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PubMed2006

Determinants of arterial wall remodeling during lipid-lowering therapy: serial intravascular ultrasound observations from the Reversal of Atherosclerosis with Aggressive Lipid Lowering Therapy (REVERSAL) trial.

BACKGROUND: Coronary plaque progression and instability are associated with expansive remodeling of the arterial wall. However, the remodeling response during plaque-stabilizing therapy and its relationship to markers of lipid metabolism and inflammation are incompletely understood. METHODS AND RESULTS: Serial intravascular ultrasound (IVUS) data from the Reversal of Atherosclerosis with Aggressive Lipid Lowering Therapy (REVERSAL) trial were obtained during 18 months of intensive versus moderate lipid-lowering therapy. In a subgroup of 210 patients, focal coronary lesions with mild luminal narrowing were identified. Lumen area, external elastic membrane (EEM) area, and plaque area were determined at the lesion and proximal reference sites at baseline and during follow-up. The remodeling ratio (RR) was calculated by dividing the lesion EEM area by the reference EEM area. The relationship between the change in remodeling, change in plaque area, lipid profile, and inflammatory markers was examined. At the lesion site, a progression in plaque area (8.9+/-25.7%) and a decrease in the RR (-3.0+/-11.2%) occurred during follow-up. In multivariable analyses, the percentage change in plaque area (P<0.0001), baseline RR (P<0.0001), baseline lesion lumen area (0.019), logarithmic value of the change in high-sensitivity C-reactive protein (P=0.027), and hypertension at baseline (P=0.014) showed a significant, direct relation with the RR at follow-up. Lesion location in the right coronary artery (P=0.006), percentage change in triglyceride levels (P=0.049), and age (P=0.037) demonstrated a significant, inverse relation with the RR at follow-up. Changes in LDL cholesterol, HDL cholesterol, and treatment group demonstrated no significant associations. CONCLUSIONS: Constrictive remodeling of the arterial wall was observed during plaque-stabilizing therapy with statin medications and appears related to their antiinflammatory effects.

Adaptation, Physiological↗
PubMed2005

The biotin-capture lipid affinity assay: a rapid method for determining lipid binding parameters for apolipoproteins.

The lipid affinity of plasma apolipoproteins is an important modulator of lipoprotein metabolism. Mutagenesis techniques have been widely used to modulate apolipoprotein lipid affinity for studying biological function, but the approach requires rapid and reliable lipid affinity assays to compare the mutants. Here, we describe a novel method that measures apolipoprotein binding to a standardized preparation of small unilamellar vesicles (SUVs) containing trace biotinylated and fluorescent phospholipids. After a 30 min incubation at various apolipoprotein concentrations, vesicle-bound protein is rapidly separated from free protein on columns of immobilized streptavidin in a 96-well microplate format. Vesicle-bound protein and lipid are eluted and measured in a fluorescence microplate reader for calculation of a dissociation constant and the maximum number of potential binding sites on the SUVs. Using human apolipoprotein A-I (apoA-I), apoA-IV, and mutants of each, we show that the assay generates binding constants that are comparable to other methods and is reproducible across time and apolipoprotein preparations. The assay is easy to perform and can measure triplicate binding parameters for up to 10 separate apolipoproteins in 3.5 h, consuming only 120 microg of apolipoprotein in total. The benefits and potential drawbacks of the assay are discussed.

Algorithms↗
PubMed1989

Effect of taurine administration on serum lipid and biliary lipid composition in man.

The effect of oral administration of taurine (3.2 g/day, 2 weeks) on the metabolism of lipids and bile acids was studied with healthy humans. Four male subjects were fed taurine. Another five male subjects were administered 1 g of cholesterol daily for two weeks and, at intervals of two weeks, cholesterol and taurine simultaneously. Serum lipoprotein and duodenal bile were analyzed. Oral administration of taurine resulted in the increase of taurine-conjugated bile acids. However, neither serum lipid nor biliary lipid composition was altered. Addition of taurine with cholesterol administration showed elevation of both the serum low density lipoprotein cholesterol level and the lithogenic index in bile. The ratio of glycine-to taurine-conjugated bile acids was changed from 4.1 to 0.63. The ratio of cholic acid/chenodeoxycholic acid was augmented from 0.57 to 0.81. The percentage of taurocholic acid, taurochenodexycholic acid and taurodeoxycholic acid were increased about 4-fold, 2.5-fold and 3-fold, respectively. Our results suggested that taurine administration alone did not influence the serum lipid level although taurine-conjugated bile acids were increased. The taurine intake would increase serum low density lipoprotein cholesterol and biliary cholesterol levels when excessive cholesterol is administered simultaneously.

Administration, Oral↗
PubMed2001

Drug-Induced lipid changes: a review of the unintended effects of some commonly used drugs on serum lipid levels.

Many drugs besides lipid-lowering drugs affect serum lipid levels in either a potentially harmful or beneficial way, and may therefore increase or decrease the risk of cardiovascular disease. Diuretics, beta-blocking agents, progestogens, combined oral contraceptives containing 'second generation' progestogens, danazol, immunosuppressive agents, protease inhibitors and enzyme-inducing anticonvulsants adversely affect the lipid profile. They increase total cholesterol, low density lipoprotein cholesterol and triglycerides by up to 40, 50 and 300%, respectively, and decrease high density lipoprotein cholesterol by a maximum of 50%. Conversely, alpha-blocking agents, estrogens, hormone replacement therapy, combined oral contraceptives containing 'third generation' progestogens, selective estrogen receptor modulators, growth hormone and valproic acid show mostly beneficial effects on the lipd profile. Some drugs, for example, isotretinoin, acitretin and antipsychotics, mainly elevate triglyceride levels. Adverse or beneficial effects on serum cholesterol levels do not always translate into a higher or lower, respectively, incidence of cardiovascular disease. because these drugs may influence cardiovascular risk through multiple pathways. In some cases, excessive cholesterol levels occur, for example, with protease inhibitor therapy, and several cases of pancreatitis attributable to drug-induced hypertriglyceridaemia have been reported. Some general guidelines on the management of drug-induced dyslipidaemia can be given. Replacement of the dyslipidaemia-inducing drug by an equivalent alternative therapy is preferred. However, such alternatives are often difficult to find. If there is no equivalent alternative and treatment with the dyslipidaemia-inducing drug must be initiated, monitoring of serum lipid levels is important. If drug use is expected to be long term, the existing guidelines for the management of dyslipidaemia in the general population can be applied to drug-induced dyslipidaemia. In cases of extreme hyperlipidaemia, medication use should be reassessed.

Adult↗
PubMed2000

Lipid profiles in Polish adolescents from high- and low-risk families: tracking unfavourable lipid levels over a one-year period.

In a country with a high cardiovascular mortality rate, lipid profiles were studied in 929 adolescents (440 from affected and 489 from non-affected families for cardiovascular disease and hypercholesterolaemia). In 334 children with elevated or borderline total cholesterol level, lipid profiles were re-measured after a 1-y period. In boys from affected families, in contrast to boys from non-affected families, significantly higher total cholesterol levels (4.36 +/- 0.81 vs 4.19 +/- 0.78 mmol/L, p < 0.05) and LDL-C level (2.1 +/- 0.72 vs 1.89 +/- 0.79 mmol/L, p < 0.05) and significantly lower HDL-cholesterol levels (1.81 +/- 0.34 vs 1.93 +/- 0.38 mmol/L, p < 0.05) were found. The odds ratio for being in the most unfavourable decile for LDL-cholesterol was significantly higher for girls from affected families (2.17, p = 0.02). A relatively high HDL-C level as well as a favourable TC/HDL-C ratio was demonstrated in all groups, being lowest in boys from affected families. A significant correlation was found between baseline lipids and their values re-measured after 1 y. It is concluded that (1) adolescents with a positive family history are at increased risk for unfavourable lipid profile, (2) adolescents with elevated total cholesterol and LDL-cholesterol levels remain hypercholesterolaemic after a 1-y period and are therefore candidates for further biochemical and clinical monitoring, and (3) children with elevated total cholesterol may not be at high risk for cardiovascular disease owing to the favourable TC/HDL-C ratio. The study results do not indicate that general cholesterol screening in Polish adolescents is necessary, as the proportion of children with elevated LDL-cholesterol is relatively low.

Adolescent↗
PubMed2001

[Blood lipid derangement common in peripheral artery disease. Lipid-lowering agents may alleviate symptoms and slow the atherosclerotic process].

In the new guidelines from the Swedish Medical Products Agency, an aggressive approach is recommended for the treatment of hyperlipidemia in all patients with manifest atherosclerotic disease. Patients with intermittent claudication should therefore receive lipid-lowering treatment on the same indications as patients with coronary artery disease. The present article reviews our knowledge of hyperlipidemia as a risk factor for the development of peripheral artery disease. Hyperlipidemia is frequently found in these patients and the most common lipid derangements are low levels of HDL-cholesterol and hypertriglyceridemia. Hard end-point data concerning morbidity and mortality during lipid-lowering treatment in this specific population is largely lacking, although previous studies indicate that lipid-lowering treatment slows the atherosclerotic process and induces pain relief.

Adult↗
PubMed1992

Estrogen modulates Ca(2+)-independent lipid-stimulated kinase in the rabbit corpus luteum of pseudopregnancy. Identification of luteal estrogen-modulated lipid-stimulated kinase as protein kinase C delta.

Rabbit corpora lutea were tested for the presence of phosphorylative responses sensitive to estrogen. Luteal Ca(2+)-independent lipid-stimulated kinase activity was detected by phosphorylation of the endogenous substrate, p76. Estrogen treatment, by way of estradiol-17 beta implant, increased levels of the lipid-stimulated phosphoprotein 2-3-fold throughout pseudopregnancy. Midpseudopregnant rabbit luteal extracts were further evaluated to determine the identity of the lipid-stimulated kinase. Results of low pH-activated phosphorylation were consistent with the identification of p76 as an autophosphorylated member of the protein kinase C (PKC) family. Partial purification of the luteal lipid-stimulated kinase was performed using sequential DEAE-cellulose/hydroxylapatite chromatographies and using gel filtration. Western immunoblot with type-specific anti-PKC delta antiserum showed coelution of kinase p76 activity with immunoreactive PKC delta. Immunoblot analysis confirmed that luteal levels of PKC delta were increased by estrogen treatment.

Animals↗
PubMed1992

Lateral lipid distribution is a major regulator of lipase activity. Implications for lipid-mediated signal transduction.

Pancreatic carboxylester lipase catalyzes the exchange of 18O between water and 13,16-cis,cis-doco-sadienoic acid (DA) in monolayers at the argon-buffer interface (Muderhwa, J.M., Schmid, P.C., and Brockman, H.L. (1992) Biochemistry 31, 141). In mixed monolayers of 18O, 18O-DA and 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC), both the extent and mechanism of 18O exchange show characteristics of a critical transition in the range of 0.5-0.6 mol fraction of DA (Muderhwa, J.M., and Brockman, H. L. (1992) Biochemistry 31, 149). To determine if the regulatory behavior exhibited on this type of surface is limited to members of the carboxylester lipase gene family (cholinesterases), comparable experiments were performed with a genetically and functionally unrelated lipase, pancreatic colipase-dependent lipase (PL). PL readily catalyzed the exchange of 18O between water and the carboxyl group of DA with enzyme at either monolayer or catalytic levels in the fatty acid-buffer interface. The oxygen exchange reaction obeyed a random, sequential mechanism, indicating that the dissociation of the enzyme.DA complex is much faster than the rate-limiting step in the overall exchange process. Kinetic analysis of oxygen exchange in pure DA monolayers showed a first-order dependence on interfacial PL and DA concentrations from which kcat/Km values were calculated. The oxygen exchange reaction proceeded with a rate constant of 16 x 10(-2) cm2 pmol-1 s-1, a value comparable to that for hydrolysis of the ester substrate, 1,3-dioleoylglycerol. With a monolayer of PL adsorbed to the interfacial phase, kcat/Km for oxygen exchange was about 600-fold lower than the value obtained with catalytic levels of adsorbed enzyme, indicating a possible restriction of substrate diffusion in the protein-covered fatty acid monolayer. With constant bulk PL concentration and mixed lipid monolayers containing DA and the non-substrate lipid, POPC, the extent of oxygen exchange increased abruptly as the abundance of DA in the interface was increased from 0.5 to 0.6 mol fraction. Concomitant with this critical transition was a change in the apparent mechanism of oxygen exchange from coupled to random, sequential. For both the extent of oxygen exchange and its mechanism shift, the critical transition was independent of the lipid packing density, i.e. surface pressure, of the interface. These results show that PL responds similarly to carboxylester lipase with respect to changes in interfacial lipid mole fraction in DA-POPC surfaces.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2005

Solid lipid nanoparticles (SLN) and nanostructured lipid carriers (NLC) for application of ascorbyl palmitate.

The aim of this study was to improve the chemical stability of ascorbyl palmitate (AP) in a colloidal lipid carrier for its topical use. For this purpose, AP-loaded solid lipid nanoparticles (SLN), nanostructured lipid carriers (NLC) and for comparison, a nanoemulsion (NE) were prepared employing the high pressure homogenization technique and stored at room temperature (RT), 4 degrees C and 40 degrees C. During 3 months, physical stability of these formulations compared to placebo formulations which were prepared by the same production method, was studied including recrystallization behaviour of the lipid with differential scanning calorimetry (DSC), particle size distribution and storage stability with photon correlation spectroscopy (PCS) and laser diffractometry (LD). After evaluating data indicating excellent physical stability, AP-loaded SLN, NLC and NE were incorporated into a hydrogel by the same production method as the next step. Degradation of AP by HPLC and physical stability in the same manner were investigated at the same storage temperatures during 3 months. As a result, AP was found most stable in both the NLC and SLN stored at 4 degrees C (p > 0.05) indicating the importance of storage temperature. Nondegraded AP content in NLC, SLN and NE was found to be 71.1% +/- 1.4, 67.6% +/- 2.9 and 55.2% +/- 0.3 after 3 months, respectively. Highest degradation was observed with NE at all the storage temperatures indicating even importance of the carrier structure.

Ascorbic Acid↗
PubMed2006

[The effects of calmodulin on the lipid-binding activity of CaM-binding protein-10 and maize non-specific lipid transfer protein].

Fluorescence-marked lipid binding experiment shows that CaMBP-10 has typical lipid binding feature of non-specific lipid transfer protein (nsLTP). We have compared the effects of calmodulin (CaM) on the lipid-binding activity of CaMBP-10 and maize nsLTP. Different influences were found in the presence of either Ca(2+) or EGTA. W-7 and TFP could abolish the influence of CaM. Therefore, it is suggested that CaM could interact specifically with both CaMBP-10 and maize nsLTP. Probably, there are different CaM regulatory mechanisms between CaMBP-10 and maize nsLTP.

Amino Acid Sequence↗
PubMedDate not supplied

[Lipid oxidation in bilayer lipid membranes linked with the reaction of oxidation of NAD.H by atmospheric oxygen].

It is shown that along with NAD.H oxidation with air oxygen peroxide oxidation of lipids forming the membrane takes place in bilayer lipid membranes modified with ubiquinone. During nicotin amide oxidation proton absorption takes place. Peroxide oxidation of lipids results in the liberation of H+ ions, which in its turn brings about the formation of protone-deficient or enriched (against aqueous solution) layers adjacent to the membrane. The potential value on the membrane is shown to depend on nicotine amide and oxygen concentration, on ubiquinone presence and lipid composition of the membrane. It has been also indicated that the transmembrane potential difference is initiated with a sharp change of aqueous solution pH by 0.05--0.4 units.

Air↗
PubMed1987

Clearance of instilled surfactant lipid from the lungs of unanesthetized sheep: lipids are differentially transported by nonlymphatic pathways.

The routes used by the lung to dispose of instilled exogenous surfactant lipid components were examined with the sheep chronic lung lymph fistula preparation. Small vesicles of radiolabeled dipalmitoyl phosphatidylcholine (DPPC) either alone or with radiolabeled cholesterol (CHOL) were instilled intratracheally, and samples of lung lymph and plasma were collected at 60-minute intervals for 12 hours. At any time point, the total amounts of either labeled DPPC or CHOL that appeared in lung lymph were small fractions (less than 0.5%) of their respective amounts in plasma. Labeled DPPC, as DPPC alone or as DPPC/CHOL (2:1 molar ratio), appeared simultaneously in plasma and lymph and displayed the same time course of appearance regardless of vesicle composition. CHOL appearance was also simultaneous in both plasma and lymph, but was distinctly slower than that of DPPC. The time differences noted between the appearance of labeled DPPC and CHOL in lymph and plasma indicate that these two lipid components of the instilled surfactant lipid component vesicles appear to be handled in different fashions during their transport from the lung. Further, the data obtained by sampling lung lymph suggest that the lung interstitial space may not play an active role in the transport of exogenously administered lipid from the lung.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1985

Binding of plasma-derived lipid transfer protein to lipoprotein substrates. The role of binding in the lipid transfer process.

Plasma-derived lipid transfer protein (LTP) facilitates the transfer of cholesteryl ester and triglyceride between all lipoproteins. Kinetic models of the transfer event have suggested that transfer is facilitated through the physical interaction (binding) of LTP with its lipoprotein substrate. Such binding has been observed previously between LTP and high density lipoprotein (HDL), but not between LTP and low (LDL) or very low (VLDL) density lipoproteins. In the present study, the interaction of LTP with plasma lipoproteins has been re-evaluated. These experiments have employed Sepharose-bound lipoproteins in order to facilitate the rapid separation of unbound and lipoprotein-associated LTP. The validity of this approach in assessing LTP-lipoprotein interactions was evidenced by the fact that free (unbound) lipoproteins could competitively inhibit or disrupt the binding of LTP to the Sepharose-bound lipoproteins. LTP was observed to bind to VLDL, LDL, and HDL. Whereas VLDL- and LDL-LTP complexes were labile and almost completely dissociated in 90 min, HDL-LTP complexes remained intact during this time. Under equilibrium conditions, LTP binding to all lipoproteins was characterized by high affinity, saturable kinetics; the apparent affinities (Kd) of VLDL, LDL, and HDL for LTP were nearly the same (congruent to 25 nM). The results of two studies correlated lipid transfer activity with LTP binding to lipoproteins: 1) LTP binding and transfer activity increased in parallel as the amount of LTP in the assay was increased and 2) the inhibition of transfer activity caused by differing amounts of an inhibitory protein correlated with similar decrements in LTP binding. The latter data also suggest that the inhibitor protein suppresses lipid transfer activity by disrupting LTP-lipoprotein interactions. It is concluded that LTP avidly binds to VLDL, LDL, and HDL via a reversible, saturable mechanism and that the binding of LTP to the lipoprotein surface is an integral component of the lipid transfer reaction.

Carrier Proteins↗
PubMed1979

[Effects of chronic inhalation intoxication with carbon disulfide on the content of various lipid metabolism indices in the serum, aorta and cardiac muscle in rabbits. II. Lipid phosphorus and phospholipid fractions in the serum, aorta and cardiac muscle].

Lipid phosphorus and single phospholipids content was checked in serum, aorta and cardiac muscle of rabbits exposed in toxicological chamber for 3 and 6 months, to carbon disulfide of low concentration (0.44 mg/l) and higher concentration (0.8 mg/l). Phospholipids were separated using thin--layer chromatography. Lipid phosphorus content in each fraction was determined colorimetrically. Statistical analysis of obtained results was done based on the Student "t" test. Lipid phosphorus content in serum, aorta and cardiac muscle was found to increase in animals exposed to CS2 in lower concentration. A decrease in lipid phosphorus content (statistically significant) was noted in the serum of rabbits intoxicated with CS2 in high concentration for 3 months. Changes in the percentage of phosphatidylcholine and sphingomyelins in cardiac muscle were found.

Animals↗
PubMed1981

[Specific effect of highly unsaturated lipids of animal origin on the blood lipid composition (author's transl)].

A beneficial effect, consisting in reduction of the risk of ischaemic cardiovascular disease, has long been attributed to fish lipids. These fish lipids were previously believed to be capable of markedly reducing the cholesterol level of the serum. However, recent studies showed that this reduction did not occur in normal subjects not affected with hypercholesteraemia, to whom fatty fish or polyunsaturated fatty acids isolated from fish were administered. On the other hand, the triglyceride level of the serum did decrease on administration of relatively large doses of these fatty acids. Moreover, the ingestion of fish lipids caused a shift in the fatty acid pattern of the serum lipids in the sense that w6 fatty acids were partially substituted for polyunsaturated fatty acids of the w3 type. This may result in changes in the synthesis of prostaglandins, which affect platelet aggregation and the bleeding time. This may indeed reduce the hazard of ischaemic cardiovascular disease.

Blood Coagulation↗
PubMed1998

Cationic lipids enhance cytokine and cell influx levels in the lung following administration of plasmid: cationic lipid complexes.

Administration of plasmid/lipid complexes to the lung airways may be associated, in addition to expression of transgene, with a range of other responses. We report here the induction of cytokines and cellular influx in the lung airway following intratracheal administration of an N-[1-(2-3-dioleyloxy)propyl]-N,N,N-trimethylammonium chloride/cholesterol/plasmid positively charged complex in mice. We show that 1) the appearance of the Th1-associated cytokines IFN-gamma and IL-12 in bronchoalveolar lavage fluid is caused by unmethylated CpG dinucleotide sequences present within the plasmid, and is enhanced by the lipid formulation; 2) cationic lipids by themselves do not induce IL-12 or IL-12p40; 3) TNF-alpha is rapidly induced by cationic lipids and plasmid/lipid complex, but not by plasmid alone; 4) an acute cellular influx is induced by cationic lipid alone and by a plasmid/lipid complex, but to a much lesser extent by plasmid alone; and 5) plasmid methylation does not influence the degree of inflammatory cell influx. The induction of the innate immune responses by plasmid/lipid complexes may be advantageous to gene therapy of lung diseases. In particular, induction of the Th1 cell-promoting cytokines by plasmid/lipid complexes could, in conjunction with an expressed transgene, be used to modulate immune responses in the lung airways in disease conditions that are deficient in Th1 cell responses or that have a dominant Th2 phenotype. Alternatively, the elimination of immunostimulatory sequences in plasmids may improve the tolerability and/or efficacy of nonviral gene therapy, especially for diseases requiring chronic administration.

Administration, Inhalation↗
PubMed2004

Effects of structured lipids containing eicosapentaenoic or docosahexaenoic acid and caprylic acid on serum and liver lipid profiles in rats.

The physiological activity and effect on lipid metabolism of four types of structured lipids (SLs), that contain caprylic acid (C8) and either eicosapentaenoic (EPA) or docosahesaenoic acid (DHA), were evaluated in male Wistar rats fed experimental diets containing 7% (wt %) of each SL and 3% (wt %) soybean oil for 28 days. Control rats were fed a diet containing 10% (wt %) soybean oil. The relative perirenal adipose tissue weights of rats fed D-8-8 and 8-D-8 diets were significantly lower than those of other groups. We observed significantly lower serum cholesterol concentrations in rats fed SLs than those of control group over experimental period. The serum lipids concentrations in rats fed diets containing SLs were significantly lower P < 0.05) than those of soybean oil group. The fatty acid compositions of WAT did not reflect the structural differences in the triglyceride. These results suggest that the physiological effects of the SLs used in this study were due to the fatty acids rather than the structural specificity. Therefore, further study will be needed to ascertain the most desirable structural configuration.

Adipose Tissue↗
PubMed2003

Protective effects of curcumin and photo-irradiated curcumin on circulatory lipids and lipid peroxidation products in alcohol and polyunsaturated fatty acid-induced toxicity.

Alcohol is a neurotoxin associated with significant morbidity and mortality. Ethanol is found to induce a dose dependent increase in lipid peroxidation (LPO). The elevation in lipid peroxidative products and the loss of antioxidant defense potential are enhanced when alcohol is taken along with polyunsaturated fatty acid (PUFA) or heated PUFA. The present study was undertaken to evaluate the effects of curcumin and photo-irradiated curcumin on alcohol and PUFA induced LPO and lipid pro fi les in plasma. The levels of vitamin C and E were decreased significantly in alcohol + raw as well as heated PUFA groups. The treatment with curcumin and photo-irradiated curcumin (IC) increased their levels significantly. The increase was more significant in the IC group than the curcumin group. The levels of cholesterol, phospholipids (PL), triglycerides (TG), free fatty acids (FFA), thiobarbituric acid reactive substances (TBARS) and hydroperoxides (HP) were increased significantly in alcohol + raw as well as heated PUFA groups and the treatment with curcumin and IC, brought back the levels. But the IC reduced the levels more significantly than curcumin. Thus, our results indicate that IC is a more potent antioxidant than curcumin.

Animals↗