Punicalagin from pomegranate ameliorates TNF-α/IFN-γ-induced inflammatory responses in HaCaT cells via regulation of SIRT1/STAT3 axis and Nrf2/HO-1 signaling pathway
Copyright © 2024. Published by Elsevier B.V..
Punicalagin (PUN) was isolated from the peel of pomegranate (Punica granatum L.), is a polyphenol with anti-inflammatory, hepatoprotective, and antioxidant activities. However, it remains unclear whether PUN alleviates the inflammation and anti-inflammatory mechanisms in pro-inflammatory cytokines-induced human keratinocyte HaCaT cells. Here, we investigated that tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) mixture-stimulated HaCaT cells were treated with various concentrations of PUN, followed by analyzed the expression of inflammation-related mediators and evaluate anti-inflammatory-related pathways. Our results demonstrated that PUN ≤ 100 μM did not reduce HaCaT cell viability, and PUN ≥ 3 μM was sufficient to decrease interleukin-6 (IL-6), IL-8, monocyte chemoattractant protein-1 (MCP-1), chemokine ligand 5 (CCL5), CCL17 and CCL20 concentrations. We found that PUN ≥ 10 μM and ≥ 3 μM significantly increased sirtuin 1 (SIRT1) expression and inhibited signal transducer and activator of transcription 3 (STAT3) phosphorylation, respectively. PUN downregulated inflammation-related proteins cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), enhanced nuclear factor erythroid-2-related factor-2 (Nrf2) and heme oxygenase-1 (HO-1) expression. Moreover, PUN decreased intercellular adhesion molecule-1 (ICAM-1) expression and inhibited monocyte adhesion to inflamed HaCaT cells. PUN also suppressed inflammatory-related pathways, including mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) signaling pathways in TNF-α/IFN-γ- stimulated HaCat cells. Collectively, there is significant evidence that PUN has effective protective defenses against TNF-α/IFN-γ-induced skin inflammation by enhancing SIRT1 to mediate STAT3 and Nrf2/HO-1 signaling pathway.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:130 |
|---|---|
| Enthalten in: |
International immunopharmacology - 130(2024) vom: 30. März, Seite 111665 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Huang, Wen-Chung [VerfasserIn] |
|---|
| Links: |
|---|
| Anmerkungen: |
Date Completed 25.03.2024 Date Revised 25.03.2024 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1016/j.intimp.2024.111665 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM368575322 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM368575322 | ||
| 003 | DE-627 | ||
| 005 | 20240325234858.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 240218s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.intimp.2024.111665 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1346.xml |
| 035 | |a (DE-627)NLM368575322 | ||
| 035 | |a (NLM)38367463 | ||
| 035 | |a (PII)S1567-5769(24)00183-8 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Huang, Wen-Chung |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Punicalagin from pomegranate ameliorates TNF-α/IFN-γ-induced inflammatory responses in HaCaT cells via regulation of SIRT1/STAT3 axis and Nrf2/HO-1 signaling pathway |
| 264 | 1 | |c 2024 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 25.03.2024 | ||
| 500 | |a Date Revised 25.03.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2024. Published by Elsevier B.V. | ||
| 520 | |a Punicalagin (PUN) was isolated from the peel of pomegranate (Punica granatum L.), is a polyphenol with anti-inflammatory, hepatoprotective, and antioxidant activities. However, it remains unclear whether PUN alleviates the inflammation and anti-inflammatory mechanisms in pro-inflammatory cytokines-induced human keratinocyte HaCaT cells. Here, we investigated that tumor necrosis factor-alpha (TNF-α) and interferon-gamma (IFN-γ) mixture-stimulated HaCaT cells were treated with various concentrations of PUN, followed by analyzed the expression of inflammation-related mediators and evaluate anti-inflammatory-related pathways. Our results demonstrated that PUN ≤ 100 μM did not reduce HaCaT cell viability, and PUN ≥ 3 μM was sufficient to decrease interleukin-6 (IL-6), IL-8, monocyte chemoattractant protein-1 (MCP-1), chemokine ligand 5 (CCL5), CCL17 and CCL20 concentrations. We found that PUN ≥ 10 μM and ≥ 3 μM significantly increased sirtuin 1 (SIRT1) expression and inhibited signal transducer and activator of transcription 3 (STAT3) phosphorylation, respectively. PUN downregulated inflammation-related proteins cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS), enhanced nuclear factor erythroid-2-related factor-2 (Nrf2) and heme oxygenase-1 (HO-1) expression. Moreover, PUN decreased intercellular adhesion molecule-1 (ICAM-1) expression and inhibited monocyte adhesion to inflamed HaCaT cells. PUN also suppressed inflammatory-related pathways, including mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB) signaling pathways in TNF-α/IFN-γ- stimulated HaCat cells. Collectively, there is significant evidence that PUN has effective protective defenses against TNF-α/IFN-γ-induced skin inflammation by enhancing SIRT1 to mediate STAT3 and Nrf2/HO-1 signaling pathway | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a HaCaT cells | |
| 650 | 4 | |a MAPKs | |
| 650 | 4 | |a NF-κB | |
| 650 | 4 | |a Nrf2/HO-1 | |
| 650 | 4 | |a Punicalagin | |
| 650 | 4 | |a SIRT1/STAT3 axis | |
| 650 | 7 | |a Tumor Necrosis Factor-alpha |2 NLM | |
| 650 | 7 | |a Sirtuin 1 |2 NLM | |
| 650 | 7 | |a EC 3.5.1.- |2 NLM | |
| 650 | 7 | |a Interferon-gamma |2 NLM | |
| 650 | 7 | |a 82115-62-6 |2 NLM | |
| 650 | 7 | |a punicalagin |2 NLM | |
| 650 | 7 | |a 65995-63-3 |2 NLM | |
| 650 | 7 | |a NF-E2-Related Factor 2 |2 NLM | |
| 650 | 7 | |a Heme Oxygenase-1 |2 NLM | |
| 650 | 7 | |a EC 1.14.14.18 |2 NLM | |
| 650 | 7 | |a STAT3 Transcription Factor |2 NLM | |
| 650 | 7 | |a NF-kappa B |2 NLM | |
| 650 | 7 | |a Anti-Inflammatory Agents |2 NLM | |
| 650 | 7 | |a SIRT1 protein, human |2 NLM | |
| 650 | 7 | |a EC 3.5.1.- |2 NLM | |
| 650 | 7 | |a STAT3 protein, human |2 NLM | |
| 650 | 7 | |a Hydrolyzable Tannins |2 NLM | |
| 700 | 1 | |a Liou, Chian-Jiun |e verfasserin |4 aut | |
| 700 | 1 | |a Shen, Szu-Chuan |e verfasserin |4 aut | |
| 700 | 1 | |a Hu, Sindy |e verfasserin |4 aut | |
| 700 | 1 | |a Chao, Jane C-J |e verfasserin |4 aut | |
| 700 | 1 | |a Huang, Chun-Hsun |e verfasserin |4 aut | |
| 700 | 1 | |a Wu, Shu-Ju |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t International immunopharmacology |d 2001 |g 130(2024) vom: 30. März, Seite 111665 |w (DE-627)NLM112639542 |x 1878-1705 |7 nnns |
| 773 | 1 | 8 | |g volume:130 |g year:2024 |g day:30 |g month:03 |g pages:111665 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.intimp.2024.111665 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 130 |j 2024 |b 30 |c 03 |h 111665 | ||