Nepetin inhibits IL-1β induced inflammation via NF-κB and MAPKs signaling pathways in ARPE-19 cells

Chen, Xi; Han, Ruifang; Peng, Hao; Wang, Liming; Liu, Meixin; Jin, Meihua; Kong, Dexin; Li, Xuan

doi:10.1016/j.biopha.2018.02.054

Cited by 56 publications

(34 citation statements)

References 43 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These results suggested that inhibiting apoptosis was involved in the beneficial effect of tempol against IH-induced pancreatic injury. MAPK and NF-κB signaling pathways are confirmed to play crucial roles in inflammatory response (Chen et al 2018, Gao et al 2018. Suppressing the abnormal activation of MAPK and NF-κB pathways has been reported to attenuate IH-induced inflammation (Kang et al 2017, Liu et al 2017.…”

Section: Discussionmentioning

confidence: 99%

Tempol Alleviates Chronic Intermittent Hypoxia-Induced Pancreatic Injury Through Repressing Inflammation and Apoptosis

Wang

Han

et al. 2019

Physiol Res

View full text Add to dashboard Cite

Obstructive sleep apnea (OSA) has been demonstrated to be implicated in disorder of insulin secretion and diabetes mellitus. In this study, we aimed to evaluate the protective role of tempol, a powerful antioxidant, in chronic intermittent hypoxia (IH)-induced pancreatic injury. The rat model of OSA was established by IH exposure. The pathological changes, increased blood-glucose level, and raised proinsulin/insulin ratio in pancreatic tissues of rats received IH were effectively relieved by tempol delivery. In addition, the enhanced levels of pro-inflammatory cytokines, TNF-α, IL-1β, IL-6, and inflammatory mediators, PGE2, cyclooxygenase-2 (COX-2), NO, and inducible nitric oxide synthase (iNOS) in pancreatic tissue were suppressed by tempol. Moreover, tempol inhibited IH-induced apoptosis in pancreatic tissue as evidenced by upregulated Bcl-2 level, and downregulated Bax and cleaved caspase-3 levels. Finally, the abnormal activation of mitogen-activated protein kinase (MAPK) and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathways induced by IH was restrained by tempol administration. In summary, our study demonstrates that tempol relieves IH-induced pancreatic injury by inhibiting inflammatory response and apoptosis, which provides theoretical basis for tempol as an effective treatment for OSA-induced pancreatic injury.

show abstract

Section: Discussionmentioning

confidence: 99%

Tempol Alleviates Chronic Intermittent Hypoxia-Induced Pancreatic Injury Through Repressing Inflammation and Apoptosis

Wang

Han

et al. 2019

Physiol Res

View full text Add to dashboard Cite

show abstract

“…It was well known that NF-κB used to serving as the upstream of NLRP3 53 . However, overexpression of NLRP3 can also lead to the increase of IL-1β and IL-18, and many literatures reported that IL-1β feedback loop could promote the activation of NF-κB signaling pathway [54][55][56][57][58][59] . Therefore, in our results, overexpression of NLRP3 caused the activation of NF-κB signaling pathway, although NF-κB served as the upstream of NLRP3.…”

Section: Discussionmentioning

confidence: 99%

Scutellarin ameliorates pulmonary fibrosis through inhibiting NF-κB/NLRP3-mediated epithelial–mesenchymal transition and inflammation

et al. 2020

View full text Add to dashboard Cite

Idiopathic pulmonary fibrosis (IPF) is featured with inflammation and extensive lung remodeling caused by overloaded deposition of extracellular matrix. Scutellarin is the major effective ingredient of breviscapine and its anti-inflammation efficacy has been reported before. Nevertheless, the impact of scutellarin on IPF and the downstream molecular mechanism remain unclear. In this study, scutellarin suppressed BLM-induced inflammation via NF-κB/NLRP3 pathway both in vivo and in vitro. BLM significantly elevated p-p65/p65 ratio, IκBα degradation, and levels of NLRP3, caspase-1, caspase-11, ASC, GSDMDNterm, IL-1β, and IL-18, while scutellarin reversed the above alterations except for that of caspase-11. Scutellarin inhibited BLM-induced epithelial–mesenchymal transition (EMT) process in vivo and in vitro. The expression levels of EMT-related markers, including fibronectin, vimentin, N-cadherin, matrix metalloproteinase 2 (MMP-2) and MMP-9, were increased in BLM group, and suppressed by scutellarin. The expression level of E-cadherin showed the opposite changes. However, overexpression of NLRP3 eliminated the anti-inflammation and anti-EMT functions of scutellarin in vitro. In conclusion, scutellarin suppressed inflammation and EMT in BLM-induced pulmonary fibrosis through NF-κB/NLRP3 signaling.

show abstract

“…IL-1 β activation of NF- κ B signaling is closely associated with RD diseases [ 15 , 16 ] and pAKT is related to inhibition of the NF- κ B inflammatory pathway [ 36 ]. Previous studies show that IL-1 β -activates NF- κ B, resulting in its translocation from the cytoplasm into the nucleus, followed by induction of cytokine and chemokine expressions in ARPE-19 cells [ 43 ]. Our present results showed that luteolin promoted AKT phosphorylation (Figures 2(f) and 2(g) ), inhibited NF- κ B p65 activation, and suppressed THP-1 cell adhesion ( Figure 4 ).…”

Section: Discussionmentioning

confidence: 99%

Luteolin Attenuates IL-1β-Induced THP-1 Adhesion to ARPE-19 Cells via Suppression of NF-κB and MAPK Pathways

Huang

Liou

Shen

et al. 2020

Mediators of Inflammation

View full text Add to dashboard Cite

Cytokine-induced endothelial dysfunction leads to inflammation and vascular adhesion molecule production in retinal pigment epithelium (RPE) cells. Inflammation is a critical mediator in retinal degeneration (RD) diseases, including age-related macular degeneration (AMD), and RD progression may be prevented through anti-inflammatory activity in RPE cells. The flavonoid polyphenol luteolin (LU) has anti-inflammatory and antidiabetes activities, but its effects regarding retinal protection remain unknown. Here, we examined the ability of luteolin to alleviate markers of inflammation related to RD in cytokine-primed APPE-19 cells. We found that luteolin decreased the levels of interleukin- (IL-) 6, IL-8, soluble intercellular adhesion molecule-1 (sICAM-1), and monocyte chemoattractant protein-1 (MCP-1) and attenuated adherence of the human monocytic leukemia cell line THP-1 to IL-1β-stimulated ARPE-19 cells. Luteolin also increased anti-inflammatory protein heme oxygenase-1 (HO-1) levels. Interestingly, luteolin induced protein kinase B (AKT) phosphorylation, thus inhibiting nuclear factor- (NF-) κB transfer from cytoplasm into the nucleus and suppressing mitogen-activated protein kinase (MAPK) inflammatory pathways. Furthermore, cotreatment with MAPK inhibitors and luteolin decreased inflammatory cytokine and chemokine levels, and further suppressed THP-1 adhesion. Overall, these results provide evidence that luteolin protects ARPE-19 cells from IL-1β-stimulated increases of IL-6, IL-8, sICAM-1, and MCP-1 production by blocking the activation of MAPK and NF-κB signaling pathways, thus ameliorating the inflammatory response.

show abstract

Nepetin inhibits IL-1β induced inflammation via NF-κB and MAPKs signaling pathways in ARPE-19 cells

Cited by 56 publications

References 43 publications

Tempol Alleviates Chronic Intermittent Hypoxia-Induced Pancreatic Injury Through Repressing Inflammation and Apoptosis

Tempol Alleviates Chronic Intermittent Hypoxia-Induced Pancreatic Injury Through Repressing Inflammation and Apoptosis

Scutellarin ameliorates pulmonary fibrosis through inhibiting NF-κB/NLRP3-mediated epithelial–mesenchymal transition and inflammation

Luteolin Attenuates IL-1β-Induced THP-1 Adhesion to ARPE-19 Cells via Suppression of NF-κB and MAPK Pathways

Contact Info

Product

Resources

About