Anti-oxidant and anti-inflammatory effects of ellagic and punicic acid in an in vitro model of cardiac fibrosis

Mannino, Federica; Imbesi, Chiara; Bitto, Alessandra; Minutoli, Letteria; Squadrito, Francesco; D’Angelo, Tommaso; Booz, Christian; Pallio, Giovanni; Irrera, Natasha

doi:10.1016/j.biopha.2023.114666

Cited by 21 publications

(5 citation statements)

References 48 publications

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“…To prevent stricture formation and treat corrosive esophageal burn (CEB) injury, ketotifen [33], tamoxifen [34], Ankaferd Blood Stopper [35], carvacrol [36], hypericum perforatum oil [37], contractubex [30], ethyl pyruvate, N-acetyl cysteine [38], platelet-rich plasma [39], alpha lipoic [40], bromelain [41], hesperidin [42] and mitomycin C [43] were studied. Due to its antioxidant, anti-inflammatory, antifibrotic [44], antitumoral [45], antiviral [46] and antidiabetic [47] effects, this study investigated the efficacy of Ellagic acid (EA) for the treatment of CEB injury, as previous experimental studies explored various therapeutic agents. However, to the best of our knowledge, none of these agents demonstrated conclusive effectiveness in the treatment of CEB injury.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Ellagic Acid on Experimental Corrosive Esophageal Burn Injury

Keşim,

Aşır,

Ayaz

et al. 2024

CIMB

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This study aimed to investigate the antioxidant effect of Ellagic acid (EA) on wound healing in sodium hydroxide (NaOH)-induced corrosive esophageal burn injury. The interaction networks and functional annotations were conducted using Cytoscape software. A total of 24 Wistar albino rats were divided into control, corrosive esophageal burn (CEB) and CEB + EA groups. Burn injury was created by 20% NaOH and 30 mg/kg EA was per oral administered to rats. At the end of the 28-day experimental period, Malondialdehyde (MDA) content was measured. Esophageal tissue samples were processed for histological staining. The EA–target interaction network was revealed to be involved in regulating crucial cellular mechanisms for burn wound healing, with epidermal growth factor (EGF) identified as a central mediator. An increase in animal weight in the CEB + EA group was observed in the EA-treated group after CEB injury. Burn injury increased MDA content, but EA treatment decreased its level after CEB injury. Stenosis index, collagen degeneration, inflammation, fibrosis and necrosis levels were increased after CEB injury. EA treatment improved histopathology in the CEB + EA group compared to the CEB group. The expression of EGF was decreased in the CEB group but upregulated in the EA-treated group, suggesting a potential involvement of EA in cellular processes and tissue regeneration. EA, through its antioxidative and tissue regenerative properties, significantly contributes to alleviating the adverse effects of CEB injury, promoting wound healing.

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Section: Discussionmentioning

confidence: 99%

The Effects of Ellagic Acid on Experimental Corrosive Esophageal Burn Injury

Keşim,

Aşır,

Ayaz

et al. 2024

CIMB

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“…At the end of the treatment period, cells were incubated with 5 μL of CM-H2DCFDA probe (Thermo Fisher, Carlsbad, CA, USA) for 1 h at 37 °C with a percentage of 5% CO 2 . After three washing with sterile PBS, cells were observed with a fluorescent microscope and the fluorescent intensity was quantified using ImageJ 1.53e software for Windows (Softonic, Barcelona, Spain) [ 41 ].…”

Section: Methodsmentioning

confidence: 99%

Blunting Neuroinflammation by Targeting the Immunoproteasome with Novel Amide Derivatives

Imbesi

Ettari

Irrera

et al. 2023

IJMS

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Neuroinflammation is an inflammatory response of the nervous tissue mediated by the production of cytokines, chemokines, and reactive oxygen species. Recent studies have shown that an upregulation of immunoproteasome is highly associated with various diseases and its inhibition attenuates neuroinflammation. In this context, the development of non-covalent immunoproteasome-selective inhibitors could represent a promising strategy for treating inflammatory diseases. Novel amide derivatives, KJ3 and KJ9, inhibit the β5 subunit of immunoproteasome and were used to evaluate their possible anti-inflammatory effects in an in vitro model of TNF-α induced neuroinflammation. Differentiated SH-SY5Y and microglial cells were challenged with 10 ng/mL TNF-α for 24 h and treated with KJ3 (1 µM) and KJ9 (1 µM) for 24 h. The amide derivatives showed a significant reduction of oxidative stress and the inflammatory cascade triggered by TNF-α reducing p-ERK expression in treated cells. Moreover, the key action of these compounds on the immunoproteasome was further confirmed by halting the IkB-α phosphorylation and the consequent inhibition of NF-kB. As downstream targets, IL-1β and IL-6 expression resulted also blunted by either KJ3 and KJ9. These preliminary results suggest that the effects of these two compounds during neuroinflammatory response relies on the reduced expression of pro-inflammatory targets.

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“…Intracellular ROS production was evaluated by using a 5-(and-6)-chloromethyl-2 ′ ,7 ′ -dichlorodihydrofluorescein diacetate (CM-H2DCFDA) probe (Thermo Fisher, Milan, Italy) in HMC3 cells challenged with LPS alone or with levosimendan or dobutamine for 24 h. At the end of the treatment, cells were incubated with a CM-H2DCFDA probe (5 µM) for 1 h at 37 • C with 5% CO 2 and then washed with sterile PBS 2-3 times. After washing, cells were observed with a fluorescent microscope [27]. Fluorescence quantification was performed by using ImageJ software for Windows (Softonic, Barcelona, Spain).…”

Section: Intracellular Ros Productionmentioning

confidence: 99%

Levosimendan and Dobutamin Attenuate LPS-Induced Inflammation in Microglia by Inhibiting the NF-κB Pathway and NLRP3 Inflammasome Activation via Nrf2/HO-1 Signalling

Mannino,

Urzì Brancati,

Lauro

et al. 2024

Biomedicines

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Hypovolemic shock is a circulatory failure, due to a loss in the effective circulating blood volume, that causes tissue hypoperfusion and hypoxia. This condition stimulates reactive oxygen species (ROS) and pro-inflammatory cytokine production in different organs and also in the central nervous system (CNS). Levosimendan, a cardioprotective inodilator, and dobutamine, a β1-adrenergic agonist, are commonly used for the treatment of hypovolemic shock, thanks to their anti-inflammatory and antioxidant effects. For this reason, we aimed at investigating levosimendan and dobutamine’s neuroprotective effects in an “in vitro” model of lipopolysaccharide (LPS)-induced neuroinflammation. Human microglial cells (HMC3) were challenged with LPS (0.1 µg/mL) to induce an inflammatory phenotype and then treated with levosimendan (10 µM) or dobutamine (50 µM) for 24 h. Levosimendan and dobutamine significantly reduced the ROS levels and markedly increased Nrf2 and HO-1 protein expression in LPS-challenged cells. Levosimendan and dobutamine also decreased p-NF-κB expression and turned off the NLRP3 inflammasome together with its downstream signals, caspase-1 and IL-1β. Moreover, a reduction in TNF-α and IL-6 expression and an increase in IL-10 levels in LPS-stimulated HMC3 cells was observed following treatment. In conclusion, levosimendan and dobutamine attenuated LPS-induced neuroinflammation through NF-κB pathway inhibition and NLRP3 inflammasome activation via Nrf2/HO-1 signalling, suggesting that these drugs could represent a promising therapeutic approach for the treatment of neuroinflammation consequent to hypovolemic shock.

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Anti-oxidant and anti-inflammatory effects of ellagic and punicic acid in an in vitro model of cardiac fibrosis

Cited by 21 publications

References 48 publications

The Effects of Ellagic Acid on Experimental Corrosive Esophageal Burn Injury

The Effects of Ellagic Acid on Experimental Corrosive Esophageal Burn Injury

Blunting Neuroinflammation by Targeting the Immunoproteasome with Novel Amide Derivatives

Levosimendan and Dobutamin Attenuate LPS-Induced Inflammation in Microglia by Inhibiting the NF-κB Pathway and NLRP3 Inflammasome Activation via Nrf2/HO-1 Signalling

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