curcumin and Coronary-Disease

This study assessed the effects of curcumin intake on psychological status, markers of inflammation and oxidative damage in patients with type 2 diabetes mellitus (T2DM) and coronary heart disease (CHD).. This randomized, double-blind, placebo-controlled trial was performed in 60 patients with T2DM and CHD, aged 45-85 years with 2- and 3-vessel CHD. Patients were randomized into two groups to receive either 1000 mg/day curcumin (n = 30) or placebo (n = 30) for 12 weeks. Using RT-PCR method, gene expression related to insulin metabolism and inflammatory markers on mononuclear cells from peripheral blood was evaluated.. Curcumin intake significantly decreased Pittsburgh Sleep Quality Index (PSQI) (β -1.27; 95% CI, -2.27, -0.31; P = 0.01) compared to the placebo group. Curcumin intake caused a significant reduction in malondialdehyde (MDA) (β -0.20 μmol/L; 95% CI, -0.36, -0.04; P = 0.01), significant increase in total antioxidant capacity (TAC) (β 75.82 mmol/L; 95% CI, 3.400, 148.25; P = 0.04) and glutathione (GSH) levels (β 63.48 μmol/L; 95% CI, 26.58, 100.37; P = 0.001) when compared with the placebo. Additionally, curcumin intake upregulated peroxisome proliferator-activated receptor gamma (PPAR-γ) (P = 0.01).. Curcumin intake for 12 weeks in patients with T2DM and CHD had beneficial effects on PSQI, TAC, GSH, MDA values, and gene expression of PPAR-γ. This study was retrospectively registered in the Iranian website (www.irct.ir) for registration of clinical trials (http://www.irct.ir: IRCT20170513033941N63).

Topics: Blood Glucose; C-Reactive Protein; Coronary Disease; Curcumin; Diabetes Mellitus, Type 2; Humans; Inflammation; Iran; Oxidative Stress

Coronary heart disease(CHD) is a common cardiovascular disease in clinical practice. Curcumae Rhizoma(CR), an important herbal medicine for breaking blood stasis and resolving mass, is often used for the treatment of CHD caused by blood stasis syndrome. However, the anti-CHD components, targets, and mechanism are still unclear. Therefore, in this study, the chemical components of CR were separated and identified by ultra high performance liquid chromatography-quadrupole-time-of-flight mass spectrometry(UPLC-Q-TOF-MS/MS). Based on the identified components, network pharmacology analysis, including target prediction and functional enrichment, was applied to screen out the main active components against CHD, and the potential mechanism was discussed. Finally, molecular docking was performed to verify the binding between the active components and the targets. The results showed that among the 52 chemical components identified in CR, 28 were related to CHD, involving 75 core targets. The core components included(4S)-4-hydroxy-gweicurculactone, curcumadione, and curcumenone, and the core targets included phosphatidylinositol-4,5-bisphosphate 3-kinase, catalytic subunit alpha(PIK3 CA), mitogen-activated protein kinase 1(MAPK1), and mitogen-activated protein kinase 3(MAPK3). In summary, through the active components, such as(4S)-4-hydroxy-gweicurculactone, curcumadione, and curcumenone, CR regulates the nerve repair, vasoconstriction, lipid metabolism, and inflammatory response, thereby exerts therapeutic effect on CHD.

Topics: Coronary Disease; Curcuma; Drugs, Chinese Herbal; Humans; Molecular Docking Simulation; Tandem Mass Spectrometry

Coronary microembolization (CME) is a common complication during the percutaneous coronary intervention (PCI). CME-induced local myocardial inflammation and myocardial apoptosis are the primary causes of progressive cardiac dysfunction. Curcumin exerts a protective role in various cardiovascular diseases; however, its effects in CME are yet to be clarified. Therefore, the current study investigated the effects of curcumin on myocardial inflammatory responses, myocardial apoptosis, and cardiac dysfunctions induced by CME in rats.. A total of 40 Sprague-Dawley rats were randomly divided into the following groups: Sham operation (sham group), CME group, curcumin, and control with 10 rats in each group. The ascending aortas were clamped, and the CME-model group was established by injecting microspheres into the apex of the left ventricle. An equivalent amount of normal saline was injected to establish the sham group. The cardiac functions, serum c-troponin I level, and apoptotic index was examined. Also, the levels of Toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MYD88), nuclear factor κB (NF-κB) p65, BCL2-associated X protein (Bax), B-cell lymphoma 2 (Bcl-2), cleaved caspase-3, tumor necrosis factor α (TNF-α), and interleukin-1β (IL-1β) were detected.. Myocardial dysfunction enhanced serum c-troponin I, and apoptotic index were induced following CME. Moreover, CME elevated the expression of TLR4, MyD88, NF-κB p65, cleaved caspase-3, TNF-α, and IL-1β, while the Bcl-2/Bax ratio decreased. Curcumin reversed these effects by CME, while the gastric lavage control did not exert any effect.. Curcumin was responsible for the anti-CME-induced myocardial injury. The effector mechanism might be related to the reduction of cardiomyocyte apoptosis and inhibition of myocardial inflammatory responses mediated by TLR4/MyD88/NF-κB signaling pathway.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Coronary Disease; Curcumin; Embolism; Gene Expression Regulation; Heart Injuries; Male; Myeloid Differentiation Factor 88; Myocardial Infarction; Myocytes, Cardiac; NF-kappa B; Rats; Rats, Sprague-Dawley; Toll-Like Receptor 4

Chronic inflammation and oxidative stress increase with advancing age and appear to be involved in the pathogenesis of coronary heart disease, the leading cause of death worldwide. There is a need for animal models that reflect the increases in pro-inflammatory cytokines and oxidative damage observed during aging in humans. We therefore aimed to investigate the suitability of the fast-aging senescence-accelerated mouse-prone 8 (SAMP8) strain and its normally aging control senescence-accelerated mouse-resistant 1 (SAMR1) to study the age-dependent changes in cytokines, oxidative damage and antioxidants in the heart. To this end, 2-months-old male SAMR1 and SAMP8 mice were fed a Western type diet (control groups) for 5 months. Two groups of SAMP8 mice were simultaneously fed identical diets fortified with 0.5 g curcumin or 1.0 g Ginkgo biloba extract EGb 761(®) per kg diet. Heart tissue homogenates were analysed for protein carbonyls, glutathione, glutathione disulfide, methionine, cysteine and uric acid as well as the cytokines tumor-necrosis factor-α, interleukin-1β, interleukin-6, and monocyte chemoattractant protein 1. Neither the strain (SAMR1 or SAMP8) nor antioxidant intake (curcumin or EGb 761(®)) affected the concentrations of the measured parameters. In conclusion, our data do not support the suitability of the SAMP8 and SAMR1 strains as a model to study age-related changes in pro-inflammatory cytokines and oxidative stress parameters in the heart.

Topics: Age Factors; Aging; Animals; Antioxidants; Atherosclerosis; Coronary Disease; Curcumin; Cytokines; Female; Ginkgo biloba; Heart; Humans; Inflammation; Interleukin-1beta; Interleukin-6; Male; Mice; Mice, Inbred C57BL; Mice, Inbred Strains; Models, Animal; Oxidative Stress; Plant Extracts; Protein Carbonylation