PMID- 33171640
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231112
IS  - 1424-8247 (Print)
IS  - 1424-8247 (Electronic)
IS  - 1424-8247 (Linking)
VI  - 13
IP  - 11
DP  - 2020 Nov 8
TI  - Punicalagin Regulates Key Processes Associated with Atherosclerosis in THP-1 
      Cellular Model.
LID - 10.3390/ph13110372 [doi]
LID - 372
AB  - Atherosclerosis may lead to cardiovascular diseases (CVD), which are the primary 
      cause of death globally. In addition to conventional therapeutics for CVD, use of 
      nutraceuticals that prevents cholesterol deposition, reduce existing plaques and 
      hence anti-atherosclerotic effects of nutraceuticals appeared to be promising. As 
      such, in the present study we evaluated the beneficial effects of punicalagin, a 
      phytochemical against an atherosclerotic cell model in vitro. Cytotoxicity assays 
      were examined for 10 microM concentration of punicalagin on THP-1 macrophages. 
      Real-time-polymerase chain reaction (RT-PCR) was used to analyze monocyte 
      chemoattractant protein-1 (MCP-1) and Intercellular adhesion molecule (ICAM-1) 
      expressions. Monocyte migration and cholesterol efflux assays were performed to 
      investigate punicalagin's further impact on the key steps of atherosclerosis. 
      Cytotoxicity assays demonstrated no significant toxicity for punicalagin (10 microM) 
      on THP-1 macrophages. Punicalagin inhibited the IFN-gamma-induced overexpression of 
      MCP-1 and ICAM-1 in macrophages by 10 fold and 3.49 fold, respectively, compared 
      to the control. Punicalagin also reduced the MCP-1- mediated migration of 
      monocytes by 28% compared to the control. Percentages of cellular cholesterol 
      efflux were enhanced in presence or absence of IFN-gamma by 88% and 84% compared to 
      control with 58 %and 62%, respectively. Punicalagin possesses anti-inflammatory 
      and anti-atherosclerotic effects. Punicalagin also did not exhibit any 
      cytotoxicity and therefore can be considered a safe and potential candidate for 
      the treatment and prevention of atherosclerosis.
FAU - Almowallad, Sanaa
AU  - Almowallad S
AD  - Department of Biochemistry, Faculty of Sciences, King Abdul Aziz University, 
      Jeddah 21589, Saudi Arabia.
AD  - Cell Culture Unit, King Fahad Medical Research Centre, King Abdul Aziz 
      University, Jeddah 22252, Saudi Arabia.
AD  - Department of Biochemistry, Faculty of Sciences, University of Tabuk, Tabuk 
      71491, Saudi Arabia.
FAU - Huwait, Etimad
AU  - Huwait E
AD  - Department of Biochemistry, Faculty of Sciences, King Abdul Aziz University, 
      Jeddah 21589, Saudi Arabia.
AD  - Cell Culture Unit, King Fahad Medical Research Centre, King Abdul Aziz 
      University, Jeddah 22252, Saudi Arabia.
FAU - Al-Massabi, Rehab
AU  - Al-Massabi R
AD  - Department of Biochemistry, Faculty of Sciences, King Abdul Aziz University, 
      Jeddah 21589, Saudi Arabia.
AD  - Cell Culture Unit, King Fahad Medical Research Centre, King Abdul Aziz 
      University, Jeddah 22252, Saudi Arabia.
AD  - Department of Biochemistry, Faculty of Sciences, University of Tabuk, Tabuk 
      71491, Saudi Arabia.
FAU - Saddeek, Salma
AU  - Saddeek S
AD  - Department of Biochemistry, Faculty of Sciences, King Abdul Aziz University, 
      Jeddah 21589, Saudi Arabia.
AD  - Cell Culture Unit, King Fahad Medical Research Centre, King Abdul Aziz 
      University, Jeddah 22252, Saudi Arabia.
AD  - Department of Chemistry, Faculty of Sciences, University of Hafr Al Batin, Hafr 
      Al Batin 31991, Saudi Arabia.
FAU - Gauthaman, Kalamegam
AU  - Gauthaman K
AD  - Center of Excellence in Genomic Medicine Research, King Abdulaziz University, 
      Jeddah 21589, Saudi Arabia.
AD  - Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, 
      King Abdulaziz University, Jeddah 21589, Saudi Arabia.
FAU - Prola, Alexandre
AU  - Prola A
AD  - Department of Cell Physiology and Metabolism, Faculty of Medicine, University of 
      Geneva, 1 rue Michel-Servet, CH-1211, Geneva 1202, Switzerland.
LA  - eng
PT  - Journal Article
DEP - 20201108
PL  - Switzerland
TA  - Pharmaceuticals (Basel)
JT  - Pharmaceuticals (Basel, Switzerland)
JID - 101238453
PMC - PMC7695206
OTO - NOTNLM
OT  - atherosclerosis
OT  - cholesterol efflux
OT  - inflammation
OT  - monocyte migration
OT  - punicalagin
COIS- The authors declare no conflict of interest.
EDAT- 2020/11/12 06:00
MHDA- 2020/11/12 06:01
PMCR- 2020/11/01
CRDT- 2020/11/11 01:01
PHST- 2020/10/20 00:00 [received]
PHST- 2020/11/05 00:00 [revised]
PHST- 2020/11/06 00:00 [accepted]
PHST- 2020/11/11 01:01 [entrez]
PHST- 2020/11/12 06:00 [pubmed]
PHST- 2020/11/12 06:01 [medline]
PHST- 2020/11/01 00:00 [pmc-release]
AID - ph13110372 [pii]
AID - pharmaceuticals-13-00372 [pii]
AID - 10.3390/ph13110372 [doi]
PST - epublish
SO  - Pharmaceuticals (Basel). 2020 Nov 8;13(11):372. doi: 10.3390/ph13110372.