Ameliorative effect of gossypin against acute lung injury in experimental sepsis model of rats

Çınar, İrfan; Şirin, Büşra; Aydin, Pelin; Toktay, Erdem; Çadırcı, Elif; Halici, Iclal; Halıcı, Zekai

doi:10.1016/j.lfs.2019.02.039

Cited by 63 publications

(57 citation statements)

References 74 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For example, in cecal ligation and puncture‐induced sepsis model, gossypin protects against sepsis‐mediated ALI via repressing oxidative stress, inflammation derived from NF‐κB/NLRP3 activations. [ 31 ] Here, we also observed that NLRP3 inflammasome was markedly activated following sepsis induced ALI both in vivo and in vitro.…”

Section: Discussionsupporting

confidence: 61%

Downregulating lncRNA PRNCR1 ameliorates LPS‐induced pulmonary vascular endothelial cell injury by modulating miR‐330‐5p/TLR4 axis

Sun

Zhu

et al. 2020

J Biochem & Molecular Tox

View full text Add to dashboard Cite

Pulmonary vascular endothelial cell (PVEC) injury following acute lung injury or acute respiratory distress syndrome seriously affects disease development. Recently, accumulating evidence has suggested that long noncoding RNA (lncRNA) exerts significant effects in vascular endothelial cell injury. However, PRNCR1, a novel lncRNA, remains scarcely understood in terms of its functions in PVEC injury. Both in vivo and in vitro models of PVEC injury were constructed by lipopolysaccharide (LPS) administration. The relative expressions of PRNCR1, miR‐330‐5p, and TLR4 were detected by quantitative reverse transcription‐polymerase chain reaction, Western blot, and immunohistochemistry. Besides, gain and loss assays of PRNCR1/miR‐330‐5p were conducted to verify their effects on LPS‐induced PVEC injury. Cell Counting Kit‐8 assay used to measure cell viability and flow cytometry was used to detect apoptosis. Besides, the protein levels of caspase 3, nuclear factor‐κB (NF‐κB), and inflammatory cytokines (including tumor necrosis factor‐α, interleukin‐1β [IL‐1β], and IL‐6) were evaluated via Western blot and enzyme‐linked immunosorbent assay. Moreover, a dual‐luciferase activity experiment and RNA immunoprecipitation were applied to confirm the targeting relationship between PRNCR1 and miR‐330‐5p, miR‐330‐5p, and TLR4. PRNCR1 and TLR4 levels were significantly upregulated in LPS‐treated PVEC, both in vivo and in vitro, while miR‐330‐5p were downregulated. Inhibiting PRNCR1 or overexpressing miR‐330‐5p markedly attenuated LPS‐induced PVEC injury, expressions of TLR4, NF‐κB, and inflammatory cytokines. Mechanistically, PRNCR1 functioned as a competitive endogenous RNA by sponging miR‐330‐5p and then promoting TLR4 expression. PRNCR1 was upregulated in LPS‐induced PVEC and aggravated its injury via modulating the miR‐330‐5p/TLR4 axis.

show abstract

Section: Discussionsupporting

confidence: 61%

Downregulating lncRNA PRNCR1 ameliorates LPS‐induced pulmonary vascular endothelial cell injury by modulating miR‐330‐5p/TLR4 axis

Sun

Zhu

et al. 2020

J Biochem & Molecular Tox

View full text Add to dashboard Cite

show abstract

“…The systemic inflammatory response to severe infection was mainly mediated by activation of NF-κB. 15,16 In the present study, increased P-IκB-α and P-NF-κB p65 protein levels in LPS-stimulated rats was rescued by sufentanil administration. This finding suggested that sufentanil inhibited the activation of NF-κB and reduced the production of TNF-α and IL-6, thus playing an anti-inflammatory and protective role in ALI.…”

Section: Discussionsupporting

confidence: 58%

In vitro and in vivo assessment of the protective effect of sufentanil in acute lung injury

2021

View full text Add to dashboard Cite

Objectives To investigate the mechanisms underlying the protective effect of sufentanil against acute lung injury (ALI). Material and Methods Rats were administered lipopolysaccharide (LPS) by endotracheal instillation to establish a model of ALI. LPS was used to stimulate BEAS-2B cells. The targets and promoter activities of IκB were assessed using a luciferase reporter assay. Apoptosis of BEAS-2B cells was evaluated by terminal deoxynucleotidyl transferase dUTP nick end labeling. Results Sufentanil treatment markedly reduced pathological changes in lung tissue, pulmonary edema and secretion of inflammatory factors associated with ALI in vivo and in vitro. In addition, sufentanil suppressed apoptosis induced by LPS and activated NF-κB both in vivo and in vitro. Furthermore, upregulation of high mobility group box protein 1 (HMGB1) protein levels and downregulation of miR-129-5p levels were observed in vivo and in vitro following sufentanil treatment. miR-129-5p targeted the 3ʹ untranslated region and its inhibition decreased promoter activities of IκB-α. miR-129-5p inhibition significantly weakened the protective effect of sufentanil on LPS-treated BEAS-2B cells. Conclusion Sufentanil regulated the miR-129-5p/HMGB1 axis to enhance IκB-α expression, suggesting that sufentanil represents a candidate drug for ALI protection and providing avenues for clinical treatment.

show abstract

“…Sepsis, a common acute and critical disease, is mainly characterized by sustained hypotension, metabolic acidosis, and systemic inflammatory response syndrome [1]. It can lead to multiple organ injuries and even death.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Coenzyme Q Protects Sepsis-Induced Acute Lung Injury by Activating PI3K/Akt/GSK-3β/mTOR Pathway in Rats

Ren

Zeng

2019

BioMed Research International

View full text Add to dashboard Cite

The aim of our study was to assess the effects of mitochondrial coenzyme Q (MitoQ) on sepsis-induced acute lung injury (ALI) and investigate its possible mechanisms. The cecal ligation and puncture (CLP) method was used to establish a septic ALI model. Rats were randomly divided into Con group, CLP group, MitoQ group, and MitoQ + LY294002 group. The survival rate of the rats was recorded, and the survival rate curve was plotted. Moreover, the ratio of wet/dry weight (W/D) in lung tissue was measured. The activity of myeloperoxidase (MPO) was measured by using the MPO colorimetric activity assay kit. The levels of high-mobility group box 1 (HMGB1) and interleukin-6 (IL-6), macrophage inflammatory protein 2 (MIP2), and keratinocyte chemoattractant (KC) were analyzed by ELISA. The histopathological changes were measured by HE staining, and the lung injury was scored. TUNEL assay was applied to detect the apoptotic cells in lung tissue. The protein expressions were detected by western blot. MitoQ increased the survival rate and alleviated pulmonary edema in septic ALI rats. In addition, MitoQ inhibited the MPO activity and decreased the levels of HMGB1 and IL-6. After treatment with MitoQ, alveolar wall edema, inflammatory cell infiltration, and red blood cell exudation were relieved. MitoQ inhibited cell apoptosis in lung tissue of septic ALI rats. Meanwhile, MitoQ treatment remarkedly increased the expression of p-Akt, p-GSK-3β, and p-mTOR but decreased Bax, caspase-3, caspase-9, Beclin-1, and LC-3II/LC-3I. The effects of MitoQ were significantly reversed by the PI3K inhibitor (LY294002). Our study demonstrated that MitoQ could protect sepsis-induced acute lung injury by activating the PI3K/Akt/GSK-3β/mTOR pathway in rats.

show abstract

Ameliorative effect of gossypin against acute lung injury in experimental sepsis model of rats

Cited by 63 publications

References 74 publications

Downregulating lncRNA PRNCR1 ameliorates LPS‐induced pulmonary vascular endothelial cell injury by modulating miR‐330‐5p/TLR4 axis

Downregulating lncRNA PRNCR1 ameliorates LPS‐induced pulmonary vascular endothelial cell injury by modulating miR‐330‐5p/TLR4 axis

In vitro and in vivo assessment of the protective effect of sufentanil in acute lung injury

Mitochondrial Coenzyme Q Protects Sepsis-Induced Acute Lung Injury by Activating PI3K/Akt/GSK-3β/mTOR Pathway in Rats

Contact Info

Product

Resources

About