Search

Your search keyword '"Troiani D"' showing total 217 results
Start Over Author "Troiani D"
217 results on '"Troiani D"'

4. Noise-induced cochlear damage involves ppar down-regulation through the interplay between oxidative stress and inflammation

Author

Paciello, F. (ORCID:0000-0002-8473-8074), Pisani, A., Rolesi, R., Escarrat, V., Galli, J. (ORCID:0000-0001-6353-6249), Paludetti, G. (ORCID:0000-0003-2480-1243), Grassi, C. (ORCID:0000-0001-7253-1685), Troiani, D. (ORCID:0000-0002-5665-7410), Fetoni, A. R. (ORCID:0000-0001-5405-4301), Paciello, F. (ORCID:0000-0002-8473-8074), Pisani, A., Rolesi, R., Escarrat, V., Galli, J. (ORCID:0000-0001-6353-6249), Paludetti, G. (ORCID:0000-0003-2480-1243), Grassi, C. (ORCID:0000-0001-7253-1685), Troiani, D. (ORCID:0000-0002-5665-7410), and Fetoni, A. R. (ORCID:0000-0001-5405-4301)

Abstract

The cross-talk between oxidative stress and inflammation seems to play a key role in noise-induced hearing loss. Several studies have addressed the role of PPAR receptors in mediating antioxidant and anti-inflammatory effects and, although its protective activity has been demonstrated in several tissues, less is known about how PPARs could be involved in cochlear dysfunction induced by noise exposure. In this study, we used an in vivo model of noise-induced hearing loss to investigate how oxidative stress and inflammation participate in cochlear dysfunction through PPAR signaling pathways. Specifically, we found a progressive decrease in PPAR expression in the cochlea after acoustic trauma, paralleled by an increase in oxidative stress and inflammation. By comparing an antioxidant (Q-ter) and an anti-inflammatory (Anakinra) treatment, we demonstrated that oxidative stress is the primary element of damage in noise-induced cochlear injury and that increased inflammation can be considered a consequence of PPAR down-regulation induced by ROS production. Indeed, by decreasing oxidative stress, PPARs returned to control values, reactivating the negative control on inflammation in a feedback loop.

Published
2021

6. Publisher Correction: The dual role of curcumin and ferulic acid in counteracting chemoresistance and cisplatin-induced ototoxicity (Scientific Reports, (2020), 10, 1, (1063), 10.1038/s41598-020-57965-0)

Author

Paciello, F. (ORCID:0000-0002-8473-8074), Fetoni, A. R. (ORCID:0000-0001-5405-4301), Mezzogori, D., Rolesi, R., Di Pino, A., Paludetti, G. (ORCID:0000-0003-2480-1243), Grassi, C. (ORCID:0000-0001-7253-1685), Troiani, D. (ORCID:0000-0002-5665-7410), Paciello, F. (ORCID:0000-0002-8473-8074), Fetoni, A. R. (ORCID:0000-0001-5405-4301), Mezzogori, D., Rolesi, R., Di Pino, A., Paludetti, G. (ORCID:0000-0003-2480-1243), Grassi, C. (ORCID:0000-0001-7253-1685), and Troiani, D. (ORCID:0000-0002-5665-7410)

Abstract

In the original version of this Article, the author Anna Rita Fetoni was incorrectly indexed. This error has now been corrected.

Published
2020

7. Publisher Correction: The dual role of curcumin and ferulic acid in counteracting chemoresistance and cisplatin-induced ototoxicity (Scientific Reports, (2020), 10, 1, (1063), 10.1038/s41598-020-57965-0)

Author

Paciello, Fabiola, Fetoni, Anna Rita, Mezzogori, D., Rolesi, Rolando, Di Pino, Antonella, Paludetti, Gaetano, Grassi, Claudio, Troiani, Diana, Paciello F. (ORCID:0000-0002-8473-8074), Fetoni A. R. (ORCID:0000-0001-5405-4301), Rolesi R., Di Pino A., Paludetti G. (ORCID:0000-0003-2480-1243), Grassi C. (ORCID:0000-0001-7253-1685), Troiani D. (ORCID:0000-0002-5665-7410), Paciello, Fabiola, Fetoni, Anna Rita, Mezzogori, D., Rolesi, Rolando, Di Pino, Antonella, Paludetti, Gaetano, Grassi, Claudio, Troiani, Diana, Paciello F. (ORCID:0000-0002-8473-8074), Fetoni A. R. (ORCID:0000-0001-5405-4301), Rolesi R., Di Pino A., Paludetti G. (ORCID:0000-0003-2480-1243), Grassi C. (ORCID:0000-0001-7253-1685), and Troiani D. (ORCID:0000-0002-5665-7410)

Abstract

In the original version of this Article, the author Anna Rita Fetoni was incorrectly indexed. This error has now been corrected.

Published
2020

8. Abstract

Author

Andries, L. J., Sys, S. U., Meulemans, A. L., Schuurkes, J. A. J., Vanheel, B., Van de Voorde, J., De Smet, P., Li, J., Van Driessche, W., Flamion, B., Foulon, S., Abramow, M., Calders, P., Eechaute, W., Lacroix, E., Weyne, I., Hoeben, D., Burvenich, C., Fransen, P., Andries, L. J., Van Bedaf, D., Demolder, M., Sys, S. U., Ouedraogo, R., Lebrun, P., Herchuelz, A., Antoine, M. -H., Vandenput, S., Votion, D., Anciaux, N., Duvivier, D. H., Art, T., Lekeux, P., Votion, D., Ghafir, Y., Vandenput, S., Art, T., Lekeux, P., Geurts, M., Hermans, E., Maloteaux, J. -M., Perrad, B., Noel, B., Lagache, F., Bister, J. L., Paquay, R., Bister, J. L., Derycke, G., Vandermeir, M. A., Paquay, R., de Brouwer, S., Porret, C. -A., Stergiopulos, N., Meister, J. -J., Verbeke, M., Van de Voorde, J., Lameire, N., De Clerck, N. M., De Schuytter, J., Tytgato, J., Buyse, G., Eggermont, J., Droogmans, G., Nilius, B., Daenens, P., Salomone, S., Feron, O., Dessy, C., Morel, N., Godfraind, T., Aloisi, A. M., Sacerdote, P., Lodi, L., Carli, G., Carobi, C., Garinei, G., Miniaci, U. C., Scotto, P., Sabatino, M., Sardo, P., Iurato, L., La Grutta, V., Bagni, M. A., Cecchi, G., Cecchini, E., Colomo, F., Garzella, P., Bottinelli, R., Harridge, S. D. H., Canepari, M., Reggiani, C., Reggiani, Saltin, Bambagioni, D., Fanò, G., Menchetti, G,, Danieli-Betto, P., Esposito, A., Betto, R., Megighian, A., Midrio, M., Betto, D. Danieli, Esposito, A., Megighian, A., Midrio, M., Orizio, C., Liberati, D., Locatelli, C., De Grandis, D., Veicsteinas, A., Angoli, D., Delia, D., Wanke, E., Bramucci, M., Miano, A., Quassinti, L., Maccari, E., Murri, O., Amici, D., Cibelli, G., Jüngling, S., Schoch, S., Gerdest, H. H., Thiel, G., Demori, I., Bottazzi, C., Voci, A., Fugassa, E., Barreca, A., Minuto, F., Gallo, G., Fulle, S., Belia, S., Menchetti, G., Cacchio, M., Fanò, G., Gastaldi, G., Laforenza, U., Ferrari, G., Rindi, G., Doni, M. G., Padoin, E., Residori, O., Cesaro, M., Toma, L., Rubini, A., Mutinelli, F, Paulesu, L., Romagnolie, R., Cintorino, M., Pippia, P., Meloni, M. A., Sciola, L., Spano, A., Cogoli-Greuter, M., Cogoli, A., Sardini, A., Mintenig, G. M., Valverde, M. A., Sepùlveda, F. V., Gill, D. R., Hyde, S. C., Higgins, C. F., McNaughton, P. A., Spena, A., Arcuri, M. T., Bonofiglio, S., Chimenti, R., Covello, C., De Cicco, T., Mazzulla, S., Martino, G., Tottene, A., Moretti, A., Pietrobon, D., Baccari, M. C., Calamai, F., Staderini, G., Cova, E., Marelli, R., Sommi, P., Ventura, U., Lombardi, A. M., Fabris, R., Pagano, C., Federspil, G., Vettor, R., Mancinelli, R., Tonali, P., Servidei, S., Romani, R., Tringali, A., Azzena, G. B., Mulè, F., Serio, R., Postorino, A., Pagano, C., Rizzato, M., Granzotto, M., Lombardi, A. M., Fabris, R., Vettor, R., Federspil, G., Sommi, P., Ricci, V., Romano, M., Ivey, K. J., Ventura, U., Vacca, G., Papillo, B., Mary, D. A. S. G., Battaglia, A., Grossini, E., Vacca, G., Papillo, B., Battaglia, A., Grossini, E., Accili, E. A., Redaelli, G., DiFrancesco, D., Antoniotti, S., Distasi, C., Lovisolo, D., Munaron, L., Bertaso, F., Assandri, R., Mazzanti, M., Bianchi, L., Arcangeli, A., Faravelli, L., Becchetti, A., Coronello, M., Mini, E., Francini, F., Olivotto, M., Wanke, E., Bigiani, A., Kim, D. -J., Roper, S. D., Carabelli, V., Lovallo, M., Magnelli, V., Zucker, H., Carbone, E., D’Angelo, E., Rossi, P., De Filippi, G., Taglietti, V., Faravelli, L., Bianchi, L., Arcangeli, A., Francini, F., Olivotto, M., Wanke, E., Francini, F., Bencini, C., Squecco, R., Guatteo, E., Bacci, A., Franceschetti, S., Avanzini, G., Wanke, E., Magnelli, V., Carbone, E., Mazzanti, M., Assandri, R., Ferroni, A., DiFrancesco, D., Navangione, A., Vellani, V., Rispoli, G., Peres, A., Centinaio, E., Giovannardi, S., Russo, G., Marcotti, W., Prigioni, I., Trequattrini, C., Harper, A. A., Petris, A., Franciolini, F., Zaza, A., Micheletti, M., Brioschi, A., Antonutto, G., Capelli, C., Girardis, M., Zamparo, P., di Prampero, P. E., Antonutto, G., Girardis, M., Tuniz, D., di Prampero, P. E., Filippi, G. M., Troiani, D., Grassi, B., Poole, D. C., Richardson, R. S., Knight, D. R., Erickson, B. K., Wagner, P. D., Aimi, B., Stilli, D., Gallo, P., Sgoifo, A., Lagrasta, C., Olivetti, G., Reali, N., Casti, A., Musso, E., Alloatti, G., Penna, C., Gallo, M. P., Levi, R. C., Fenoglio, I., Appendino, G., Gallo, P., Sgoifo, A., Medici, D., Aimi, B., Manghi, M., Stilli, D., Musso, E., Sgoifo, A., Pasini, E., Gallo, P., Aimi, B., Stilli, D., Ceconi, C., Musso, E., Baldissera, F., Cavallari, P., Locatelli, M., Bartesaghi, R., Gessi, T., Benfenati, F., Valtorta, F., Onofri, F., Poo, M., Greengard, P., Biagini, G., Sala, D., Viani§, P., Kozlov, A. V., Zini, I., Bravin, M., Tempia, F., Strata, P., Brescia, G., Di Benedetto, C., Corsi, P., Cangiano, G., Buttiglione, M., Ambrosini, M., Gennarini, G., Casadio, A., Levi, R. C., Montarolo, P. G., Cesare, P., Stoughton, R., McNaughton, P. A., D’Arcangelo, G., Dodt, H. U., Brancati, A., Zieglgänsberger, W., Errico, P., Ferraresi, A., Barmack, N. H., Pettorossi, V. E., Gasparini, S., D’Ambrosio, R., Janigro, D., DiFrancesco, D., Gritti, I., Marintti, M., Calcaterra, R., Freddi, R., Mancia, M., Imeri, I., Bianchi, S., Mancia, M., Lui, F., Gregory, K. M., Blanks, R. H. I., Giolli, R. A., Benassi, C., Corazza, R., Magherini, P. C., Bardoni, R., Belluzzi, O., Mancinelli, R., Manni, E., Azzena, G. B., Tringali, A., Romani, R., Diana, M., Fratta, W., Manzoni, D., Andre, P., Pompeiano, O., Mazzocchio, R., Rossi, A., Melis, F., Kitura, A., Caria, M. A., Asanuma, H., Melone, M, De Biasi, S, Minelli, A, Conti, F, Minelli, A, Karschin, C, DeBiasi, S, Brecha, N C, Conti, F, Monda, M., Amaro, S., Sullo, A., De Luca, B., Monda, M., Amaro, S., Sullo, A., De Luca, B., Pantò, M. R., Cicirata, F., Parenti, R., Serapide, M. F., Parenti, R., Wassef, M., Cicirata, F., Podda, M. V., Solinas, A., Chessa, G., Deriu, F., Mameli, O., Tolu, E., Pompeiano, O., Andre, P., Manzoni, D., Porro, C. A., Francescato, M. P., Cettolo, V., Diamond, M. E., Baraldi, P., Bazzocchi, M., Rivosecchi, R., Konnerth, A., Rossi, M. L., Martini, M., Pelucchi, B., Fesce, R., Santarelli, L., Schacher, S., Montarolo, P. G., Santarelli, R., Grassi, C., Valente, A., Nisticò, S., Bagetta, G., Azzena, G. B., Scuri, Rossana, Garcia-Gil, Mercedes, Mozzachiodi, Riccardo, Brunelli, Marcello, Stefani, G., Onofri, F., Vaccaro, P., Nielander, H. B., Benfenati, F., Tancredi, V., D’Antuono, M., Siniscalchi, A., Brancati, A., Avoli, M., Vellani, V., Navangione, A., Rispoli, G., Verzè, L., Buffo, A., Rossi, F., Oestreicher, A. B., Gispen, W. H., Strata, P., Zamboni, G., Amici, R., Jones, C. A., Perez, E., Domeniconi, R., Parmeggiani, P. L., Zoli, Michele, Le Novàre, Nicolas, Changeux, Jean -Pierre, Lafortuna, C. L., Reinach, E., Saibene, F., Scotto, P., Zocchi, L., Agostoni, E., and Cremaschi, D.

Published
1996
Full Text
View/download PDF

21. Protective properties of antioxidant drugs in noise-induced hearing loss in the guinea pig

Author

Fetoni AR, Ralli M, Sergi B, Parrilla C, Troiani D, Paludetti G, Fetoni, Ar, Ralli, M, Sergi, B, Parrilla, C, Troiani, D, and Paludetti, G

Abstract

Oxidative stress plays a significant role in noise-induced hearing loss (NIHL), as it largely participates in the mechanisms that underlie cell death after noise exposure and lead to sensorineural hearing loss. Many antioxidant drugs have been tested to prevent NIHL. We present three molecules with antioxidant properties (vitamin E, idebenone, N-L-acetylcysteine) that have been studied in our laboratory, and compare their protective effects. We induced acoustic trauma in treated guinea pigs, evaluated their hearing function via electrophysiological measurements at 1, 7 and 21 days, and performed morphological studies with scanning electron microscopy and TUNEL assay. All molecules had a certain effect in protecting hair cells from oxidative stress; vitamin E offered almost complete protection (8095%), N-L-acetylcysteine and idebenone also significantly reduced the threshold shift and hair cell loss. Our results support the effectiveness of antioxidant drugs in protecting against NIHL and provide a rationale for exploring therapeutic strategies in humans.

Published
2008

28. alpha-Tocopherol protective effects on gentamicin ototoxicity: an experimental study

Author

Fetoni, Ar, Sergi, B, Ferraresi, Aldo, Paludetti, Gaetano, Troiani, D., Fetoni, A, Sergi, B, Ferraresi, A, Paludetti, G, and Troiani, D

Subjects
aminoglycoside antibiotics, gentamicin, ototoxicity, antioxidant therapy, alpha-tocopherol protection, OHCs
Abstract

Gentamicin, acting as an iron chelator, activates membrane lipid peroxidation (MPL) and induces free radical formation, as observed in vitro and in vivo. Antioxidants, such as alpha-tocopherol, are able to suppress MLP, thus attenuating tissue damage. The present study was designed to investigate the possible protective effects of alpha-tocopherol on gentamicin ototoxicity. The study was carried out on albino guinea pigs (250-350 g). The animals were divided into four groups: group A (n = 4), injected with corn oil daily at a dose of 100 mg/kg body weight intramuscularly (IM); group B (n = 10), treated with corn oil at a dose of 100 mg/kg body weight and gentamicin base at a dose of 100 mg/kg body weight (IM); group C (n = 10). treated with gentamicin alone at a dose of 100 mg/kg body weight (IM); and group D (n = 10), treated with gentamicin at the same dose plus alpha-tocopherol acetate at dose of 100 mg/kg body weight (IM). Electrocochleographic recordings were made from an implanted round-window electrode. All animals were treated for 14 days. The compound action potentials (CAPs) were measured at 2-16 kHz at days 0, 10, 14 and 18 after treatment. Changes in cochlear function were characterized as CAP threshold shifts. Morphological changes were analysed by scanning electron microscopy. Gentamicin induced progressive high-frequency hearing loss of 50-60 dB SPL. alpha-Tocopherol co-therapy slowed the progression of hearing loss. The significant loss of outer hair cells (OHCs) in the cochlear basal turn in gentamicin-treated animals was not observed in the cochleas of animals protected with alpha-tocopherol. This study supports the hypothesis that alpha-tocopherol interferes with gentamicin-induced free radical formation, and suggests that this drug may be useful in protecting OHC function from aminoglycoside ototoxicity, thus reducing hearing loss.

Published
2004

29. Protective effects of alpha-tocopherol and tiopronin against cisplatin-induced ototoxicity

Author

FETONI A, SERGI B, FERRARESI A, PALUDETTI G, TROIANI D, Fetoni, A, Sergi, B, Ferraresi, A, Paludetti, G, and Troiani, D

Abstract

OBJECTIVE: To investigate the possible protective effects of alpha-tocopherol and tiopronin against cisplatin-induced cochlear damage. Cisplatin ototoxicity and nephrotoxicity seem to result from the inhibition of cochlear antioxidant defences, causing an increase in the amount of reactive oxygen species. Antioxidants, such as alpha-tocopherol and tiopronin, are able to suppress lipid peroxidation, thus attenuating tissue damage. MATERIAL AND METHODS: Hartley albino guinea pigs were used. The animals were treated for 7 consecutive days with either (I) cisplatin alone, (II) cisplatin+alpha-tocopherol acetate, (III) cisplatin+tiopronin, (IV) cisplatin+alpha-tocopherol acetate+tiopronin, (V) alpha-tocopherol acetate alone or (VI) tiopronin alone. Changes in cochlear function were characterized by means of compound action potential threshold shifts. After the functional testing, tympanic bullae were removed and processed for morphological examination of the sensorineural epithelium. Renal function was evaluated by measuring serum blood urea nitrogen and creatinine levels. RESULTS: Cisplatin induced progressive high-frequency hearing loss of 40-50 dB SPL. Alpha-tocopherol and tiopronin co-therapy significantly slowed the progression of hearing loss. Treatment with alpha-tocopherol acetate or tiopronin alone was less effective. Morphological observations showed an important loss of outer hair cells and degeneration of the organ of Corti in the basal and middle turns. Injection of both alpha-tocopherol and tiopronin reduced cochlear outer hair cell loss more than treatment with a single drug. Beneficial effects of alpha-tocopherol and tiopronin on cisplatin-induced nephrotoxicity were observed. CONCLUSION: This study supports the hypothesis that alpha-tocopherol and tiopronin interfere with cisplatin-induced damage, and suggests that concurrent treatment with the two drugs can be useful in protecting against hearing loss.

Published
2004

31. Protective effects of alpha-tocopherol against gentamicin-induced Oto-vestibulo toxicity: an experimental study

Author

FETONI A, SERGI B, SCARANO E, PALUDETTI G, FERRARESI A, TROIANI D, Fetoni, A, Sergi, B, Scarano, E, Paludetti, G, Ferraresi, A, and Troiani, D

Abstract

OBJECTIVE: Free radicals are involved in gentamicin ototoxicity and vestibular dysfunction and it has been demonstrated that free radical scavengers, such as alpha-tocopherol, are able to inactive free radicals, attenuating tissue damage This study was designed to investigate the possible protective effects of alpha-tocopherol against gentamicin-induced oto-vestibulo toxicity. MATERIAL AND METHODS: Adult albino guinea pigs were divided into four groups and were treated for 2 weeks as follows: Group A, controls; Group B, gentamicin plus corn oil; Group C, gentamicin only; and Group D, gentamicin plus alpha-tocopherol. To evaluate vestibular function, the animals underwent sinusoidal oscillations in the dark about their vertical and longitudinal axes to evoke horizontal and vertical vestibulo-ocular reflexes (VORs), respectively. Electrocochleographic recordings were performed using an implanted round window electrode. The compound action potentials (CAPs) at 2, 4, 8 and 16 kHz were measured every 5 days Morphological changes were analysed by means of scanning electron microscopy. RESULTS: Gentamicin induced a consistent reduction in VOR responses and a progressive high-frequency hearing loss of 50-60 dB sound pressure level. Alpha-Tocopherol co-therapy slowed the progression of hearing loss and significantly attenuated the final threshold shifts The impairment of vestibular function was reduced, as evidenced by an increased VOR gain. The massive loss of outer hair cells in the cochlear basal turn and of cristae ampullaris stereocilia in gentamicin-treated animals was not observed in the cochlea of animals protected with alpha-tocopherol. CONCLUSION: This study supports the hypothesis that alpha-tocopherol interferes with gentamicin-induced free radical formation, and suggests that this drug may be useful in preventing aminoglycoside oto-vestibulo toxicity.

Published
2003

Catalog

Books, media, physical & digital resources
See catalog results