Luteolin Protects HUVECs from TNF-α-induced Oxidative Stress and Inflammation via its Effects on the Nox4/ROS-NF-κB and MAPK Pathways

Xia, Fan; Wang, Changyuan; Jin, Yue; Liu, Qi; Meng, Qiang; Liu, Kexin; Sun, Huijun

doi:10.5551/jat.23697

Cited by 124 publications

(94 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Several reports indicate that Nox4 has a protective function in distinct pathological conditions, for example obesity, pulmonary arterial hypertension, kidney fibrosis and myocardial infarction 14, 46-49 . Conversely, other articles suggest that Nox4 induces apoptosis, especially in cancer cells, endothelial cells and cardiac myocytes 45, 48, 50, 51 . Nox4 exerts these effects by inactivating the protein tyrosine phosphatase-1B (PTP1B) and enhancing vascular endothelial growth factor receptor-2 (VEGFR2) and mTOR signaling, as well as by regulating endothelial nitric oxide synthase (eNOS) expression, phosphorylation of members of the Bcl-2 family and mitochondrial oxidative stress.…”

Section: Discussionmentioning

confidence: 98%

Polymerase δ-Interacting Protein 2 Promotes Postischemic Neovascularization of the Mouse Hindlimb

Amanso

Lassègue

Joseph

et al. 2014

ATVB

View full text Add to dashboard Cite

Objective Collateral vessel formation can functionally compensate for obstructive vascular lesions in patients with atherosclerosis. Neovascularization processes are triggered by fluid shear stress, hypoxia, growth factors, chemokines, proteases and inflammation, as well as reactive oxygen species (ROS) in response to ischemia. Poldip2 is a multifunctional protein that regulates focal adhesion turnover and vascular smooth muscle cell migration and modifies extracellular matrix composition. We therefore tested the hypothesis that loss of Poldip2 impairs collateral formation. Approach and Results The mouse hindlimb ischemia model has been used to understand mechanisms involved in postnatal blood vessel formation. Poldip2+/- mice were subjected to femoral artery excision, and functional and morphological analysis of blood vessel formation was performed after injury. Heterozygous deletion of Poldip2 decreased the blood flow recovery and spontaneous running activity at 21 days after injury. H2O2 production, as well as the activity of matrix metalloproteinases-2 and -9, was reduced in these animals compared with Poldip2+/+ mice. Infiltration of macrophages in the peri-injury muscle was also decreased; however, macrophage phenotype was similar between genotypes. In addition, the formation of capillaries and arterioles was impaired, as was angiogenesis, in agreement with a decrease in proliferation observed in endothelial cells treated with siRNA against Poldip2. Finally, regression of newly formed vessels and apoptosis was more pronounced in Poldip2+/- mice. Conclusions Together, these results suggest that Poldip2 promotes ischemia-induced collateral vessel formation via multiple mechanisms that likely involve ROS-dependent activation of matrix metalloproteinase activity as well as enhanced vascular cell growth and survival.

show abstract

Section: Discussionmentioning

confidence: 98%

Polymerase δ-Interacting Protein 2 Promotes Postischemic Neovascularization of the Mouse Hindlimb

Amanso

Lassègue

Joseph

et al. 2014

ATVB

View full text Add to dashboard Cite

show abstract

“…NADPH oxidase plays a key role in ROS generation and Nox4 is the most abundant Nox isoform in the vasculature and p22phox is a modulatory subunit for NADPH oxidase (Xia et al, 2014), thus the effects of RDNP on H 2 O 2 -induced Nox4 and p22phox mRNA and protein expressions in HUVECs were examined. Both Nox4 and p22phox mRNA in H 2 O 2 group increased obviously.…”

Section: Rdnp Inhibited H 2 O 2 -Induced Nox4 and P22phox Over-expresmentioning

confidence: 99%

Rhizoma Dioscoreae Nipponicae polysaccharides protect HUVECs from H2O2-induced injury by regulating PPARγ factor and the NADPH oxidase/ROS–NF-κB signal pathway

et al. 2015

Self Cite

View full text Add to dashboard Cite

“…SOD absorbance was measured at the wavelength at 550 nm. MDA absorbance was measured at the wavelength at 532 nm [17]. …”

Section: Methodsmentioning

confidence: 99%

Huang Gan Formula Eliminates the Oxidative Stress Effects of Advanced Oxidation Protein Products on the Divergent Regulation of the Expression of AGEs Receptors via the JAK2/STAT3 Pathway

Deng

et al. 2017

Evidence-Based Complementary and Alternative Medicine

View full text Add to dashboard Cite

Chronic kidney disease (CKD) has a high prevalence and low cure rate and represents a significant health issue. Oxidative stress is common in CKD due to metabolic disorders, inflammation, and impaired renal function changing normal proteins into advanced oxidation protein products (AOPPs). Huang Gan formula (HGF) is a new type of traditional Chinese herbal medicine. Although we previously investigated the protective effects of HGF against oxidative stress, the mechanism of HGF in CKD is still not fully understood. In this study, we used western blotting, quantitative polymerase chain reaction, and biochemical assays to show that HGF significantly decreased AOPP-induced oxidative stress damage. Moreover, the protective effects of HGF might be associated with upregulation of the advanced glycation end product receptor 1 (AGE-R1) and downregulation of the receptor for advance glycation end products (RAGE). Treatment with HGF and the Janus kinase 2 (JAK2) inhibitor, AG4-90, significantly attenuated AOPP-induced JAK2/STAT3 protein levels. These findings indicate that HGF inhibits AOPP-mediated biological responses by inactivating the JAK2/STAT3 pathway. In conclusion, HGF eliminated AOPP-induced effects in human mesangial cells (HMCs) by interrupting JAK2/STAT3 signaling, which altered RAGE/AGE-R1 expression and reduced oxidative stress in CKD.

show abstract

Luteolin Protects HUVECs from TNF-α-induced Oxidative Stress and Inflammation via its Effects on the Nox4/ROS-NF-κB and MAPK Pathways

Cited by 124 publications

References 46 publications

Polymerase δ-Interacting Protein 2 Promotes Postischemic Neovascularization of the Mouse Hindlimb

Polymerase δ-Interacting Protein 2 Promotes Postischemic Neovascularization of the Mouse Hindlimb

Rhizoma Dioscoreae Nipponicae polysaccharides protect HUVECs from H2O2-induced injury by regulating PPARγ factor and the NADPH oxidase/ROS–NF-κB signal pathway

Huang Gan Formula Eliminates the Oxidative Stress Effects of Advanced Oxidation Protein Products on the Divergent Regulation of the Expression of AGEs Receptors via the JAK2/STAT3 Pathway

Contact Info

Product

Resources

About