Bergamottin alleviates LPS-induced acute lung injury by inducing SIRT1 and suppressing NF-κB

An, Ning; Yang, Tao; Zhang, Xiaoxia; Xu, Mei-Xia

doi:10.1177/17534259211062553

Cited by 10 publications

(4 citation statements)

References 36 publications

(42 reference statements)

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“…Bergamottin has been drawing increasing interest recently owing to its anti-inflammatory properties. It is reported that Bergamottin alleviates LPS-induced acute lung injury by inducing SIRT1 and inhibiting NF-κB ( An et al, 2021 ). Research also suggests that Bergamottin prevents LPS-induced endotoxic shock by modulating the NF-κB signaling pathway ( Liu et al, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

Bergamottin (Ber) ameliorates the progression of osteoarthritis via the Sirt1/NF-κB pathway

Shen,

Zhang,

et al. 2024

Front. Pharmacol.

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Osteoarthritis (OA) is a common chronic disease characterized by progressive cartilage degeneration and secondary synovial inflammation. Bergamottin (Ber) is an important natural derivative of the furanocoumarin compound, extracted from natural foods, such as the pulp of grapefruits and pomelos. Ber exhibits several characteristicsthat are beneficial to human health, such as anti-inflammation, antioxidant, and anti-cancer effects. However, the role of Ber in the treatment of OA has not been elucidated to date. Therefore, in the present study, in vitro experiments were conducted, which demonstrated that Ber reduces the secretion of inducible nitric oxide synthase (iNOS), nitric oxide (NO), cyclooxygenase-2 (COX2), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and prostaglandin E2 (PGE2) under the stimulation of interleukin-1β (IL-1β). Ber also reversed the IL-1 β-mediated aggrecan and type II collagen degradation within the extracellular matrix (ECM). In addition, in vivo experiments were conducted, in which Ber ameliorated the progression of OA in mice. It was revealed that Ber exerted its cellular effect by activating the Sirt1/NF-kB pathways. In conclusion, the present study demonstrated the therapeutic potential of Ber in the context of OA.

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Section: Discussionmentioning

confidence: 99%

Bergamottin (Ber) ameliorates the progression of osteoarthritis via the Sirt1/NF-κB pathway

Shen,

Zhang,

et al. 2024

Front. Pharmacol.

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“…The protein concentration and the inflammatory cell number of BALF in the P5 group increased by 3.32-fold and 4.66-fold, respectively, compared to the untreated group. Typical features of ALI are the alveolar accumulation of protein-rich fluid and activated immune cells due to pulmonary endothelial barrier disruption and increased vascular permeability [ 38 , 39 ]. The results indicate that GF-17 can induce inflammatory reactions in the lungs, leading to inflammatory injury in the lungs.…”

Section: Discussionmentioning

confidence: 99%

A Rapid In Vivo Toxicity Assessment Method for Antimicrobial Peptides

Chi,

Peng,

Zhang

et al. 2024

Toxics

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Antimicrobial peptides (AMPs) represent a promising antibiotic alternative to overcome drug-resistant bacteria by inserting into the membrane of bacteria, resulting in cell lysis. However, therapeutic applications of AMPs have been hindered by their ability to lyse eukaryotic cells. GF-17 is a truncated peptide of LL-37, which has perfect amphipathicity and a higher hydrophobicity, resulting in higher haemolytic activity. However, there is no significant difference in the cytotoxicity against human lung epithelial cells between the GF-17 and LL-37 groups, indicating that there are significant differences in the sensitivity of different human cells to GF-17. In this study, LL-37 and GF-17 were administered to mouse lungs via intranasal inoculation. Blood routine examination results showed that LL-37 did not affect the red blood cells, platelet, white blood cells and neutrophil counts, but GF-17 decreased the white blood cells and neutrophil counts with the increasing concentration of peptides. GF-17-treated mice suffer a body weight loss of about 2.3 g on average in 24 h, indicating that GF-17 is highly toxic to mice. The total cell counts in the bronchoalveolar lavage fluid from GF-17-treated mice were 4.66-fold that in the untreated group, suggesting that GF-17 treatment leads to inflammation in the lungs of mice. Similarly, the histological results showed the infiltration of neutrophils in the lungs of GF-17-treated mice. The results suggest that the administration of GF-17 in the lungs of mice does not affect the red blood cells and platelet counts in the blood but promotes neutrophil infiltration in the lungs, leading to an inflammatory response. Therefore, we established a mouse acute lung injury model to preliminarily evaluate the in vivo toxicity of AMPs. For AMPs with a clinical application value, systematic research is still needed to evaluate their acute and long-term toxicity.

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“…Herein, we found LPS can promote the secretion of TNF-α, IL-1β, and IL-6 while safflor yellow A could mitigate the excessive synthesis of these cytokines, which indicated its anti-inflammatory effects in Beas-2B cells. More experimental evidences have disclosed activation of NF-κB signaling pathway was involved in ALI/ARDS (Cao et al 2018 ; An et al 2021 ), which could regulate the secretion of these pro-inflammatory cytokines in transcription (Hayden and Ghosh 2011 ). Under unstressed conditions, NF-κB dimers are bound to IκBα to form the complex and sequestered in cytosol (Oeckinghaus et al 2011 ).…”

Section: Discussionmentioning

confidence: 99%

Safflor Yellow A Protects Beas-2B Cells Against LPS-Induced Injury via Activating Nrf2

Chen

Zheng

2023

Rev. Bras. Farmacogn.

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Acute lung injury and its severe form acute respiratory distress syndrome are lethal lung diseases. So far, effective therapy for the diseases is deficient and the prognosis is poor. Recently, it was found activating nuclear factor erythroid 2-related factor 2 could attenuate the injury including inflammation, oxidative stress, and apoptosis in those diseases. To discover novel therapy, we have evaluated safflor yellow A and explored the underlying mechanisms using Beas-2B cells injured by lipopolysaccharide. As a result, safflor yellow A could improve the viability of Beas-2B cells treated with lipopolysaccharide. Further investigations have revealed safflor yellow A suppressed oxidative stress induced by lipopolysaccharide via reducing reactive oxygen species and malondialdehyde, and elevating superoxide dismutase, catalase, and glutathione peroxidase. Meanwhile, the inflammation resulting from lipopolysaccharide was ameliorated through decreasing the pro-inflammatory cytokines including tumor necrosis factor-α, interleukin-1β, and interleukin-6. It was also found nuclear factor κB was inactivated by safflor yellow A. In addition, safflor yellow A downregulated cysteinyl aspartate specific proteinase-3 and Bcl-2-associated X protein and upregulated B-cell lymphoma-2 to inhibited apoptosis of Beas-2B cells induced by lipopolysaccharide. The activation of nuclear factor erythroid 2-related factor 2 was observed in Beas-2B cells, which was associated with the protective effects of safflor yellow A. And molecular docking elucidated safflor yellow A interacted with Kelch-like ECH-associated protein 1 to activate nuclear factor erythroid 2-related factor 2. These results can provide evidences for the discovery of novel therapy for further evaluation of safflor yellow A in the treatment of acute lung injury and acute respiratory distress syndrome. Graphical Abstract

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Bergamottin alleviates LPS-induced acute lung injury by inducing SIRT1 and suppressing NF-κB

Cited by 10 publications

References 36 publications

Bergamottin (Ber) ameliorates the progression of osteoarthritis via the Sirt1/NF-κB pathway

Bergamottin (Ber) ameliorates the progression of osteoarthritis via the Sirt1/NF-κB pathway

A Rapid In Vivo Toxicity Assessment Method for Antimicrobial Peptides

Safflor Yellow A Protects Beas-2B Cells Against LPS-Induced Injury via Activating Nrf2

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