Platelets Rich Plasma Increases Antioxidant Defenses of Tenocytes via Nrf2 Signal Pathway
Tendinopathies are common disabling conditions in equine and human athletes. The etiology is still unclear, although reactive oxygen species (ROS) and oxidative stress (OS) seem to play a crucial role. In addition, OS has been implicated in the failure of tendon lesion repair. Platelet-rich plasma (...
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MDPI AG
2023-08-01
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author | Alessia Tognoloni Desiree Bartolini Marco Pepe Antonio Di Meo Ilaria Porcellato Kubra Guidoni Francesco Galli Elisabetta Chiaradia |
author_facet | Alessia Tognoloni Desiree Bartolini Marco Pepe Antonio Di Meo Ilaria Porcellato Kubra Guidoni Francesco Galli Elisabetta Chiaradia |
author_sort | Alessia Tognoloni |
collection | DOAJ |
description | Tendinopathies are common disabling conditions in equine and human athletes. The etiology is still unclear, although reactive oxygen species (ROS) and oxidative stress (OS) seem to play a crucial role. In addition, OS has been implicated in the failure of tendon lesion repair. Platelet-rich plasma (PRP) is rich in growth factors that promote tissue regeneration. This is a promising therapeutic approach in tendon injury. Moreover, growing evidence has been attributed to PRP antioxidant effects that can sustain tissue healing. In this study, the potential antioxidant effects of PRP in tenocytes exposed to oxidative stress were investigated. The results demonstrated that PRP reduces protein and lipid oxidative damage and protects tenocytes from OS-induced cell death. The results also showed that PRP was able to increase nuclear levels of redox-dependent transcription factor Nrf2 and to induce some antioxidant/phase II detoxifying enzymes (superoxide dismutase 2, catalase, heme oxygenase 1, NAD(P)H oxidoreductase quinone-1, glutamate cysteine ligase catalytic subunit and glutathione, S-transferase). Moreover, PRP also increased the enzymatic activity of catalase and glutathione S-transferase. In conclusion, this study suggests that PRP could activate various cellular signaling pathways, including the Nrf2 pathway, for the restoration of tenocyte homeostasis and to promote tendon regeneration and repair following tendon injuries. |
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id | doaj.art-026a6c6930a444b3b95d1f6e49e4786c |
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issn | 1661-6596 1422-0067 |
language | English |
last_indexed | 2024-03-10T23:21:05Z |
publishDate | 2023-08-01 |
publisher | MDPI AG |
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series | International Journal of Molecular Sciences |
spelling | doaj.art-026a6c6930a444b3b95d1f6e49e4786c2023-11-19T08:15:15ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-08-0124171329910.3390/ijms241713299Platelets Rich Plasma Increases Antioxidant Defenses of Tenocytes via Nrf2 Signal PathwayAlessia Tognoloni0Desiree Bartolini1Marco Pepe2Antonio Di Meo3Ilaria Porcellato4Kubra Guidoni5Francesco Galli6Elisabetta Chiaradia7Department of Veterinary Medicine, University of Perugia, 06126 Perugia, ItalyDepartment of Pharmaceutical Sciences, University of Perugia, 06122 Perugia, ItalyDepartment of Veterinary Medicine, University of Perugia, 06126 Perugia, ItalyDepartment of Veterinary Medicine, University of Perugia, 06126 Perugia, ItalyDepartment of Veterinary Medicine, University of Perugia, 06126 Perugia, ItalyDepartment of Veterinary Medicine, University of Perugia, 06126 Perugia, ItalyDepartment of Pharmaceutical Sciences, University of Perugia, 06122 Perugia, ItalyDepartment of Veterinary Medicine, University of Perugia, 06126 Perugia, ItalyTendinopathies are common disabling conditions in equine and human athletes. The etiology is still unclear, although reactive oxygen species (ROS) and oxidative stress (OS) seem to play a crucial role. In addition, OS has been implicated in the failure of tendon lesion repair. Platelet-rich plasma (PRP) is rich in growth factors that promote tissue regeneration. This is a promising therapeutic approach in tendon injury. Moreover, growing evidence has been attributed to PRP antioxidant effects that can sustain tissue healing. In this study, the potential antioxidant effects of PRP in tenocytes exposed to oxidative stress were investigated. The results demonstrated that PRP reduces protein and lipid oxidative damage and protects tenocytes from OS-induced cell death. The results also showed that PRP was able to increase nuclear levels of redox-dependent transcription factor Nrf2 and to induce some antioxidant/phase II detoxifying enzymes (superoxide dismutase 2, catalase, heme oxygenase 1, NAD(P)H oxidoreductase quinone-1, glutamate cysteine ligase catalytic subunit and glutathione, S-transferase). Moreover, PRP also increased the enzymatic activity of catalase and glutathione S-transferase. In conclusion, this study suggests that PRP could activate various cellular signaling pathways, including the Nrf2 pathway, for the restoration of tenocyte homeostasis and to promote tendon regeneration and repair following tendon injuries.https://www.mdpi.com/1422-0067/24/17/13299tenocytesplatelet-rich plasmaNrf2protein oxidationtendinopathyoxidative stress |
spellingShingle | Alessia Tognoloni Desiree Bartolini Marco Pepe Antonio Di Meo Ilaria Porcellato Kubra Guidoni Francesco Galli Elisabetta Chiaradia Platelets Rich Plasma Increases Antioxidant Defenses of Tenocytes via Nrf2 Signal Pathway International Journal of Molecular Sciences tenocytes platelet-rich plasma Nrf2 protein oxidation tendinopathy oxidative stress |
title | Platelets Rich Plasma Increases Antioxidant Defenses of Tenocytes via Nrf2 Signal Pathway |
title_full | Platelets Rich Plasma Increases Antioxidant Defenses of Tenocytes via Nrf2 Signal Pathway |
title_fullStr | Platelets Rich Plasma Increases Antioxidant Defenses of Tenocytes via Nrf2 Signal Pathway |
title_full_unstemmed | Platelets Rich Plasma Increases Antioxidant Defenses of Tenocytes via Nrf2 Signal Pathway |
title_short | Platelets Rich Plasma Increases Antioxidant Defenses of Tenocytes via Nrf2 Signal Pathway |
title_sort | platelets rich plasma increases antioxidant defenses of tenocytes via nrf2 signal pathway |
topic | tenocytes platelet-rich plasma Nrf2 protein oxidation tendinopathy oxidative stress |
url | https://www.mdpi.com/1422-0067/24/17/13299 |
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