The protective effect of Luteolin on myocardial ischemia/reperfusion (I/R) injury through TLR4/NF-κB/NLRP3 inflammasome pathway

Zhang, Xu; Du, Qianming; Yang, Yan; Wang, Jianbo; Dou, Shuping; Liu, Chao; Duan, Junguo

doi:10.1016/j.biopha.2017.05.033

Cited by 126 publications

(91 citation statements)

References 22 publications

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“…It can be extrapolated that the increase in serum level of XO was an indication of hyperuricemia which is major pointer to oxidative stress, inflammation, renal damage and hypertension, arteriosclerosis, and myocardial infarction . The ability of Luteolin to inhibit the activities of MPO and XO confirms the antioxidant, anti‐inflammatory, cardioprotective and reno‐protective effect of Luteolin . Cardiovascular complication was also evident from the ECG as indicated with increased P wave duration, prolonged QRS duration, QT and QTc intervals, R amplitude, and increase heart rate.…”

Section: Discussionmentioning

confidence: 89%

Luteolin‐mediated Kim‐1/NF‐kB/Nrf2 signaling pathways protects sodium fluoride‐induced hypertension and cardiovascular complications

et al. 2018

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The use of sodium fluoride (NaF) as a major ingredient for tooth paste, mouth wash, and mouth rinse has become inevitable in our day-to-day life. However, flavonoids such as Luteolin might be of great value in the prevention of toxicity associated with accidental or inevitable ingestion of NaF. In the study, 40 male Wistar albino rats were randomly divided into four groups with 10 rats in a group. Group A was the control group and received normal saline, Group B was exposed to NaF at 300 ppm (300 mg/L) in drinking water daily for a week, Groups C and D were exposed to 300 ppm (300 mg/L) of NaF and coadministered with Luteolin orally daily at a dosage of 100 mg/kg and 200 mg/kg for the same time point. Our results indicated that NaF caused significant increases in systolic blood pressure, diastolic blood pressure, mean arterial pressure, malondialdehyde, protein carbonyl, myeloperoxidase, advanced oxidative protein products, together with significant reductions in glutathione peroxidase, superoxide dismutase, catalase, glutathione reductase, reduced glutathione, and nitric oxide (NO) bioavailability. The electrocardiogram results showed that NaF alone caused significant prolongation of QT and QTc intervals. Immunohistochemistry revealed that NaF caused increase expressions of Kidney injury marker 1 (Kim-1), nuclear factor 518 BioFactors Research Communication kappa bet (NF-κB), nuclear factor erythroid 2-related factors 2 (Nrf2), and cardiac troponin I (CTnI). Together, Luteolin coadministration with NaF improved NO bioavailability, reduced high blood pressure, markers of oxidative stress, reversed prolongation of QT and QTc intervals, and lowered the expressions of Kim-1, NF-κB, and CTnI. © 2018 BioFactors, 44(6):518-531, 2018

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Section: Discussionmentioning

confidence: 89%

Luteolin‐mediated Kim‐1/NF‐kB/Nrf2 signaling pathways protects sodium fluoride‐induced hypertension and cardiovascular complications

et al. 2018

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“…Some endogenous ligands activate NF-κB through the activation of TLR4 receptor, resulting in the release of pro-inflammatory factors such as TNF-a, IL-1β, and others [26]. The increased production and release of pro-inflammatory factors further activates NF-κB, which induces the NLRP3 inflammasome, leading to the continuous amplification of initial inflammatory signals, thus causing the so-called inflammatory waterfall effect [27,28]. This study found that TLR4/ MyD88/NF-κB signaling was significantly activated after CME, and participated in the inflammatory responses of the myocardium, resulting in decreased cardiac function and Cellular Physiology and Biochemistry Cellular Physiology and Biochemistry myocardial injury in rats.…”

Section: Discussionmentioning

confidence: 99%

Effects of the TLR4/Myd88/NF-κB Signaling Pathway on NLRP3 Inflammasome in Coronary Microembolization-Induced Myocardial Injury

Sun

et al. 2018

Cell Physiol Biochem

154

101

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Background/Aims: Coronary microembolization (CME) is a common complication of acute coronary syndrome (ACS) and percutaneous coronary intervention (PCI); Myocardial inflammation, caused by CME, is the main cause of cardiac injury. TLR4/MyD88/NF-κB signaling plays an important role in the development of myocardial inflammation, but its effects on CME remain unclear. To assess the cardiac protective effects of TAK-242 (TLR4 specific inhibitor) on CME-induced myocardial injury, and explore the underlying mechanism. Methods: Cardiac function, serum c-troponin I level, microinfarct were examined by cardiac ultrasound, myocardial enzyme assessment, HBFP staining. The levels of TLR4/MyD88/NF-κB signaling and NLRP3 inflammasome pathway were detected by ELISA, qRT-PCR and western blot. Results: The results showed inflammatory responses in the myocardium after CME, with increased expression levels of pro-inflammatory factors TNF-α, IL-1β and IL-18. Meanwhile, TLR4/MyD88/NF-κB signaling and the NLRP3 inflammasome were involved in the inflammatory process. TAK-242 administration before CME effectively inhibited the inflammatory response in the rat myocardium after CME and reduced myocardial injury, mainly by inhibiting TLR4/ MyD88/NF-κB signaling and reducing NLRP3 inflammasome activation. In addition, in vitro assays with neonatal rat cardiomyocytes further confirmed that TLR4/MyD88/NF-κB signaling was significantly activated in the inflammatory response of LPS-induced cardiomyocytes, via activation of the NLRP3 inflammasome. Inhibition of TLR4/MyD88/NF-κB signaling resulted in increased survival of cardiomyocytes mainly by reducing the release of inflammatory cytokines and decreasing NLRP3 inflammasome activation. Conclusions: TLR4/MyD88/NF-κB signaling participates in the inflammatory response of the myocardium after CME, activating the NLRP3 inflammasome, promoting the inflammatory cascade, and aggravating myocardial injury. Blocking TLR4/MyD88/NF-κB signaling may help reduce myocardial injury and improve cardiac function after CME.

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“…; Zhang et al . ). Using this model, we first investigated whether mild heat pretreatment at 39°C for 24 h or exposure to 10% serum from human subjects who had undergone 8 weeks of passive heat therapy could protect endothelial cells against H/R‐induced inflammatory and oxidative stress and hypothesized that both would reduce NF‐κB activation, release of pro‐inflammatory cytokines [e.g.…”

Section: Introductionmentioning

confidence: 97%

“…Therefore, in the present study, we investigated whether heat therapy could induce cellular stress resistance, and the key associated mechanisms, using an H/R model in cultured endothelial cells. H/R, which is the ex vivo equivalent of ischaemia-reperfusion injury, induces inflammatory and oxidative stress primarily through activation of the transcription factor nuclear factor-kappa B (NF-κB) (Natarajan et al 2002;Xie et al 2005;Zhang et al 2017). Using this model, we first investigated whether mild heat pretreatment at 39°C for 24 h or exposure to 10% serum from human subjects who had undergone 8 weeks of passive heat therapy could protect endothelial cells against H/R-induced inflammatory and oxidative stress and hypothesized that both would reduce NF-κB activation, release of pro-inflammatory cytokines [e.g.…”

Section: Introductionmentioning

confidence: 99%

Passive heat therapy protects against endothelial cell hypoxia‐reoxygenation via effects of elevations in temperature and circulating factors

Brunt

Wiedenfeld-Needham

Comrada

et al. 2018

The Journal of Physiology

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Repeated exposure to passive heat stress ('heat therapy') has widespread physiological benefits, including cellular protection against novel stressors. Increased heat shock protein (HSP) expression and upregulation of circulating factors may impart this protection. We tested the isolated abilities of mild heat pretreatment and serum from human subjects (n = 10) who had undergone 8 weeks of heat therapy to protect against cellular stress following hypoxia-reoxygenation (H/R), a model of ischaemic cardiovascular events. Cultured human umbilical vein endothelial cells were incubated for 24 h at 37°C (control), 39°C (heat pretreatment) or 37°C with 10% serum collected before and after 8 weeks of passive heat therapy (four to five times per week to increase rectal temperature to ≥ 38.5°C for 60 min). Cells were then collected before and after incubation at 1% O for 16 h (hypoxia; 37°C), followed by 20% O for 4 h (reoxygenation; 37°C) and assessed for markers of cell stress. In control cells, H/R increased nuclear NF-κB p65 protein (i.e. activation) by 106 ± 38%, increased IL-6 release by 37 ± 8% and increased superoxide production by 272 ± 45%. Both heat pretreatment and exposure to heat therapy serum prevented H/R-induced NF-κB activation and attenuated superoxide production; by contrast, only exposure to serum attenuated IL-6 release. H/R also decreased cytoplasmic haemeoxygenase-1 (HO-1) protein (known to suppress NF-κB), in control cells (-25 ± 8%), whereas HO-1 protein increased following H/R in cells pretreated with heat or serum-exposed, providing a possible mechanism of protection against H/R. These data indicate heat therapy is capable of imparting resistance against inflammatory and oxidative stress via direct heat and humoral factors.

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The protective effect of Luteolin on myocardial ischemia/reperfusion (I/R) injury through TLR4/NF-κB/NLRP3 inflammasome pathway

Cited by 126 publications

References 22 publications

Luteolin‐mediated Kim‐1/NF‐kB/Nrf2 signaling pathways protects sodium fluoride‐induced hypertension and cardiovascular complications

Luteolin‐mediated Kim‐1/NF‐kB/Nrf2 signaling pathways protects sodium fluoride‐induced hypertension and cardiovascular complications

Effects of the TLR4/Myd88/NF-κB Signaling Pathway on NLRP3 Inflammasome in Coronary Microembolization-Induced Myocardial Injury

Passive heat therapy protects against endothelial cell hypoxia‐reoxygenation via effects of elevations in temperature and circulating factors

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