Implication of Caffeic Acid for the Prevention and Treatment of Alzheimer's Disease : Understanding the Binding with Human Transferrin Using In Silico and In Vitro Approaches
© 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature..
In present times, a switch from chemical molecules towards natural products is taking place, and the latter is being increasingly explored in the management of diseases due to their broad range of therapeutic potential. Consumption of coffee is thought to reduce Alzheimer's disease (AD); however, the mechanism is still unexplored. Primarily, it is thought that components of coffee are the key players in making it a neuroprotectant. Caffeic acid (CA) is found in high quantities in coffee; thus, it is being increasingly explored to decipher its neuroprotection by various mechanisms. Iron is a toxic element in a free form capable of causing oxidative damage and ultimately contributing to the pathogenesis of AD. Thus, maintaining the proper iron levels is vital and human transferrin (Htf), a glycoprotein, is a key player in this aspect. In this work, we explored the binding mechanism of CA with Htf at the atomistic level, employing molecular docking and extensive molecular dynamics simulation (MD) approaches coupled with spectroscopic techniques in a bid to decipher the mode of interaction of CA with Htf. Molecular docking results demonstrated a strong binding affinity between CA and Htf. Furthermore, MD study highlighted the Htf-CA complex's stability and the ligand's minimal impact on Htf's overall structure. In silico approaches were further backed up by experimental approaches. Strong binding of CA with Htf was ascertained by UV-visible and fluorescence spectroscopy observations. Together, the study provides a comprehensive understanding of the Htf-CA interaction, adding to the knowledge of the use of CA in the treatment of AD, thereby adding another feather to its already known neuroprotective role.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:61 |
|---|---|
| Enthalten in: |
Molecular neurobiology - 61(2024), 4 vom: 27. März, Seite 2176-2185 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Shamsi, Anas [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Alzheimer’s disease |
|---|
| Anmerkungen: |
Date Completed 28.03.2024 Date Revised 28.03.2024 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1007/s12035-023-03696-y |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM363570934 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM363570934 | ||
| 003 | DE-627 | ||
| 005 | 20240329000106.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231226s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1007/s12035-023-03696-y |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1353.xml |
| 035 | |a (DE-627)NLM363570934 | ||
| 035 | |a (NLM)37864768 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Shamsi, Anas |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Implication of Caffeic Acid for the Prevention and Treatment of Alzheimer's Disease |b Understanding the Binding with Human Transferrin Using In Silico and In Vitro Approaches |
| 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 28.03.2024 | ||
| 500 | |a Date Revised 28.03.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature. | ||
| 520 | |a In present times, a switch from chemical molecules towards natural products is taking place, and the latter is being increasingly explored in the management of diseases due to their broad range of therapeutic potential. Consumption of coffee is thought to reduce Alzheimer's disease (AD); however, the mechanism is still unexplored. Primarily, it is thought that components of coffee are the key players in making it a neuroprotectant. Caffeic acid (CA) is found in high quantities in coffee; thus, it is being increasingly explored to decipher its neuroprotection by various mechanisms. Iron is a toxic element in a free form capable of causing oxidative damage and ultimately contributing to the pathogenesis of AD. Thus, maintaining the proper iron levels is vital and human transferrin (Htf), a glycoprotein, is a key player in this aspect. In this work, we explored the binding mechanism of CA with Htf at the atomistic level, employing molecular docking and extensive molecular dynamics simulation (MD) approaches coupled with spectroscopic techniques in a bid to decipher the mode of interaction of CA with Htf. Molecular docking results demonstrated a strong binding affinity between CA and Htf. Furthermore, MD study highlighted the Htf-CA complex's stability and the ligand's minimal impact on Htf's overall structure. In silico approaches were further backed up by experimental approaches. Strong binding of CA with Htf was ascertained by UV-visible and fluorescence spectroscopy observations. Together, the study provides a comprehensive understanding of the Htf-CA interaction, adding to the knowledge of the use of CA in the treatment of AD, thereby adding another feather to its already known neuroprotective role | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Alzheimer’s disease | |
| 650 | 4 | |a Caffeic acid | |
| 650 | 4 | |a Human transferrin | |
| 650 | 4 | |a Iron | |
| 650 | 4 | |a Molecular docking | |
| 650 | 4 | |a Molecular dynamic simulation | |
| 650 | 4 | |a Spectroscopy | |
| 650 | 7 | |a Transferrin |2 NLM | |
| 650 | 7 | |a caffeic acid |2 NLM | |
| 650 | 7 | |a U2S3A33KVM |2 NLM | |
| 650 | 7 | |a Coffee |2 NLM | |
| 650 | 7 | |a Iron |2 NLM | |
| 650 | 7 | |a E1UOL152H7 |2 NLM | |
| 650 | 7 | |a Caffeic Acids |2 NLM | |
| 700 | 1 | |a Shahwan, Moyad |e verfasserin |4 aut | |
| 700 | 1 | |a Das Gupta, Debarati |e verfasserin |4 aut | |
| 700 | 1 | |a Abdullah, K M |e verfasserin |4 aut | |
| 700 | 1 | |a Khan, Mohd Shahnawaz |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Molecular neurobiology |d 1990 |g 61(2024), 4 vom: 27. März, Seite 2176-2185 |w (DE-627)NLM012626961 |x 1559-1182 |7 nnns |
| 773 | 1 | 8 | |g volume:61 |g year:2024 |g number:4 |g day:27 |g month:03 |g pages:2176-2185 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1007/s12035-023-03696-y |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 61 |j 2024 |e 4 |b 27 |c 03 |h 2176-2185 | ||