New thiazolidinedione LPSF/GQ-2 inhibits NFκB and MAPK activation in LPS-induced acute lung inflammation

Santos, Laise Aline Martins dos; Rodrigues, Gabriel Barros; Mota, Fernanda Virgínia Barreto; França, Maria Eduarda Rocha de; Barbosa, Karla Patrícia de Souza; Oliveira, W.; Rocha, Sura Wanessa Santos; Lós, Deniele Bezerra; Silva, Amanda Karolina Soares; Silva, Teresinha Gonçalves da; Peixoto, Christina Alves

doi:10.1016/j.intimp.2018.02.011

Cited by 21 publications

(9 citation statements)

References 43 publications

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“…The production of chemokines in keratinocytes requires the activation of several signaling pathways, especially mitogen-activated protein kinase and NF-kB pathways (Santos et al, 2018;, the activity of which were further evaluated in NHK treated with rhHMGB1 in our study. Our western blotting assays showed that the phosphorylation levels of p65 and extracellular signaleregulated kinase (ERK) were upregulated by rhHMGB1 in NHK (Figure 4a), but two other mitogen-activated protein kinase pathways including p38 and JNK were not activated by rhHMGB1 (see Supplementary Figure S3 online).…”

Section: Rage Is the Key Receptor That Mediates The Secretion Of Cxclmentioning

confidence: 99%

Oxidative Stress–Induced HMGB1 Release from Melanocytes: A Paracrine Mechanism Underlying the Cutaneous Inflammation in Vitiligo

Cui

Zhang

et al. 2019

Journal of Investigative Dermatology

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Vitiligo is a cutaneous depigmentation disorder caused by the destruction of epidermal melanocytes. The generation and the skin infiltration of autoreactive CD8 þ cytotoxic T cells triggered by oxidative stress play a critical role in vitiligo. High-mobility group protein B1 (HMGB1) is a classic damage-associated molecular pattern molecule with strong proinflammatory effects in inflammatory reactions. A previous study reported an enhanced expression of HMGB1 in vitiligo lesions, but the role of HMGB1 in cutaneous inflammation of vitiligo is still unknown. In the present study, we initially found that HMGB1 was released from the nucleus of melanocytes in vitiligo perilesional skin. Furthermore, cultured normal human melanocytes could release HMGB1 under treatment with hydrogen peroxide. Moreover, HMGB1 facilitated the secretion of CXCL16 and IL-8 from keratinocytes by binding to the receptor for advanced glycation end products and activating NF-kB and extracellular signaleregulated kinase signaling pathways. Subsequently, HMGB1 led to the formation of chemotaxis for the migration of CD8 þ T cells from patients with vitiligo by increasing the release of CXCL16 from keratinocytes. Additionally, HMGB1 promoted the maturation of dendritic cells from patients with vitiligo. Altogether, our study demonstrates that HMGB1 released from melanocytes contributes to the formation of oxidative stresseinduced autoimmunity in vitiligo.

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Section: Rage Is the Key Receptor That Mediates The Secretion Of Cxclmentioning

confidence: 99%

Oxidative Stress–Induced HMGB1 Release from Melanocytes: A Paracrine Mechanism Underlying the Cutaneous Inflammation in Vitiligo

Cui

Zhang

et al. 2019

Journal of Investigative Dermatology

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“…33,34 Several studies on animal models of ALI have demonstrated a critical role of NF-κB signalling, and the involvement of proteins such as p-IKK, IKKα/β, p-P65, P65, p-IκBα and IκBα in ALI have been uncovered. 35–37 In this mouse model of ALI, phosphorylation of IKK, P65 and IκBα were enhanced with LPS instillation, and PSS post treatment markedly decreased these three phosphorylated proteins. These results suggest that PSS post treatment protects against LPS-induced ALI by suppressing the activation of the NF-κB signalling pathway.…”

Section: Discussionmentioning

confidence: 85%

Propylene glycol alginate sodium sulphate attenuates LPS-induced acute lung injury in a mouse model

Zhao

Liu

et al. 2019

Innate Immun

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Propylene glycol alginate sodium sulphate, a sulphated polysaccharide, has been used to treat hyperlipidaemia and ischaemia–reperfusion injury of liver. This study aimed to investigate the effect of propylene glycol alginate sodium sulphate on LPS-induced acute lung injury. Propylene glycol alginate sodium sulphate was injected intraperitoneally into male C57BL/6 mice with or without LPS administration. Survival rates were calculated. Serum, bronchoalveolar lavage fluid and lung tissues were collected to determine lung histology, wet/dry ratio, Evans blue albumin permeability, protein levels, the counts of immune cells and the levels of inflammatory cytokines and chemokines. Serum alanine aminotransferase, aspartate transaminase, creatinine and blood urea nitrogen levels were also measured. Additionally, NF-κB signalling was detected in the lung. Propylene glycol alginate sodium sulphate treatment significantly improved the survival of mice suffering from LPS. Lung histological injury, wet/dry ratio, Evans blue albumin permeability, neutrophils and the inflammatory cytokines and chemokines were significantly reduced by propylene glycol alginate sodium sulphate treatment. NF-κB signalling was significantly inhibited by propylene glycol alginate sodium sulphate in the lung of mice subjected to LPS. Furthermore, serum alanine aminotransferase, aspartate transaminase, creatinine and blood urea nitrogen levels were also significantly decreased after propylene glycol alginate sodium sulphate administration. This study suggests that NF-κB signalling and inhibition of pro-inflammatory cytokines, chemokines and neutrophil accumulation may be involved in the process of acute lung injury attenuation by propylene glycol alginate sodium sulphate.

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“…Intranasal instillation of LPS is a classical and widely used method to construct ALI model (Hsu et al, 2015;Huang et al, 2015). This method can better simulate the pathological process of ALI, control the degree of ALI, only cause local severe injury, and will not cause systemic inflammatory response and organ failure (Santos et al, 2018). Recently, a study has confirmed that PTER can protect female mice in this ALI model (Yang et al, FIGURE 10 | PTER activated the protein expressions of Nrf2/HO-1 signaling pathway in the lungs.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Pterostilbene on Lipopolysaccharide-Induced Acute Lung Injury in Mice by Inhibiting NF-κB and Activating Nrf2/HO-1 Signaling Pathways

et al. 2021

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Pterostilbene (PTER) is a kind of stilbene compound with biological activity isolated from plants such as red sandalwood, blueberry and grape. It has anti-tumor, anti-bacterial, anti-oxidation and other pharmacological activities. However, the underlying mechanism of the protective effect of PTER on lipopolysaccharide (LPS)-induced acute lung injury (ALI) remained not clarified. In this study, LPS was used to establish a mouse model of ALI. Bronchoalveolar lavage fluid (BALF) was collected for inflammatory cells, and the wet-to-dry weight ratio of the lungs was measured. The activities of myeloperoxidase (MPO), antioxidant indexes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and oxidation index such as malondialdehyde (MDA) in lung tissues of mice were measured by the corresponding kits. The levels of Cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), TNF-α, IL-6 and IL-1β in lung tissues of mice were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The activities of Nrf2, HO-1, p-p65 and p-IκB were determined by western blotting. The results showed that the model of LPS-induced ALI was successfully replicated, and it was found that PTER could significantly improve the pathological degree of ALI such as sustained the integrity of the lung tissue structure, alleviated pulmonary interstitial edema and alveolar wall thickening, reduced infiltrated inflammatory cells. PTER could decrease the number of inflammatory cells and obviously inhibit the increase of W/D ratio caused by LPS. PTER could also significantly reduce LPS-induced MPO and MDA, and increase LPS-decreased SOD, CAT and GSH-Px in the lungs. In addition, it was also found that PTER has the ability to decrease LPS-induced production of COX-2, iNOS, TNF-α, IL-6 and IL-1β. The underlying mechanism involved in the protective effect of PTER on ALI were via activating Nrf2 and HO-1, and inhibiting the phosphorylation of p65 and IκB. These results suggested that PTER can protect LPS-induced ALI in mice by inhibiting inflammatory response and oxidative stress, which provided evidence that PTER may be a potential therapeutic candidate for LPS-induced ALI intervention.

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New thiazolidinedione LPSF/GQ-2 inhibits NFκB and MAPK activation in LPS-induced acute lung inflammation

Cited by 21 publications

References 43 publications

Oxidative Stress–Induced HMGB1 Release from Melanocytes: A Paracrine Mechanism Underlying the Cutaneous Inflammation in Vitiligo

Oxidative Stress–Induced HMGB1 Release from Melanocytes: A Paracrine Mechanism Underlying the Cutaneous Inflammation in Vitiligo

Propylene glycol alginate sodium sulphate attenuates LPS-induced acute lung injury in a mouse model

Protective Effects of Pterostilbene on Lipopolysaccharide-Induced Acute Lung Injury in Mice by Inhibiting NF-κB and Activating Nrf2/HO-1 Signaling Pathways

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