Lycopene Inhibits Toll-Like Receptor 4-Mediated Expression of Inflammatory Cytokines in House Dust Mite-Stimulated Respiratory Epithelial Cells

Choi, Jiyeon; Lim, Joo Weon; Kim, Hye Young

doi:10.3390/molecules26113127

Cited by 16 publications

(8 citation statements)

References 67 publications

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“…66 Moreover, lycopene could reduce the risk of pancreatic cancer by regulating NF-κB signaling pathway, 67 and inhibiting TLR4 expression and inflammatory cytokines secretion in respiratory epithelial cells. 68 Notably, the inhibition of the TLR4/NF-κB signaling pathway could restore insulin secretion and protect islet β cell function in HFD-induced mice. 69 Therefore, these findings suggest that lycopene may improve islet function via regulation of the TLR4/MyD88/NF-κB signaling pathway.…”

Section: Food and Function Papermentioning

confidence: 99%

Lycopene ameliorates islet function and down-regulates the TLR4/MyD88/NF-κB pathway in diabetic mice and Min6 cells

et al. 2023

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Section: Food and Function Papermentioning

confidence: 99%

Lycopene ameliorates islet function and down-regulates the TLR4/MyD88/NF-κB pathway in diabetic mice and Min6 cells

et al. 2023

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“…In addition, TLR4 can activate TRAF6 by regulating TRIF, and then induce the expression of cytokines such as IL-1, IL-4, IL-8, IL-12, and IFN-γ through the activation of JNK, P38, and other MAPK pathways. Choi et al [ 38 ] found that LP inhibited the expression of inflammatory cytokines by downregulating the expression of TLR4 protein and alleviating oxidative stress injury in respiratory epithelial cells A549 stimulated by house dust mites. Our previous study showed that LP prevented DSS-induced UC in mice by regulating the TLR4/TRIF/NF-κB signaling pathway [ 24 ].…”

Section: Discussionmentioning

confidence: 99%

Preventive Mechanism of Lycopene on Intestinal Toxicity Caused by Cyclophosphamide Chemotherapy in Mice by Regulating TLR4-MyD88/TRIF-TRAF6 Signaling Pathway and Gut-Liver Axis

Xiao

Niu

et al. 2022

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Cyclophosphamide (CYC) is the first-line chemotherapy drug for cancer in clinical practice, and its intestinal toxicity seriously affects the treatment effect and prognosis of patients. Lycopene (LP) is the main pigment of ripe tomatoes and has strong antioxidant activity. However, the mechanism by which LP prevents CYC-induced intestinal injury remains unclear. The aim of this study was to investigate the mechanism of LP in preventing intestinal toxicity caused by CYC chemotherapy in mice. The results showed that LP significantly prevented spleen and thymus atrophy induced by CYC. In terms of intestinal injury, LP significantly increased the levels of superoxide dismutase (SOD), secretory immunoglobulin A (sIgA), interleukin (IL)-4, IL-12, and interferon (IFN)-γ, decreased the content of lipid oxidation (MDA), upregulated the protein expressions of toll-like receptors 4 (TLR4), myeloid differentiation factor 88 (MyD88), tumor necrosis factor receptor-associated factor 6 (TRAF6), toll/IL-1receptor domain containing adaptor protein inducing IFN-β (TRIF), p-P38 MAPK (P38), and p- nuclear factor kappa-B (NF-κB) p65, and improved the small intestine tissue injury induced by CYC. In terms of liver injury, LP significantly increased the content of glutathione (GSH), decreased the contents of MDA, nitric oxide (NO), IL-1β, IL-6, and tumor necrosis factor (TNF)-α, and repaired the liver tissue injury induced by CYC. Importantly, 10 mg/kg LP significantly prevented intestinal microbiota dysregulation in CYC mice. These results suggested that LP significantly prevented intestinal injury induced by CYC in mice by regulating the TLR4-MyD88/TRIF-TRAF6 signaling pathway and gut-liver axis.

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“…To measure the nuclear translocation of PPar-γ, cells on coverslips placed in six-well plates were pretreated with α-lipoic acid for 2 h and then stimulated with cerulein/resistin for 45 min. Immunofluorescence staining was performed as previously described (48). Briefly, cells were fixed with 4% formaldehyde for 10 min at 20-25˚C, permeabilized with 0.2% Triton X-100 for 10 min at 20-25˚C, blocked with blocking buffer containing 1% BSa and 0.1% gelatin for 1 h at 20-25˚C, and then incubated with the primary antibody against PPar-γ (dilution 1/200) for 1 h at 20-25˚C.…”

Section: Preparation Of Whole-cell Extracts and Nuclear Extractsmentioning

confidence: 99%

α‑lipoic acid inhibits cerulein/resistin‑induced expression of interleukin‑6 by activating peroxisome proliferator‑activated receptor‑γ in pancreatic acinar cells

2022

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cerulein-induced pancreatitis resembles human acute pancreatitis in terms of pathological events, such as enzymatic activation and inflammatory cell infiltration in the pancreas. cerulein is a cholecystokinin analog that increases levels of reactive oxygen species (roS) and interleukin-6 (il-6) expression level in pancreatic acinar cells. Serum levels of resistin, which is secreted from adipocytes, are reportedly higher in patients with acute pancreatitis than in healthy individuals. Previously, it was shown that the adipokine resistin can aggravate the cerulein-induced increase in roS levels and il-6 expression level in pancreatic acinar cells. Peroxisome proliferator-activated receptor-gamma (PPar-γ) is a key regulator of the transcription and expression of antioxidant enzymes, including heme oxygenase 1 (Ho-1) and catalase. α-lipoic acid, a naturally occurring dithiol antioxidant, can prevent cerulein-induced pancreatic damage in rats. in the present study, it was aimed to investigate whether α-lipoic acid can attenuate the cerulein/resistin-induced increase in il-6 expression and roS levels via PPar-γ activation in pancreatic acinar AR42J cells. The anti-inflammatory mechanism of α-lipoic acid was determined using reverse transcription-quantitative Pcr, western blot analysis, enzyme-linked immunosorbent assay, immunofluoresc2ence staining and fluorometry. Treatment with cerulein and resistin increased roS levels and il-6 expression level, which were inhibited by α-lipoic acid in pancreatic acinar cells. α-lipoic acid increased the nuclear translocation and expression level of PPar-γ and the expression levels of its target genes: Ho-1 and catalase. The PPar-γ antagonist GW9662 and Ho-1 inhibitor zinc protoporphyrin reversed the inhibitory effect of α-lipoic acid on cerulein/resistin-induced increase in roS and il-6 levels. in conclusion, α-lipoic acid inhibits the cerulein/resistin-induced increase in roS production and il-6 expression levels by activating PPar-γ and inducing the expression of Ho-1 and catalase in pancreatic acinar cells.

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Lycopene Inhibits Toll-Like Receptor 4-Mediated Expression of Inflammatory Cytokines in House Dust Mite-Stimulated Respiratory Epithelial Cells

Cited by 16 publications

References 67 publications

Lycopene ameliorates islet function and down-regulates the TLR4/MyD88/NF-κB pathway in diabetic mice and Min6 cells

Lycopene ameliorates islet function and down-regulates the TLR4/MyD88/NF-κB pathway in diabetic mice and Min6 cells

Preventive Mechanism of Lycopene on Intestinal Toxicity Caused by Cyclophosphamide Chemotherapy in Mice by Regulating TLR4-MyD88/TRIF-TRAF6 Signaling Pathway and Gut-Liver Axis

α‑lipoic acid inhibits cerulein/resistin‑induced expression of interleukin‑6 by activating peroxisome proliferator‑activated receptor‑γ in pancreatic acinar cells

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