Abstract
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 µM 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 µM) on THP-1 macrophages. Punicalagin inhibited the IFN-γ-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-γ 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.
Highlights
Cardiovascular-related diseases (CVD) remain the leading cause of death globally in comparison to other chronic illnesses
Punicalagin-induced cytotoxicity was measured by lactate dehydrogenase (LDH) assays whereas cell viability was measured by crystal violet using 10 μM concentration of punicalagin on THP-1 macrophages
Punicalagin treatment induced no significant difference in macrophage viability mcoamcrpoaprhedagwe itvhiavbeihliitcyle-ctoremapteadrecdellws i(tFhiguverehi1cble).-tFreuarttehdermceollrse,(cFoigmubriene1db)fi.nFduinrtghsefrrmomorec,rycsotaml bviinoeledt fainnddiLnDgsHfraosmsacyrsy,s1t0alμvMiolceotnacnedntLrDatHionasosfaypsu,n1i0caμlMagicnonwcaesntursaetidonfoorffpuurtnhiecraPlaCgRin. was used for further PCR
Summary
Cardiovascular-related diseases (CVD) remain the leading cause of death globally in comparison to other chronic illnesses. In 2012, CVD was responsible for 31%, or 17.5 million deaths across the globe, and the number of fatalities is estimated to rise to approximately 23.3 million within the decade [1]. Atherosclerosis remains the primary cause of deadly heart diseases [3] and occurs when long-lasting inflammation affects the vascular system. Atherosclerosis is a progressive illness that results from the accumulation of fatty acids and lipids in medium- and large-sized arteries, which become precursors to the buildup of plaque [4]. Size of plaque increase and may eventually rupture, releasing vast amounts of necrotic fragments into the bloodstream, increasing the probability of blood clots leading to myocardial infarctions, stroke, or both [5]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
