The Effects of Quercetin on Acute Lung Injury and Biomarkers of Inflammation and Oxidative Stress in the Rat Model of Sepsis

Gerin, Fethullah; Şener, Ümit; Erman, Hayriye; Yılmaz, Ahsen; Aydın, Bayram; Armutçu, Ferah; Gürel, Ahmet

doi:10.1007/s10753-015-0296-9

Cited by 69 publications

(49 citation statements)

References 29 publications

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“…MPO is a marker of oxidative stress except for neutrophil infiltration. In addition, therapeutic strategies to protect the mitochondria by decreasing oxidative stress during sepsis have been recognized [48–50]. Our study showed that the levels of ROS detected by DHE fluorescence and MPO by immunofluorescence were markedly increased after the CLP treatment and decreased in the KO-CLP mice compared with the WT-CLP mice in the lung and liver.…”

Section: Discussionmentioning

confidence: 60%

5-HT Drives Mortality in Sepsis Induced by Cecal Ligation and Puncture in Mice

Zhang

Liu

et al. 2017

Mediators of Inflammation

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Sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated host response to infection with a high mortality. 5-Hydroxytryptamine (5-HT) is an important regulatory factor in inflammation. The aim of this study is to investigate the role of 5-HT on cecal ligation and puncture- (CLP-) induced sepsis in the mouse model. CLP was performed on C57B/6 wild-type (WT) mice and tryptophan hydroxylase 1 (TPH1) knockout (KO) mice. The results showed that the 5-HT-sufficient group mice had a significantly lower survival rate than the 5-HT-deficient group in CLP-induced sepsis and septic shock. The KO-CLP sepsis group received a lower clinical score than the WT-CLP sepsis group. Meanwhile, the body temperature of mice in the KO-CLP sepsis group was higher than that in the WT-CLP sepsis group and was much closer to the normal body temperature 24 hours after CLP. The tissue histopathology analysis revealed that 5-HT markedly exacerbated histological damages in the peritoneum, lung, liver, kidney, intestinal tissue, and heart in sepsis. Moreover, significant lower levels of TNF-α, IL-6, bacterial loads, MPO, and ROS were discovered in the KO-CLP sepsis group in contrast to the WT-CLP sepsis group. In conclusion, 5-HT drives mortality and exacerbates organ dysfunction by promoting serum cytokines and bacterial loads as well as facilitating oxidative stress in the process of sepsis.

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Section: Discussionmentioning

confidence: 60%

5-HT Drives Mortality in Sepsis Induced by Cecal Ligation and Puncture in Mice

Zhang

Liu

et al. 2017

Mediators of Inflammation

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“…Finally, we found that CFH independently increases lung F 2 -isoprostanes and isofurans, markers of increased oxidant stress, in this polymicrobial sepsis model. Increased oxidant stress in the lung during sepsis has been well described in cecal ligation and puncture models [40][41][42][43] but none of these studies examined CFH as a potential mediator of oxidant injury. The CLP model of sepsis also has elevated circulating CFH, raising the possibility that some of its oxidant effects could be due to CFH [44].…”

Section: Discussionmentioning

confidence: 99%

Cell-free hemoglobin increases inflammation, lung apoptosis, and microvascular permeability in murine polymicrobial sepsis

et al. 2020

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Increased endothelial permeability is central to the pathogenesis of sepsis and leads to organ dysfunction and death but the endogenous mechanisms that drive increased endothelial permeability are not completely understood. We previously reported that cell-free hemoglobin (CFH), elevated in 80% of patients with sepsis, increases lung microvascular permeability in an ex vivo human lung model and cultured endothelial cells. In this study, we augmented a murine model of polymicrobial sepsis with elevated circulating CFH to test the hypothesis that CFH increases microvascular endothelial permeability by inducing endothelial apoptosis. Mice were treated with an intraperitoneal injection of cecal slurry with or without a single intravenous injection of CFH. Severity of illness, mortality, systemic and lung inflammation, endothelial injury and dysfunction and lung apoptosis were measured at selected time points. We found that CFH added to CS increased sepsis mortality, plasma inflammatory cytokines as well as lung apoptosis, edema and inflammation without affecting large vessel reactivity or vascular injury marker concentrations. These results suggest that CFH is an endogenous mediator of increased endothelial permeability and apoptosis in sepsis and may be a promising therapeutic target. OPEN ACCESS Citation: Meegan JE, Shaver CM, Putz ND, Jesse JJ, Landstreet SR, Lee HNR, et al. (2020) Cell-free hemoglobin increases inflammation, lung apoptosis, and microvascular permeability in murine polymicrobial sepsis. PLoS ONE 15(2):

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“…We have already demonstrated that ExoS can cause an in ammatory response and improve clearance in the lungs in vitro and vivo [26]. It is also well known that quercetin is a useful substance for various diseases [27][28][29]. However, it is not known whether quercetin prevents disease by inhibiting the expression of ExoS due to infection of the host via T3SS of P. aeruginosa.…”

Section: Discussionmentioning

confidence: 99%

Quercetin attenuates the production of pro-inflammatory cytokines in H292 human lung epithelial cells infected with Pseudomonas aeruginosa, by modulating ExoS production

Ahn

Park

Jang

et al. 2020

Preprint

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Background: The type three secretion system (T3SS) is a major virulence system of Pseudomonas aeruginosa (P. aeruginosa). The effector protein Exotoxin S (ExoS) produced by P. aeruginosa is secreted into the host cells via the T3SS. For the purpose of screening the inhibitors with regard to ExoS secretion, we developed the sandwich-type enzyme-linked immunosorbent assay (ELISA) system. From the initial screening, quercetin was selected because it has the prominent effect of ExoS inhibition and also is known to have anti-inflammatory and antioxidant effects on mammalian cells.Results: In this study, we investigated the effects of quercetin on the expression and secretion of ExoS using the ELISA and Western blot analysis methods. The results showed that the secretion of ExoS was significantly decreased by 10, 20uM quercetin. Also, pscF and popD, which are composed of the T3SS needle, are reduced by quercetin at the mRNA level, and we confirmed the inhibitory effect of quercetin on cytokines in P. aeruginosa-infected H292 cells by real-time polymerase chain reaction (PCR). Conclusion: Collectively, quercetin inhibits the secretion of ExoS by reducing both ExoS production and the expression of the needle protein of T3SS. Furthermore, these results suggest that quercetin has the potential to be used as an anti-toxic treatment for the disease caused by P. aeruginosa infection.

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The Effects of Quercetin on Acute Lung Injury and Biomarkers of Inflammation and Oxidative Stress in the Rat Model of Sepsis

Cited by 69 publications

References 29 publications

5-HT Drives Mortality in Sepsis Induced by Cecal Ligation and Puncture in Mice

5-HT Drives Mortality in Sepsis Induced by Cecal Ligation and Puncture in Mice

Cell-free hemoglobin increases inflammation, lung apoptosis, and microvascular permeability in murine polymicrobial sepsis

Quercetin attenuates the production of pro-inflammatory cytokines in H292 human lung epithelial cells infected with Pseudomonas aeruginosa, by modulating ExoS production

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