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- Publisher Website: 10.1016/j.bcp.2019.05.027
- Scopus: eid_2-s2.0-85066627841
- PMID: 31158339
- WOS: WOS:000474498800022
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Article: Apigenin and its methylglyoxal-adduct inhibit advanced glycation end products-induced oxidative stress and inflammation in endothelial cells
Title | Apigenin and its methylglyoxal-adduct inhibit advanced glycation end products-induced oxidative stress and inflammation in endothelial cells |
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Authors | |
Keywords | AGEs-RAGE interaction Apigenin Di-methylglyoxal apigenin HUVECs |
Issue Date | 2019 |
Publisher | Elsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharm |
Citation | Biochemical Pharmacology, 2019, v. 166, p. 231-241 How to Cite? |
Abstract | Protein glycation in the body can lead to malfunction of intracellular and extracellular proteins. Reactive carbonyl species (RCS) have been identified to be key intermediates in the reactions. The reaction products, generally termed as advanced glycation end products (AGEs), have been implicated in the development of diabetic complications. In this study, the activity of apigenin (API), a natural flavone in scavenging RCS and the molecular mechanism involved in its protective effect against AGEs-induced oxidative stress and inflammation were examined in vitro. Results showed that API could directly trap methylglyoxal (MGO) to form API-MGO adducts, thus inhibiting AGEs formation. API and di-apigenin adduct (DMA) were found to inhibit AGEs-induced oxidative stress and inflammation in human umbilical vein endothelial cells (HUVECs) by significantly suppressing reactive oxygen species (ROS) production (30% relative to control) and decreasing the protein expression of pro-inflammatory cytokines and adhesion molecules by 30–70%. Further mechanistic investigation revealed that the protective effect was likely mediated via suppression of the extracellular-signal-regulated kinase 1/2 (ERK)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway initiated by AGEs-RAGE (receptor for AGEs) interaction and induction of ERK/nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathway with subsequent up-regulation of antioxidant defense molecules. In summary, our results suggest that API possesses great potential to protect against AGEs-associated health disorders by modulating cellular inflammatory and antioxidant defense signaling pathways. |
Persistent Identifier | http://hdl.handle.net/10722/275416 |
ISSN | 2023 Impact Factor: 5.3 2023 SCImago Journal Rankings: 1.365 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Zhou, Q | - |
dc.contributor.author | Cheng, KW | - |
dc.contributor.author | Gong, J | - |
dc.contributor.author | Li, ETS | - |
dc.contributor.author | Wang, M | - |
dc.date.accessioned | 2019-09-10T02:42:09Z | - |
dc.date.available | 2019-09-10T02:42:09Z | - |
dc.date.issued | 2019 | - |
dc.identifier.citation | Biochemical Pharmacology, 2019, v. 166, p. 231-241 | - |
dc.identifier.issn | 0006-2952 | - |
dc.identifier.uri | http://hdl.handle.net/10722/275416 | - |
dc.description.abstract | Protein glycation in the body can lead to malfunction of intracellular and extracellular proteins. Reactive carbonyl species (RCS) have been identified to be key intermediates in the reactions. The reaction products, generally termed as advanced glycation end products (AGEs), have been implicated in the development of diabetic complications. In this study, the activity of apigenin (API), a natural flavone in scavenging RCS and the molecular mechanism involved in its protective effect against AGEs-induced oxidative stress and inflammation were examined in vitro. Results showed that API could directly trap methylglyoxal (MGO) to form API-MGO adducts, thus inhibiting AGEs formation. API and di-apigenin adduct (DMA) were found to inhibit AGEs-induced oxidative stress and inflammation in human umbilical vein endothelial cells (HUVECs) by significantly suppressing reactive oxygen species (ROS) production (30% relative to control) and decreasing the protein expression of pro-inflammatory cytokines and adhesion molecules by 30–70%. Further mechanistic investigation revealed that the protective effect was likely mediated via suppression of the extracellular-signal-regulated kinase 1/2 (ERK)/nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway initiated by AGEs-RAGE (receptor for AGEs) interaction and induction of ERK/nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathway with subsequent up-regulation of antioxidant defense molecules. In summary, our results suggest that API possesses great potential to protect against AGEs-associated health disorders by modulating cellular inflammatory and antioxidant defense signaling pathways. | - |
dc.language | eng | - |
dc.publisher | Elsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharm | - |
dc.relation.ispartof | Biochemical Pharmacology | - |
dc.subject | AGEs-RAGE interaction | - |
dc.subject | Apigenin | - |
dc.subject | Di-methylglyoxal apigenin | - |
dc.subject | HUVECs | - |
dc.title | Apigenin and its methylglyoxal-adduct inhibit advanced glycation end products-induced oxidative stress and inflammation in endothelial cells | - |
dc.type | Article | - |
dc.identifier.email | Li, ETS: etsli@hku.hk | - |
dc.identifier.email | Wang, M: mfwang@hku.hk | - |
dc.identifier.authority | Li, ETS=rp00737 | - |
dc.identifier.authority | Wang, M=rp00800 | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1016/j.bcp.2019.05.027 | - |
dc.identifier.pmid | 31158339 | - |
dc.identifier.scopus | eid_2-s2.0-85066627841 | - |
dc.identifier.hkuros | 303494 | - |
dc.identifier.volume | 166 | - |
dc.identifier.spage | 231 | - |
dc.identifier.epage | 241 | - |
dc.identifier.isi | WOS:000474498800022 | - |
dc.publisher.place | United States | - |
dc.identifier.issnl | 0006-2952 | - |