Oxidative stress and inflammation are key contributors to the development of numerous inflammatory, metabolic, and neurodegenerative diseases. Increasing evidence highlights the role of diet, particularly the Mediterranean diet, in modulating these processes through the intake of bioactive compounds. Nuts represent an important source of polyphenols, unsaturated fatty acids, vitamins, and minerals; however, the biological potential of specific nut fractions and by-products remains only partially explored. This PhD thesis investigated the antioxidant, anti- inflammatory, and regenerative effects of bioactive compounds derived from almonds and cashews using validated experimental models of acute inflammation, wound healing, and neuroinflammation induced by a metabolic condition known as hyperhomocysteinemia. Almond skin extract was evaluated in a carrageenan-induced paw edema model, while the wound-healing properties of almond oil were assessed in a murine excisional wound model. In addition, the effects of cashew nut supplementation were examined in a methionine-induced hyperhomocysteinemia model, focusing on oxidative stress, neuroinflammation, and neuronal damage. The results demonstrate that nut-derived compounds significantly reduce oxidative stress and inflammatory markers, limit tissue damage, and promote repair processes. These protective effects are consistently associated with activation of the Nrf2/HO-1 antioxidant pathway and inhibition of NF-κB signaling. In the central nervous system, cashew supplementation attenuated glial activation, reduced apoptotic signaling, and preserved neuronal integrity. Overall, this work supports the potential of nuts and their by-products as sustainable sources of bioactive compounds with antioxidant, anti-inflammatory, and neuroprotective properties, suggesting their possible application in nutraceutical and preventive strategies against inflammation and oxidative stress related disorders.

Health Benefits of Nuts Bioactive Compounds: Focus on Oxidative Stress and Inflammatory markers

ARANGIA, ALESSIA
2026-02-27

Abstract

Oxidative stress and inflammation are key contributors to the development of numerous inflammatory, metabolic, and neurodegenerative diseases. Increasing evidence highlights the role of diet, particularly the Mediterranean diet, in modulating these processes through the intake of bioactive compounds. Nuts represent an important source of polyphenols, unsaturated fatty acids, vitamins, and minerals; however, the biological potential of specific nut fractions and by-products remains only partially explored. This PhD thesis investigated the antioxidant, anti- inflammatory, and regenerative effects of bioactive compounds derived from almonds and cashews using validated experimental models of acute inflammation, wound healing, and neuroinflammation induced by a metabolic condition known as hyperhomocysteinemia. Almond skin extract was evaluated in a carrageenan-induced paw edema model, while the wound-healing properties of almond oil were assessed in a murine excisional wound model. In addition, the effects of cashew nut supplementation were examined in a methionine-induced hyperhomocysteinemia model, focusing on oxidative stress, neuroinflammation, and neuronal damage. The results demonstrate that nut-derived compounds significantly reduce oxidative stress and inflammatory markers, limit tissue damage, and promote repair processes. These protective effects are consistently associated with activation of the Nrf2/HO-1 antioxidant pathway and inhibition of NF-κB signaling. In the central nervous system, cashew supplementation attenuated glial activation, reduced apoptotic signaling, and preserved neuronal integrity. Overall, this work supports the potential of nuts and their by-products as sustainable sources of bioactive compounds with antioxidant, anti-inflammatory, and neuroprotective properties, suggesting their possible application in nutraceutical and preventive strategies against inflammation and oxidative stress related disorders.
27-feb-2026
bioactive compounds; oxidative stress; inflammation; neuroinflammation; nuts
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/3349249
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