curcumin and astaxanthine

The blockade of the progression or onset of pathological events is essential for the homeostasis of an organism. Some common pathological mechanisms involving a wide range of diseases are the uncontrolled inflammatory reactions that promote fibrosis, oxidative reactions, and other alterations. Natural plant compounds (NPCs) are bioactive elements obtained from natural sources that can regulate physiological processes. Inflammation is recognized as an important factor in the development and evolution of chronic renal damage. Consequently, any compound able to modulate inflammation or inflammation-related processes can be thought of as a renal protective agent and/or a potential treatment tool for controlling renal damage. The objective of this research was to review the beneficial effects of bioactive natural compounds on kidney damage to reveal their efficacy as demonstrated in clinical studies.. This systematic review is based on relevant studies focused on the impact of NPCs with therapeutic potential for kidney disease treatment in humans.. Clinical studies have evaluated NPCs as a different way to treat or prevent renal damage and appear to show some benefits in improving OS, inflammation, and antioxidant capacity, therefore making them promising therapeutic tools to reduce or prevent the onset and progression of KD pathogenesis.. This review shows the promising clinical properties of NPC in KD therapy. However, more robust clinical trials are needed to establish their safety and therapeutic effects in the area of renal damage.

Topics: Antioxidants; Berberine; Beta vulgaris; Betalains; Biological Products; Catechin; Curcumin; Disulfides; Flavonoids; Humans; Isothiocyanates; Kidney; Kidney Diseases; Plant Extracts; Pomegranate; Protective Agents; Resveratrol; Sulfinic Acids; Sulfoxides; Xanthophylls

Increasing prevalence of nonalcoholic fatty liver disease (NAFLD) in parallel with the obesity epidemic has been a major public health concern. NAFLD is the most common chronic liver disease in the United States, ranging from fatty liver to steatohepatitis, fibrosis and cirrhosis in the liver. In response to chronic liver injury, fibrogenesis in the liver occurs as a protective response; however, prolonged and dysregulated fibrogenesis can lead to liver fibrosis, which can further progress to cirrhosis and eventually hepatocellular carcinoma. Interplay of hepatocytes, macrophages and hepatic stellate cells (HSCs) in the hepatic inflammatory and oxidative milieu is critical for the development of NAFLD. In particular, HSCs play a major role in the production of extracellular matrix proteins. Studies have demonstrated that bioactive food components and natural products, including astaxanthin, curcumin, blueberry, silymarin, coffee, vitamin C, vitamin E, vitamin D, resveratrol, quercetin and epigallocatechin-3-gallate, have antifibrotic effects in the liver. This review summarizes current knowledge of the mechanistic insight into the antifibrotic actions of the aforementioned bioactive food components.

Topics: Blueberry Plants; Coffee; Curcumin; Food; Hepatic Stellate Cells; Hepatocytes; Humans; Liver Cirrhosis; Macrophages; Non-alcoholic Fatty Liver Disease; Oxidative Stress; Resveratrol; Vitamins; Xanthophylls

Non-alcoholic fatty liver disease (NAFLD) is a clinical condition characterized by lipid infiltration of the liver, highly prevalent in the general population affecting 25% of adults, with a doubled prevalence in diabetic and obese patients. Almost 1/3 of NAFLD evolves in Non-Alcoholic SteatoHepatitis (NASH), and this can lead to fibrosis and cirrhosis of the liver. However, the main causes of mortality of patients with NAFLD are cardiovascular diseases. At present, there are no specific drugs approved on the market for the treatment of NAFLD, and the treatment is essentially based on optimization of lifestyle. However, some nutraceuticals could contribute to the improvement of lipid infiltration of the liver and of the related anthropometric, haemodynamic, and/or biochemical parameters. The aim of this paper is to review the available clinical data on the effect of nutraceuticals on NAFLD and NAFLD-related parameters. Relatively few nutraceutical molecules have been adequately studied for their effects on NAFLD. Among these, we have analysed in detail the effects of silymarin, vitamin E, vitamin D, polyunsaturated fatty acids of the omega-3 series, astaxanthin, coenzyme Q10, berberine, curcumin, resveratrol, extracts of

Topics: Antioxidants; Berberine; Curcumin; Dietary Supplements; Fatty Acids, Omega-3; Fatty Acids, Unsaturated; Humans; Meta-Analysis as Topic; Non-alcoholic Fatty Liver Disease; Obesity; Observational Studies as Topic; Plant Extracts; Probiotics; Randomized Controlled Trials as Topic; Resveratrol; Salvia miltiorrhiza; Silymarin; Ubiquinone; Vitamin D; Vitamin E; Xanthophylls

Non-alcoholic fatty liver disease (NAFLD) is a common clinicopathological condition, encompassing a range of conditions caused by lipid deposition within liver cells. To date, no approved drugs are available for the treatment of NAFLD, despite the fact that it represents a serious and growing clinical problem in the Western world. Identification of the molecular mechanisms leading to NAFLD-related fat accumulation, mitochondrial dysfunction and oxidative balance impairment facilitates the development of specific interventions aimed at preventing the progression of hepatic steatosis. In this review, we focus our attention on the role of dysfunctions in mitochondrial bioenergetics in the pathogenesis of fatty liver. Major data from the literature about the mitochondrial targeting of some antioxidant molecules as a potential treatment for hepatic steatosis are described and critically analysed. There is ample evidence of the positive effects of several classes of antioxidants, such as polyphenols (

Topics: Animals; Anthocyanins; Antioxidants; Carotenoids; Catechin; Coumestrol; Curcumin; Energy Metabolism; Fatty Liver; Glucosinolates; Humans; Imidoesters; Isothiocyanates; Lipogenesis; Mitochondria; Non-alcoholic Fatty Liver Disease; Nutritional Sciences; Oxidative Stress; Oximes; Polyphenols; Quercetin; Resveratrol; Stilbenes; Sulfoxides; Xanthophylls

This study aimed to: 1) investigate sex differences in heat-induced mitochondrial dysfunction, ROS production, and skeletal muscle injury in mice; 2) evaluate whether curcumin and astaxanthin, alone or together, would prevent those heat-induced changes.. Male and female C57BL/6J mice were treated with curcumin and astaxanthin for 10 days, then exposed to 39.5 °C heat for up to 3 h. Heat-induced hyperthermia, changes in mitochondrial morphology and function, and oxidative damage to skeletal muscle were evaluated.. Although female mice had a slightly higher basal core body temperature (Tc) than male mice, peak Tc during heat exposure was significantly lower in females than in males. Heat increased ROS levels in skeletal muscle in both sexes; interestingly, the increases in ROS were greater in females than in males. Despite the above-mentioned differences, heat induced similar levels of mitochondrial fragmentation and membrane potential depolarization, caspase 3/7 activation, and injury in male and female skeletal muscle. Individual treatment of curcumin or astaxanthin did not affect basal and peak Tc but prevented heat-induced mitochondrial dysfunction, ROS increases, and apoptosis in a dose-dependent manner. Moreover, a low-dose combination of curcumin and astaxanthin, which individually showed no effect, reduced the heat-induced oxidative damage to skeletal muscle.. Both male and female mice can develop mitochondrial dysfunction and oxidative stress in skeletal muscle when exposed to heat stress. High doses of either curcumin or astaxanthin limit heat-induced skeletal muscle injury, but a low-dose combination of these ingredients may increase their efficacy.

Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Curcumin; Diet; Female; Heat-Shock Response; Hyperthermia, Induced; Male; Mice; Mice, Inbred C57BL; Muscle, Skeletal; Muscular Diseases; Oxidative Stress; Protective Agents; Reactive Oxygen Species; Xanthophylls

The antioxidant activity of food compounds is one of the properties generating the most interest, due to its health benefits and correlation with the prevention of chronic disease. This activity is usually measured using in vitro assays, which cannot predict in vivo effects or mechanisms of action. The objective of this study was to evaluate the in vivo protective effects of six phenolic compounds (naringenin, apigenin, rutin, oleuropein, chlorogenic acid, and curcumin) and three carotenoids (lycopene B, β-carotene, and astaxanthin) naturally present in foods using a zebrafish embryo model. The zebrafish embryo was pretreated with each of the nine antioxidant compounds and then exposed to tert-butyl hydroperoxide (tBOOH), a known inducer of oxidative stress in zebrafish. Significant differences were determined by comparing the concentration-response of the tBOOH induced lethality and dysmorphogenesis against the pretreated embryos with the antioxidant compounds. A protective effect of each compound, except β-carotene, against oxidative-stress-induced lethality was found. Furthermore, apigenin, rutin, and curcumin also showed protective effects against dysmorphogenesis. On the other hand, β-carotene exhibited increased lethality and dysmorphogenesis compared to the tBOOH treatment alone.

Topics: Animals; Antioxidants; Apigenin; beta Carotene; Biological Factors; Carotenoids; Curcumin; Disease Models, Animal; Dose-Response Relationship, Drug; Embryo, Nonmammalian; Embryonic Development; Flavanones; Lycopene; Oxidative Stress; Polyphenols; tert-Butylhydroperoxide; Xanthophylls; Zebrafish

Protein-based nanoassemblies can encapsulate hydrophobic compounds into their hydrophobic region and effectively improve their aqueous solubility and stability. However, hydrolyzed food protein based micellar nanoassemblies and their interaction with different hydrophobic compounds are less understood. Here, 20 nm α-lactalbumin (α-lac) micellar nanoassemblies were constructed via self-assembly of partially hydrolyzed α-lac peptides by Bacillus licheniformis proteinase. We identified three fractions of peptides which reorganized into this kind of nanomicelle after exposure of α-lac hydrophobic groups. Moreover, four hydrophobic compounds (curcumin, quercetin, astaxanthin, coenzyme Q10) were successfully loaded into nanomicelles mainly via hydrophobic interactions. Among these four compounds, curcumin was most encapsulated in micelles due to its smaller molecular weight, high hydrophobicity and less steric hindrance. The strongest interaction was also observed between curcumin and nanomicelles. Finally, their aqueous solubility and UV stability after micellar encapsulation were significantly improved. This demonstrated that α-lac micelles are promising delivery systems for hydrophobic compounds.

Topics: Bacillus licheniformis; Bacterial Proteins; Curcumin; Drug Compounding; Hydrolysis; Hydrophobic and Hydrophilic Interactions; Lactalbumin; Micelles; Peptide Hydrolases; Quercetin; Solubility; Ubiquinone; Xanthophylls

Sympathomimetic and trace amines, including β-phenylethylamine (PEA) and amphetamine, increase blood pressure and constrict isolated blood vessels. By convention this is regarded as a sympathomimetic response, however, recent studies suggest trace amine-associated receptor (TAAR) involvement. There is also uncertainty whether these amines also release nitric oxide (NO) causing opposing vasodilatation. These questions were addressed in guinea-pig isolated aorta, a species not previously examined. Guinea-pig aortic rings were set up to measure contractile tension. Cumulative concentration-response curves were constructed for the reference α-adrenoceptor agonist, phenylephrine, PEA or d-amphetamine before and in the presence of vehicles, the α

Topics: Amphetamine; Animals; Aorta; Curcumin; Guinea Pigs; Male; NG-Nitroarginine Methyl Ester; Nitric Oxide; Phenethylamines; Phenylephrine; Prazosin; Vasoconstriction; Vasodilation; Xanthophylls

We previously developed a lutein-polyvinylpyrrolidone (PVP) complex with improved aqueous saturation solubility and stability, though the conjugation mechanism is still unclear. In this paper, experiments with astaxanthin-PVP complex and curcumin-PVP complex were carried out, which indicated that PVP could improve the solubility and stability of astaxanthin and curcumin. We aimed to construct a computational model capable of understanding the protective effect in complexes formed between PVP and antioxidants, through which the binding mode of PVP and antioxidants was investigated with molecular modelling in order to obtain the interactions, binding energy, binding site and surface area between PVP and antioxidants. Solubility enhancement was attributed to the H-bonds between PVP and antioxidants, and the saturation solubility was curcumin > lutein > astaxanthin. Binding energy, binding site and surface area were beneficial for the stability of complex, and the stability enhancement was lutein > astaxanthin > curcumin. The experimental results were in agreement with the computational results. Furthermore, we established a method for the exploration of a similar system with other polymer complexes. Additionally, the proposed PVP model could predict the interactions between PVP and various ligands, such as antioxidants and drugs.

Topics: Antioxidants; Binding Sites; Computer Simulation; Curcumin; Hydrogen Bonding; Models, Molecular; Povidone; Solubility; Xanthophylls

Advances in understanding the neurodegenerative pathologies are creating new opportunities for the development of neuroprotective therapies, such as antioxidant food factors, lifestyle modification and drugs. However, the biomarker by which the effect of the agent on neurodegeneration is determined is limited. We here address hexanoyl dopamine (HED), one of novel dopamine adducts derived from brain polyunsaturated acid, referring to its in vitro formation, potent toxicity to SH-SY5Y cells, and application to assess the neuroprotective effect of antioxidative food factors. Dopamine is a neurotransmitter, and its deficiency is a characterized feature in Parkinson's disease (PD); thus, HED provides a new insight into the understanding of dopamine biology and pathophysiology of PD and a novel biomarker for the assessment of neuroprotective therapies. We have established an analytical system for the detection of HED and its toxicity to the neuroblstoma cell line, SH-SY5Y cells. Here, we discuss the characteristics of the system and its applications to investigate the neuroprotective effect of several antioxidants that originate from food.

Topics: Antioxidants; Cell Line, Tumor; Cell Survival; Chromatography, High Pressure Liquid; Curcumin; Dioxoles; Dopamine; Humans; Lignans; Neuroblastoma; Parkinson Disease; Tandem Mass Spectrometry; Tocopherols; Tocotrienols; Xanthophylls

Advances in understanding the neurodegenerative pathologies are creating new opportunities for the development of neuroprotective therapies, such as antioxidant food factors, lifestyle modification, and drugs. However, the biomarker by which to determine the effect of the agent on neurodegeneration is limited. We here address hexanoyl dopamine (HED), one of novel dopamine adducts derived from brain polyunsaturated acid, referring to its in vitro formation, potent toxicity to SH-SY5Y cells, and application to assess the neuroprotective effect of antioxidative food factors. Dopamine is a neurotransmitter and its deficiency is a characterized feature in Parkinson's disease (PD), thereby HED represents a new addition to understanding of dopamine biology and pathophysiology of PD and a novel biomarker for the assessment of neuroprotective therapies. We have established an analytical system using for the detection of HED and its toxicity to the neuroblstoma cell line, SH-SY5Y cells. Here, we discuss the characteristics of the system and its applications to investigate the neuroprotective effect of several antioxidants that originate from food.

Topics: Antioxidants; Cell Line, Tumor; Cell Survival; Chromatography, High Pressure Liquid; Curcumin; Dioxoles; Dopamine; Food; Humans; Lignans; Neuroprotective Agents; Oxidative Stress; Parkinson Disease; Tandem Mass Spectrometry; Tocopherols; Tocotrienols; Xanthophylls

Curcumin manganese complex (CpCpx) and diacetylcurcumin manganese complex (AcylCpCpx) were determined as to their effect on the nitric oxide (NO) radical scavenging in vitro method using a sodium nitroprusside generating NO system compared with their parent compound and astaxanthin, an extreme antioxidant. All compounds effectively reduced the generation of NO radicals in a dose dependent manner. They exhibited strong NO radical scavenging activity with low IC(50) values. The IC(50) values of curcumin, diacetylcurcumin, CpCpx and AcylCpCpx obtained are 20.39+/-4.10 microM, 28.76+/-1.48 microM, 9.79+/-1.50 microM and 8.09+/-0.99 microM, respectively. CpCpx and AcylCpCpx show greater NO radical scavenging than their parent compounds, curcumin and acetylcurcumin, respectively. However, the IC(50) values of curcumin and related compounds were found to be less than astaxanthin, an extreme antioxidant, with the lower IC(50) value of 3.42+/-0.50 microM.

Topics: beta Carotene; Curcumin; Free Radical Scavengers; Manganese; Nitric Oxide; Nitroprusside; Quercetin; Structure-Activity Relationship; Xanthophylls