Ferulic Acid Grafted Into Β-Cyclodextrin Nanosponges Ameliorates Paraquat-Induced Human Mrc-5 Fibroblast Injury Publisher Pubmed



Meamar R¹ ; Haddad S¹ ; Nasiri R² ; Borojeni GS^{3, 4} ; Kolahdoozan M³ ; Eizadimood N¹ ; Pourisfahani SA¹ ; Mahvari R¹ ; Rezaei A^{5, 6} ; Fesharaki M¹ Show Affiliations
Source: Environmental Toxicology Published:2024

Abstract

Paraquat (PQ) is a commercially important and effective herbicide in the world. Nevertheless, it has higher toxicity causing acute organ damage and different complications, mainly in the lungs and kidneys. Ferulic acid (FA), 4-hydroxy-3-methoxycinnamic acid imposes multiple pharmacological impacts. No protective effect of FA on PQ poisoning-caused human embryonic lung fibroblast damage has not been reported. Despite their many beneficial effects, FA is characterized by poor water solubility, low bioavailability, and phytochemical instability. To solve the problem, β-cyclodextrin nanosponge (β-CD NSs) was utilized to increase the solubility of FA so that it was grafted into β-CD NSs to establish β-CD@FA NSs. The purpose of this work was to examine for the first time the protective effect of β-CD@FA NS on MRC-5 human lung cells damages induced by PQ poisoning. MTS assay was performed to investigate the viability of MRC-5 cells at different concentrations of FA/β-CD@FA NSs when cells were co-cultured with 0.2 μg/mL PQ. The flow cytometry study was carried out to determine apoptosis. Malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) levels were detected using appropriate biochemistry kits. Compared with the PQ group, the cell activity, CAT, and SOD levels were significantly increased in the FA and chiefly in β-CD@FA NSs intervention groups, whereas apoptosis and MDA levels were markedly decreased. The inflammatory factors tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), and interleukin 22 (IL-22) were detected. The results demonstrate that β-CD@FA NSs can inhibit PQ-induced cell damage by enhancing antioxidant stress capacity and regulation of inflammatory responses. © 2023 Wiley Periodicals LLC.