In vitro evidence for the involvement of H2S pathway in the effect of clodronate during inflammatory response

Abstract Clodronate is a bisphosphonate agent commonly used as anti-osteoporotic drug. Throughout its use, additional anti-inflammatory and analgesic properties have been reported, although the benefits described in the literature could not solely relate to their inhibition of bone resorption. Thus,...

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Autores principales:	Rosangela Montanaro, Alessio D’Addona, Andrea Izzo, Carlo Ruosi, Vincenzo Brancaleone
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/9d63c65bd58c4f1e8a98992d463f86f9
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spelling	oai:doaj.org-article:9d63c65bd58c4f1e8a98992d463f86f92021-12-02T17:55:03ZIn vitro evidence for the involvement of H2S pathway in the effect of clodronate during inflammatory response10.1038/s41598-021-94228-y2045-2322https://doaj.org/article/9d63c65bd58c4f1e8a98992d463f86f92021-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-94228-yhttps://doaj.org/toc/2045-2322Abstract Clodronate is a bisphosphonate agent commonly used as anti-osteoporotic drug. Throughout its use, additional anti-inflammatory and analgesic properties have been reported, although the benefits described in the literature could not solely relate to their inhibition of bone resorption. Thus, the purpose of our in vitro study is to investigate whether there are underlying mechanisms explaining the anti-inflammatory effect of clodronate and possibly involving hydrogen sulphide (H2S). Immortalised fibroblast-like synoviocyte cells (K4IM) were cultured and treated with clodronate in presence of TNF-α. Clodronate significantly modulated iNOS expression elicited by TNF-α. Inflammatory markers induced by TNF-α, including IL-1, IL-6, MCP-1 and RANTES, were also suppressed following administration of clodronate. Furthermore, the reduction in enzymatic biosynthesis of CSE-derived H2S, together with the reduction in CSE expression associated with TNF-α treatment, was reverted by clodronate, thus rescuing endogenous H2S pathway activity. Clodronate displays antinflammatory properties through the modulation of H2S pathway and cytokines levels, thus assuring the control of the inflammatory state. Although further investigation is needed to stress out how clodronate exerts its control on H2S pathway, here we showed for the first the involvement of H2S in the additive beneficial effects observed following clodronate therapy.Rosangela MontanaroAlessio D’AddonaAndrea IzzoCarlo RuosiVincenzo BrancaleoneNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-9 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Rosangela Montanaro Alessio D’Addona Andrea Izzo Carlo Ruosi Vincenzo Brancaleone In vitro evidence for the involvement of H2S pathway in the effect of clodronate during inflammatory response
description	Abstract Clodronate is a bisphosphonate agent commonly used as anti-osteoporotic drug. Throughout its use, additional anti-inflammatory and analgesic properties have been reported, although the benefits described in the literature could not solely relate to their inhibition of bone resorption. Thus, the purpose of our in vitro study is to investigate whether there are underlying mechanisms explaining the anti-inflammatory effect of clodronate and possibly involving hydrogen sulphide (H2S). Immortalised fibroblast-like synoviocyte cells (K4IM) were cultured and treated with clodronate in presence of TNF-α. Clodronate significantly modulated iNOS expression elicited by TNF-α. Inflammatory markers induced by TNF-α, including IL-1, IL-6, MCP-1 and RANTES, were also suppressed following administration of clodronate. Furthermore, the reduction in enzymatic biosynthesis of CSE-derived H2S, together with the reduction in CSE expression associated with TNF-α treatment, was reverted by clodronate, thus rescuing endogenous H2S pathway activity. Clodronate displays antinflammatory properties through the modulation of H2S pathway and cytokines levels, thus assuring the control of the inflammatory state. Although further investigation is needed to stress out how clodronate exerts its control on H2S pathway, here we showed for the first the involvement of H2S in the additive beneficial effects observed following clodronate therapy.
format	article
author	Rosangela Montanaro Alessio D’Addona Andrea Izzo Carlo Ruosi Vincenzo Brancaleone
author_facet	Rosangela Montanaro Alessio D’Addona Andrea Izzo Carlo Ruosi Vincenzo Brancaleone
author_sort	Rosangela Montanaro
title	In vitro evidence for the involvement of H2S pathway in the effect of clodronate during inflammatory response
title_short	In vitro evidence for the involvement of H2S pathway in the effect of clodronate during inflammatory response
title_full	In vitro evidence for the involvement of H2S pathway in the effect of clodronate during inflammatory response
title_fullStr	In vitro evidence for the involvement of H2S pathway in the effect of clodronate during inflammatory response
title_full_unstemmed	In vitro evidence for the involvement of H2S pathway in the effect of clodronate during inflammatory response
title_sort	in vitro evidence for the involvement of h2s pathway in the effect of clodronate during inflammatory response
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/9d63c65bd58c4f1e8a98992d463f86f9
work_keys_str_mv	AT rosangelamontanaro invitroevidencefortheinvolvementofh2spathwayintheeffectofclodronateduringinflammatoryresponse AT alessiodaddona invitroevidencefortheinvolvementofh2spathwayintheeffectofclodronateduringinflammatoryresponse AT andreaizzo invitroevidencefortheinvolvementofh2spathwayintheeffectofclodronateduringinflammatoryresponse AT carloruosi invitroevidencefortheinvolvementofh2spathwayintheeffectofclodronateduringinflammatoryresponse AT vincenzobrancaleone invitroevidencefortheinvolvementofh2spathwayintheeffectofclodronateduringinflammatoryresponse
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In vitro evidence for the involvement of H2S pathway in the effect of clodronate during inflammatory response

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