The protective role of curcumin in cardiovascular diseases

Wongcharoen, Wanwarang; Phrommintikul, Arintaya

doi:10.1016/j.ijcard.2009.01.073

Cited by 260 publications

(154 citation statements)

References 56 publications

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“…It has been used for thousands of years in China and India as an antiinflammatory medicinal agent. Antioxidant and anti-carcinogenic effects of Cur have also been reported [7,8]. In particular, its antioxidant activity contributes to cardioprotection in in vivo and in vitro models and attenuates cardiac hypertrophy and heart failure by inhibiting p300 HAT activity in animal models [8][9][10].…”

Section: Introductionmentioning

confidence: 97%

Curcumin Attenuates Doxorubicin-Induced Cardiotoxicity by Inducing Autophagy via the Regulation of JNK Phosphorylation

Katamura¹,

Iwai-Kanai²,

Nakaoka³

et al. 2014

J Clin Exp Cardiolog

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Background and Objective: Doxorubicin (DOX) has been used in cancer therapy for several decades. However, cardiac complications induced by DOX dose-dependently limit the clinical implication at optimal antitumor efficacy. Curcumin (Cur), a natural compound, has been effective as an anticancer agent in various types of cancers. It also protects against cardiac hypertrophy and heart failure, though its effect on cardiomyopathy caused by DOX treatment is unclear. To elucidate the role of curcumin on heart failure, we used the DOX induced cardiomyopathy model and primary cultured cardiac myocytes. Method and Results:Male C57/BL6 mice were randomized to 4 courses of treatment administered for 4 weeks: Phosphate-Buffered Saline (PBS), Cur, DOX, and DOX+Cur. DOX-treated mice exhibited severe cardiac dysfunction, and the mortality was higher than that in PBS-treated mice. In DOX-treated mice, the number of apoptotic cardiac myocytes was higher and the fibrotic areas were larger than in PBS-treated mice. The cardiotoxic effects of DOX were ameliorated by treatment with Cur. In DOX-treated GFP-LC3 transgenic mice, Cur induced autophagy and decreased apoptosis in the heart. Cur also induced autophagy and suppressed DOX-induced apoptosis in neonatal rat cardiac myocytes. Inhibition of autophagy by 3-methyladenine decreased the cardioprotective effect of Cur. Furthermore, Cur decreased c-Jun N-terminal kinase (JNK) phosphorylation, resulting in reduction of apoptosis. The JNK inhibitor SP600125 abolished these effects. Conclusion:Cur protects the heart from DOX-induced cardiotoxicity by inducing autophagy and decreasing cardiomyocyte apoptosis. The mechanism involves JNK-mediated modification of apoptosis. Induction of cardiac autophagy may be a novel therapeutic approach for preventing DOX-induced cardiotoxicity.

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Section: Introductionmentioning

confidence: 97%

Curcumin Attenuates Doxorubicin-Induced Cardiotoxicity by Inducing Autophagy via the Regulation of JNK Phosphorylation

Katamura¹,

Iwai-Kanai²,

Nakaoka³

et al. 2014

J Clin Exp Cardiolog

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“…In the last decades, the anti‐inflammatory and anticancer activity of curcumin has been reported (Wongcharoen & Phrommintikul, 2009), and safety of curcumin consumption and use in clinical treatment has been shown (Chainani‐Wu, 2003). Recently, the curcumin has been reported to reduce aneurysmal degeneration (Parodi et al., 2006).…”

Section: Discussionmentioning

confidence: 99%

A study on effect of curcumin on anticerebral aneurysm in the male albino rats

Miao

Wang

et al. 2017

Brain and Behavior

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IntroductionThis study investigated the curcumin effect on the cerebral aneurysm. Apoptosis is known to play a fundamental role in the pathogenesis of a cerebral aneurysm. Therefore, we investigated the effect of curcumin on apoptosis of smooth muscle cells of a cerebral aneurysm‐induced male albino rats.MethodsIn this study, the cerebral aneurysm has been induced in the male albino rats by the CaCl2 administration. After cerebral aneurysm induction, smooth muscle cells were isolated. Cells were treated with curcumin (25 & 50 mg/kg bwt) for 48 hr.ResultsCurcumin reduced altered mitochondrial morphology significantly, evidenced through fluorescence and confocal study. Curcumin treatment reduced the expression of p53, caspase‐3, and bax/bxl‐2 ratio significantly. Curcumin treatment also reversed the cellular architecture of smooth muscle cell wall significantly. Fluorescence and the confocal study confirmed the reduction in apoptosis in a cerebral aneurysm‐induced smooth muscle cells of male albino rats.ConclusionTaking all these data together, it may suggest that the curcumin could significantly reduce the CaCl2‐induced cerebral aneurysm through the inhibition of cell apoptosis in the cells.

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“…Sano (2007) determined that curcumin inhibited HAT mutp300 and TSA due to its strong antioxidant potential as well as prevented from the p300-GATA4 complex formation in animal models. It also protects from the development of atherosclerotic lesions (Olszanecki et al 2005;Wongcharoen & Phrommintikul 2009). It averts heart failure in animal models and myocardial hypertrophy development, inhibits hypertrophy inducing transcription factors such as p300-histone transacetylase and downregulates nitric oxide synthase (NOS) (Morimoto et al 2008;Wongcharoen & Phrommintikul 2009).…”

Section: Cardiovascular Role Of Curcuminmentioning

confidence: 99%

“…It also protects from the development of atherosclerotic lesions (Olszanecki et al 2005;Wongcharoen & Phrommintikul 2009). It averts heart failure in animal models and myocardial hypertrophy development, inhibits hypertrophy inducing transcription factors such as p300-histone transacetylase and downregulates nitric oxide synthase (NOS) (Morimoto et al 2008;Wongcharoen & Phrommintikul 2009). Curcumin also reduces the nitric oxide production through the mediation of AP-1, NFkB, and many vasoactive factors.…”

Section: Cardiovascular Role Of Curcuminmentioning

confidence: 99%

Curcumin and its allied analogues: epigenetic and health perspectives - a review

Imran¹,

Nadeem²,

Khan³

et al. 2017

Czech J. Food Sci.

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Curcumin (diferuoyl methane) is a yellow active ingredient present in turmeric. It is a homodimer of feruloylmethane that comprises a hydroxyl and methoxy group (heptadiene with two Michael acceptors), and α-, β-diketone. It contains various metabolites, i.e. hexahydrocurcumin (HHC), tetrahydrocurcumin (THC), octahydrocurcumin (OHC), dihydrocurcumin (DHC), curcumin sulphate, and curcumin glucuronide. Curcumin has been proven the most effective histone deacetylase (HDAC) inhibitor in HeLa nuclear extracts. It has the ability to affect the Akt, growth factors, NF-kB, and metastatic and angiogenic pathways. Curcumin has a strong therapeutic or preventive potential against several major human ailments, i.e. suppression of inflammation, cardiovascular, diabetes, tumorigenesis, chronic fatigue, antidepressant and neurological activities, depression, loss of muscle and bone, and neuropathic pain. In future, higher utilisation of curcumin as an active agent in food based products is required to curtail the human health disorders.

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The protective role of curcumin in cardiovascular diseases

Cited by 260 publications

References 56 publications

Curcumin Attenuates Doxorubicin-Induced Cardiotoxicity by Inducing Autophagy via the Regulation of JNK Phosphorylation

Curcumin Attenuates Doxorubicin-Induced Cardiotoxicity by Inducing Autophagy via the Regulation of JNK Phosphorylation

A study on effect of curcumin on anticerebral aneurysm in the male albino rats

Curcumin and its allied analogues: epigenetic and health perspectives - a review

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