O concentrations were used as those currently administered in clinical practice. Mild ozonisation did not affect cell proliferation or death, while molecular analyses showed an O-induced modulation of some genes involved in the cell response to stress (HMOX1, ERCC4, CDKN1A) and in the transcription machinery (CTDSP1). Ultrastructural cytochemistry after experiments of bromouridine incorporation consistently demonstrated an increased transcriptional rate at both the nucleoplasmic (mRNA) and the nucleolar (rRNA) level. No ultrastructural alteration of nuclear domains was observed. Our molecular, ultrastructural and cytochemical data demonstrate that a mild toxic stimulus such as mild ozonisation stimulate cell protective pathways and nuclear transcription, without altering cell viability. This could possibly account for the positive effects observed in ozone-treated patients.

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Effects of ozone on spinal cord recovery via wnt/ β-catenin pathway following spinal cord injury in rats

Abstract: The results of this study indicated that ozone therapy accelerates the healing process, increases vascularity, and reduces neuronal damage in rodents, suggesting that ozone therapy may be an adjuvant treatment in patients with SCI.

Cited by 7 publications

References 14 publications

Ozone: a natural bioactive molecule with antioxidant property as potential new strategy in aging and in neurodegenerative disorders

Ozone: a natural bioactive molecule with antioxidant property as potential new strategy in aging and in neurodegenerative disorders

MicroRNA‑381/Hes1 is a potential therapeutic target for spinal cord injury

Effects of mild ozonisation on gene expression and nuclear domains organization in vitro

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