Protective effect of Apremilast against LPS-induced acute lung injury via modulation of oxidative stress and inflammation

Al-Harbi, Naif O.; Imam, Faisal; Al-Harbi, M. M.; Al-Jeryan, Khaldoon; Al‐Shabanah, Othman A.; Alhosaini, Khaled; Alqahtani, Lamya Saif; Afzal, Muhammad; Anwer, Md. Khalid; Aldossari, Abdullah A.; Alanazi, Mohammed M.; Alsanea, Sary; Assiri, Mohammed A.

doi:10.1016/j.sjbs.2022.02.023

Cited by 3 publications

(9 citation statements)

References 73 publications

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“…The most common approach to treat the ALI, such as supportive care, which may include mechanical ventilation and medications to manage the inflammation and infection. The ultimately goal of the treatment to support the protective function to the lungs and also provide the preventive effect against damage 7–9 …”

Section: Introductionmentioning

confidence: 99%

“…Inflammation is a complex immune response that is initiated in response to tissue damage or injury. The inflammatory process involve in the activation of immune cells (macrophages and neutrophils) and also secrete the inflammatory mediators like chemokines and cytokines 3,8 . These mediators help to recruit and activate the additional immune cells in the site of injury and also contribute to the inflammation 8,20 .…”

Section: Introductionmentioning

confidence: 99%

“…The inflammatory process involve in the activation of immune cells (macrophages and neutrophils) and also secrete the inflammatory mediators like chemokines and cytokines 3,8 . These mediators help to recruit and activate the additional immune cells in the site of injury and also contribute to the inflammation 8,20 . Chronic inflammation, in which the inflammation response becomes prolonged or uncontrolled, can lead to tissue damage and contribute to the development of various diseases and disorders 8 .…”

Section: Introductionmentioning

confidence: 99%

“…These mediators help to recruit and activate the additional immune cells in the site of injury and also contribute to the inflammation 8,20 . Chronic inflammation, in which the inflammation response becomes prolonged or uncontrolled, can lead to tissue damage and contribute to the development of various diseases and disorders 8 . Chronic inflammation, in which the inflammatory response becomes persistent or uncontrolled, is a significant factor in the development and progression of many chronic diseases in humans.…”

Section: Introductionmentioning

confidence: 99%

“…Chronic inflammation, in which the inflammatory response becomes persistent or uncontrolled, is a significant factor in the development and progression of many chronic diseases in humans. These diseases include cancers, autoimmune diseases, metabolic disorders, and organ dysfunction 8,21 . Antioxidant compounds have been shown to have anti‐inflammatory effects and may help to modulate cytokine production and control the progression of parenchymal inflammation in the lungs 8 .…”

Section: Introductionmentioning

confidence: 99%

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Gossypin exert lipopolysaccharide induced lung inflammation via alteration of Nrf2/HO‐1 and NF‐κB signaling pathway

Huang

Wang²,

Hussain

et al. 2023

Environmental Toxicology

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Acute Lung Injury (ALI) is a critical medical condition that induces the injury into the lung tissue, resulting in decreased the oxygen levels in the circulation and finally causes the respiratory failure. In this study, we try to made effort for scrutinized the preventive effect of gossypin against lipopolysaccharide (LPS) induced lung inflammation and explore the underlying mechanism. LPS (7.5 mg/kg) was used for induction the lung inflammation in the rats and rats were received the oral administration of gossypin (5, 10 and 15 mg/kg). The wet to dry weight lung ratio and lung index were estimated. The bronchoalveolar lavage fluid (BALF) were collected to determination the inflammatory cells, total protein, macrophages and neutrophils. ELISA kits were used for the estimation of antioxidant, inflammatory cytokines, inflammatory parameters, nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) parameters. Finally, we used the lung tissue for scrutinize the alteration in the lung histopathology. Gossypin treatment significantly (p < .001) reduced the W/D ratio of lung tissue and lung index. Gossypin significantly (p < .001) decreased the total cells, neutrophils, macrophages and total protein in BALF. It is also altered the level of inflammatory cytokines, antioxidant and inflammatory parameters, respectively. Gossypin improved the level of Nrf2 and HO-1 at dose dependent manner. Gossypin treatment remarkably enhance the ALI severity via balancing the structural integrity of lung tissue, decrease the thickness of the alveolar wall, decline the pulmonary interstitial edema, and number of inflammatory cells in the lung tissue. Gossypin is a

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Gossypin exert lipopolysaccharide induced lung inflammation via alteration of Nrf2/HO‐1 and NF‐κB signaling pathway

Huang

Wang²,

Hussain

et al. 2023

Environmental Toxicology

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LncRNA HOTTIP promotes LPS‐induced lung epithelial cell injury by recruiting DNMT1 to epigenetically regulate SP‐C

Li,

Gao

et al. 2024

Journal of Cell Communication and Signaling

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The objective of this study was to elucidate the involvement of the long noncoding RNA (lncRNA) HOTTIP in acute lung injury and understand the underlying mechanisms. Relevant expression of mRNAs and proteins were assessed by qRT‐PCR and western blot assays. Cell viability was determined by employing the CCK‐8 assay, and apoptosis was quantified through TUNEL staining. The concentration of inflammatory factors was measured by ELISA. The degree of DNA methylation was quantified through MSP assay. The interaction between HOTTIP and DNA methyltransferase 1 (DNMT1) was examined by RIP assay. LPS upregulated HOTTIP, whereas downregulated SP‐C level in AEC II cells. HOTTIP knockdown inhibited LPS‐induced apoptosis and the secretion of inflammatory cytokines (TNF‐α, IL‐1β and IL‐6) in AEC II cells. Mechanistically, HOTTIP recruited DNMT1 to the SP‐C promoter, thereby facilitating DNA methylation of SP‐C and suppressing its expression. Additionally, inhibitory of SP‐C reversed the effects of HOTTIP or DNMT1 knockdown on apoptosis and inflammation in AEC II cells induced by LPS. HOTTIP recruited DNMT1 to epigenetically inhibit SP‐C expression, leading to the promotion of lung epithelial cell injury caused by LPS, suggesting that targeting HOTTIP may be an effective strategy for the therapy of lung epithelial cell injury.

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Irigenin attenuates lipopolysaccharide-induced acute lung injury by inactivating the mitogen-activated protein kinase (MAPK) signaling pathway

et al. 2023

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Acute lung injury (ALI) is a serious pulmonary inflammation disease with high mortality. Irigenin, an isoflavone from rhizomes of the Belamcanda chinensis, has been reported to exert anti-inflammatory, anti-oxidative, and anti-apoptotic activities in several diseases. However, it is still unclear whether irigenin can exert a beneficial effect in ALI. A network pharmacology method was utilized to predict the hub targets and potential therapeutic mechanisms of irigenin against ALI. Lipopolysaccharide (LPS) was used to establish the mice model of ALI for evaluating the effects of irigenin. According to the protein-protein interaction (PPI) network, we identified EGFR, HRAS, AKT1, SRC, and HSP90AA1 as the top five significant genes. Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) enrichment assays showed that irigenin might affect inflammatory response, cytokine production, and cell death by the mitogen-activated protein kinase (MAPK ) signaling pathway. In vivo experiment results manifested that irigenin decreased pathological changes, lung Wet/Dry weight ratio, and total protein content in bronchoalveolar lavage fluid (BALF). Irigenin also reduced the production of inflammatory cytokines, including tumor necrosis factor-a (TNF-a), interleukin-1β (IL-1β), interleukin-6 (IL-6), and interleukin-18 (IL-18), and neutrophil infiltration. Additionally, irigenin inhibited pulmonary apoptosis in LPS-treated ALI mice. Moreover, LPS-induced phosphorylation of p38, JNK, and ERK was significantly abated due to the treatment of irigenin. In summary, irigenin ameliorates LPS-induced ALI by suppressing pulmonary inflammation and apoptosis via inactivation of the MAPK signaling pathway. These findings indicated the therapeutic potential of irigenin in ALI.

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Protective effect of Apremilast against LPS-induced acute lung injury via modulation of oxidative stress and inflammation

Cited by 3 publications

References 73 publications

Gossypin exert lipopolysaccharide induced lung inflammation via alteration of Nrf2/HO‐1 and NF‐κB signaling pathway

Gossypin exert lipopolysaccharide induced lung inflammation via alteration of Nrf2/HO‐1 and NF‐κB signaling pathway

LncRNA HOTTIP promotes LPS‐induced lung epithelial cell injury by recruiting DNMT1 to epigenetically regulate SP‐C

Irigenin attenuates lipopolysaccharide-induced acute lung injury by inactivating the mitogen-activated protein kinase (MAPK) signaling pathway

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