Review Article

Regulation of Sirtuin-Mediated Protein Deacetylation by Cardioprotective Phytochemicals

Table 3

Other emerging cardioprotective phytochemicals regulating protein acetylation.

PhytochemicalTarget HDAC or HATMolecular pathwayModelCardiovascular effectReference

Honokiol↑ Sirt3↓ collagen, B-MHC, and ANFTAC induced heart failure model
In vivo
PE and Ang II-induced cardiac hypertrophy
In vitro
Blocks cardiac hypertrophic response
Ameliorates preexisting hypertrophy
↓ oxidative stress
[37]
Oroxylin A↑ Sirt3↑ aldehyde dehydrogenaseInsulin-induced cardiac dysfunction
In vitro
Preserved cardiac myocyte contractility[87]
Epigallocatechin-3-gallate↑ Sirt1↑ AMPK-α
↑ eNOS
High-fat diet-induced hypercholesterolemia
In vivo
↓ serum cholesterol
↓ oxidative stress
Improved morphology of myocardial tissue
[90]
↓ Ac-FoxO1
↓ Nrf2
High-glucose-induced-autophagy
In vitro
↓ ROS
↓ autophagy
[89]
Quercetin↑ Sirt1↑ AMPK-α
↑ eNOS
↓ NOX2
↓ NOX4
↓ NF-κB
OxLDL-induced endothelial oxidative stress
In vitro
Preserved mitochondrial function
↓ inflammation
[91]
Berberine↑ Sirt1↑ SOD
↑ Bcl-2
↓ Bax, caspase 3
Ischemia/reperfusion-induced myocardial Infraction
In vivo
Simulated ischemia/reperfusion model
In vitro
↓ infract size
↓ oxidative stress
↓ apoptosis
↓ LDH
Maintained LVEF and LVFS
Inhibited increase in IL-6 and TNF-α
[92]
Bakuchiol↑ Sirt1GC-1α
↑ Bcl2
↓ Bax, caspase 3
↑ SOD, SDH, Cyt-c oxidase
Ischemia reperfusion-induced myocardial infraction
Ex vivo
Simulated ischemia/reperfusion model
In vitro
Rat cardiac myocytes
↓ apoptosis
↓ oxidative stress
Maintained mitochondrial bioenergetics
[93]
n-Tyrosol↑ Sirt1↑ Akt
↑ eNOS
↑ Foxo3a
TAC induced myocardial infraction
In vivo
↓ infract size
↓ apoptosis
↓ fibrosis
↑ LVIDd
↑ EF
↑ FS
[94]
α-Lipoic acid↑ Sirt1↓ PARP-2TAC-induced cardiac hypertrophy
In vivo
Ang II-induced hypertrophy
In vitro
↓ cardiac hypertrophy[95]
Docosahexaenoic acid↑ Sirt1↑ eNOSIn vitro
Ex vivo
↑ NO synthesis
↑ bioavailable NO
[26]
Sulforaphane↑ Sirt1↑ Nrf2, NQo1, HO-1
↓ PAI-I, TNF-α, CTFG, TGF-β
Preserved LKB1/AMPK/PGC-1α
T2DM-induced cardiomyopathy
In vivo
↓ cardiac remodeling
↓ cardiac dysfunction
↓ cardiac lipid accumulation
↓ oxidative stress
↓ inflammation
↓ fibrosis
[96]
Caffeic acid ethanolamide↑ Sirt1
↑ Sirt3
↑ SOD, HIF1-αIsoproterenol-induced cardiac dysfunction
In vivo
In vitro
Restored oxygen consumption rates
Preserved ATP levels
↓ cardiac remodeling
↓ oxidative stress
Preserved mitochondrial function
[97]

AMPK: adenosine monophosphate-activated kinase; ANF: atrial natriuretic factor; Ang II: angiotensin II; B-MHC: myosin heavy chain B; CTFG: connective tissue growth factor; Cyt-c: cytochrome c; Dox: doxorubicin; EF: ejection fraction; eNOS: endothelial nitrix oxide synthase; FS: fractional shortening; HIF1-α: hypoxia inducible factor 1-α; HO-1: heme oxygenase; LDH: lactate dehydrogenase; LKB1; liver kinase B 1; LVID internal diameter in diastole; left ventricular, LVEF: left ventricular ejection fraction; NE: norepinephrine; NQo1: NAD(P)H quinone dehydrogenase 1; PAI-I: plasminogen activator inhibitor 1; PARP-2: poly(ADP-ribose) polymerase 2; PGC1-α: peroxisome proliferator activator of transcription (PPARy) coactivator 1α; PE: phenylephrine TAC: transverse aortic constriction; T2DM: type 2 diabetes mellitus; SHD: succinate dehydrogenase; SOD: superoxide dismutase.