Background. Castanea sativa (Mill.) (Fam. Fagaceae) agro-industry provides substantial by-products, source of tannins and flavonoids, which recently showed anti-inflammatory properties in Helicobacter pylori infection [1,2]. H. pylori triggers immune cells infiltration, chronic inflammation and oxidative stress, favouring DNA damage and cancer [3]. Based on this evidence, we investigated the protection of C. sativa byproducts towards gastric inflammation induced by TNFα, pivotal during H. pylori inflammation [4]. Methodologies. Polyphenolic profile of various extracts from barks, fruit shells and burs of C. sativa, including those obtained from in vitro digestion, was spectrophotometrically evaluated [5]. All the samples were tested in human gastric epithelium models (AGS and GES-1 cells) towards TNFα-induced cell damage. Intracellular ROS levels, cell regeneration, cytokines and LDH release were measured [6]. Antioxidant defence and DNA damage were investigated by immunofluorescence of Nrf2 and phosphorylated H2AX histone [6,7]. Results. All extracts restored intracellular ROS levels and cell regeneration. Fruit shell hydroalcoholic extract lowered LDH and cytokines release. Modulation of Nrf2 pathway and decreased DNA damage were observed. Conclusions. Chestnut by-products are a possible strategy towards gastric inflammation and oxidative stress and may promote environmental sustainability and circular economy. Further studies are needed to clarify the phytochemicals and the mechanisms involved. Bibliografia [1] Braga et al. Nat Prod Res 2015, 29(1), 1–18. [2] Sangiovanni et al. Pharmacol Res 2018, 134, 145–155. [3] Wang et al. Biochim Biophys Acta - Rev Cancer 2024, 1879(5), 189139. [4] Piazza et al. Nutrients 2023, 15(6), 1504. [5] Di Sotto et al. Molecules 2019, 24:3103. [6] Di Sotto et al. Biomedicines 2022,10,2257. [7] Di Giacomo et al. Antioxidants 2023, 12(9), 1771.

Role of Castanea sativa (Mill.) by-products in gastric inflammation control: a possible strategy towards Helicobacter pylori infection / Percaccio, Ester; Baldani, Claudia; Corsetti, Letizia; Piazza, Stefano; Sangiovanni, Enrico; Di Giacomo, Silvia; Di Sotto, Antonella. - (2025). ( Piante&Salute 2025 Padova, Italy ).

Role of Castanea sativa (Mill.) by-products in gastric inflammation control: a possible strategy towards Helicobacter pylori infection

Percaccio Ester
Primo
;
Baldani Claudia;Corsetti Letizia;Di Sotto Antonella
Ultimo
2025

Abstract

Background. Castanea sativa (Mill.) (Fam. Fagaceae) agro-industry provides substantial by-products, source of tannins and flavonoids, which recently showed anti-inflammatory properties in Helicobacter pylori infection [1,2]. H. pylori triggers immune cells infiltration, chronic inflammation and oxidative stress, favouring DNA damage and cancer [3]. Based on this evidence, we investigated the protection of C. sativa byproducts towards gastric inflammation induced by TNFα, pivotal during H. pylori inflammation [4]. Methodologies. Polyphenolic profile of various extracts from barks, fruit shells and burs of C. sativa, including those obtained from in vitro digestion, was spectrophotometrically evaluated [5]. All the samples were tested in human gastric epithelium models (AGS and GES-1 cells) towards TNFα-induced cell damage. Intracellular ROS levels, cell regeneration, cytokines and LDH release were measured [6]. Antioxidant defence and DNA damage were investigated by immunofluorescence of Nrf2 and phosphorylated H2AX histone [6,7]. Results. All extracts restored intracellular ROS levels and cell regeneration. Fruit shell hydroalcoholic extract lowered LDH and cytokines release. Modulation of Nrf2 pathway and decreased DNA damage were observed. Conclusions. Chestnut by-products are a possible strategy towards gastric inflammation and oxidative stress and may promote environmental sustainability and circular economy. Further studies are needed to clarify the phytochemicals and the mechanisms involved. Bibliografia [1] Braga et al. Nat Prod Res 2015, 29(1), 1–18. [2] Sangiovanni et al. Pharmacol Res 2018, 134, 145–155. [3] Wang et al. Biochim Biophys Acta - Rev Cancer 2024, 1879(5), 189139. [4] Piazza et al. Nutrients 2023, 15(6), 1504. [5] Di Sotto et al. Molecules 2019, 24:3103. [6] Di Sotto et al. Biomedicines 2022,10,2257. [7] Di Giacomo et al. Antioxidants 2023, 12(9), 1771.
2025
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/1764818
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