Hemin inhibits NLRP3 inflammasome activation in sepsis-induced acute lung injury, involving heme oxygenase-1

Luo, Yunpeng; Jiang, Lei; Kang, Kai; Fei, Dong-sheng; Meng, Xianglin; Nan, Chuanchuan; Pan, Shangha; Zhao, Mingran; Zhao, Mingyan

doi:10.1016/j.intimp.2014.02.017

Cited by 137 publications

(105 citation statements)

References 39 publications

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“…13 Inhibition of ROS production presumably suppresses inflammasome activation. 40 Another previous study showed that quercetin can increase superoxide dismutase levels, reduce malondialdehyde production and protect against SCI through regulation of secondary oxidative stress. 23 We showed that SCI induction increases ROS levels; however, quercetin obviously inhibited this process.…”

Section: Discussionmentioning

confidence: 98%

Quercetin suppresses NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury

et al. 2016

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Study design: Randomized experimental study. Objectives: To investigate the molecular mechanisms of quercetin in spinal cord injury (SCI) rats. Setting: China. Methods: One hundred female Sprague-Dawley rats were randomly assigned into four groups: sham group, SCI group, SCI+Vehicle (Veh) group, and the SCI+Quercetin (Que) group. The influences of quercetin on proinflammatory cytokine levels, histological changes and locomotion scale were estimated. Results: SCI significantly promoted nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome activation and increased proinflammatory cytokine productions in the SCI group as compared with the sham group. Quercetin administration significantly decreased reactive oxygen species production, inhibited NLRP3 inflammasome activation and reduced inflammatory cytokine levels. Moreover, quercetin administration attenuated histopathology and promoted locomotion recovery. Conclusion: Quercetin can attenuate tissue damage and improve neurological function recovery, and the mechanism may be related to the inhibition of NLRP3 inflammasome activation.

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Section: Discussionmentioning

confidence: 98%

Quercetin suppresses NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury

et al. 2016

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“…Hemin-induced HO-1 inhibits NLRP3 inflammasome formation in acute lung injury [68]. Induction of HO-1 attenuates lipopolysaccharide-induced inflammasome formation in human gingival epithelial cells [69].…”

Section: Discussionmentioning

confidence: 99%

Heme Oxygenase-1 Promotes Neuron Survival through Down-Regulation of Neuronal NLRP1 Expression after Spinal Cord Injury

Lin

Wang

2017

The Spine Journal

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“…Our study found that NLRP3 activation is involved in the pathogenesis of LPS-induced PRTC cells' apoptosis and CLP-induced sepsis. In fact, NLRP3 activation has been demonstrated to have a contribution to multiple disease by increasing IL-1β and IL-18 secretion and amplifying the inﬂammatory response, including acute lung injury [10] and acute liver failure [38]. Renal inflammation is a universal response to infectious and noninfectious triggers [39].…”

Section: Discussionmentioning

confidence: 99%

“…NLRP3 contributes to renal ischemia-reperfusion injury by a direct effect on renal tubular epithelium and that shows a tissue-speciﬁc role in which leukocyte-associated NLRP3 is associated with tubular apoptosis [8,9]. Evidence also showed that dysregulated NLRP3 inﬂammasome activation participates in the pathogenesis of sepsis and acute lung injury [10]. However, in sepsis induced-AKI, the role of NLRP3 is yet to be researched.…”

Section: Introductionmentioning

confidence: 99%

Mangiferin Attenuate Sepsis-Induced Acute Kidney Injury via Antioxidant and Anti-Inflammatory Effects

Peng

Zhu

et al. 2014

Am J Nephrol

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Background: Acute kidney injury (AKI) is a frequent and serious complication of sepsis. A growing body of evidence now suggests that inflammatory reactions and tubular dysfunction induced by oxidative stressinvolved in the mechanisms of the disease. This study aimed to determine the role of anti-inflammatory and anti-oxidant activities of mangiferin (MA) in sepsis-induced AKI. Methods: We investigated the effects of MA on apoptosis of rat kidney proximal tubular cell (RPTC), together with renal function and morphological alterations of mice undergoing cecal-ligation and puncture (CLP). The levels of oxidative stress in kidney tissues were also determined. Moreover, we mainly focus on the effects of MA in regulating the production of NLRP3 and Nrf2 in the present study. Results: The exposure to LPS (5 Vg/ml) yielded a signiﬁcant increase of apoptosis in RPTC cells, which was largely inhibited by MA pretreatment. MA attenuates renal dysfunction and ameliorates the morphological changes in the septic mice induced by CLP. MA inhibits oxidative stress, decreases serum levels of IL-1F and IL-18, and prevents tubular epithelial cells apoptosis in kidneys of CLP mice model. Data in this study also suggest that MA promotes Nrf2 expression and suppresses renal NLRP3 inflammasome activation. Conclusion: In summary, MA protects against sepsis-induced AKI through NLRP3 inflammasome inhibition and Nrf2 up-regulation. Thus, the mangiferin could thus be a promising candidate for development of a multi-potent drug. i 2014 S. Karger AG, Basel

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Hemin inhibits NLRP3 inflammasome activation in sepsis-induced acute lung injury, involving heme oxygenase-1

Cited by 137 publications

References 39 publications

Quercetin suppresses NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury

Quercetin suppresses NLRP3 inflammasome activation and attenuates histopathology in a rat model of spinal cord injury

Heme Oxygenase-1 Promotes Neuron Survival through Down-Regulation of Neuronal NLRP1 Expression after Spinal Cord Injury

Mangiferin Attenuate Sepsis-Induced Acute Kidney Injury via Antioxidant and Anti-Inflammatory Effects

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