Effects of turmeric extract on hemin-induced low-density lipoprotein oxidation

Chaniad, Prapaporn; Morales, Noppawan Phumala; Rojsitthisak, Pornchai; Luechapudiporn, Rataya

doi:10.1111/jfbc.12507

Cited by 9 publications

(12 citation statements)

References 45 publications

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“…Curcumin ( Figure 1A ) is a nature-derived polyphenol that possesses various biological activities, such as antioxidant ( Calabrese et al, 2008 ; Khan et al, 2019 ), anti-inflammatory ( Buadonpri et al, 2009 ; Chaniad et al, 2018 ; Shimizu et al, 2019 ), antiviral ( Praditya et al, 2019 ), antitumor ( Aggarwal et al, 2003 ; Muangnoi et al, 2019a ; Muangnoi et al, 2019b ), and anti-psoriasis ( Gomez et al, 2019 ) properties. Owing to its diverse biological activities and low toxicity, curcumin is an attractive compound for drug development ( Strimpakos and Sharma, 2008 ; Pouliquen, 2014 ; Ratnatilaka Na Bhuket et al, 2017 ; Pagano et al, 2018 ; Rafiee et al, 2019 ).…”

Section: Introductionmentioning

confidence: 99%

In Vitro Hepatic Metabolism of Curcumin Diethyl Disuccinate by Liver S9 from Different Animal Species

et al. 2020

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Liver S9 (LS9) is a nearly complete collection of all hepatic drug-metabolizing enzymes. It is a low-cost model for predicting drug metabolic activity. This study aimed to identify the suitability of using LS9 of different animal sources in drug metabolism profiling with respect to the possible translation of the in vitro outcomes to clinical studies. The in vitro hepatic metabolism of curcumin diethyl disuccinate (CDD) in LS9 of rats, dogs, monkeys, and humans was evaluated. The identity of CDD metabolites and the metabolism kinetic parameters, including degradation rate constant, in vitro / in vivo intrinsic clearance, and half-life, were determined. CDD was rapidly metabolized into monoethylsuccinyl curcumin and curcumin in LS9 of all tested species mainly by carboxylesterases (CESs), including CES1 and CES2, and butyrylcholinesterase. The in vitro intrinsic clearance of CDD was in the order of human > dog > monkey > rat, whereas that of monoethylsuccinyl curcumin in the order of dog > monkey > human > rat; this parameter was not correlated with their respective in vivo clearance, which followed the order of dog > monkey > rat > human. Therefore, in vitro drug metabolism data inferred from LS9 of nonhuman origin, especially from monkeys and dogs, cannot be used as preclinical data for human trials, as humans have a smaller liver-to-body weight ratio than monkeys, dogs, and rats. The in vivo drug metabolism is dictated by the anatomical factors of the test subject.

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Section: Introductionmentioning

confidence: 99%

In Vitro Hepatic Metabolism of Curcumin Diethyl Disuccinate by Liver S9 from Different Animal Species

et al. 2020

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“…This hydroxyl radical rapidly reacts with polyunsaturated fatty acids (PUFAs) in the core cholesteryl esters of LDL and initiates a chain reaction process. Here, the he-oxLDL system was used to evaluate the protective effect of lusianthridin on LDL oxidation [15].…”

Section: Discussionmentioning

confidence: 99%

“…Moreover, hemin also causes changes in lipid composition of the LDL core, especially in cholesteryl arachidonate (CA) and cholesteryl linoleate (CL), which comprise polyunsaturated fatty acids (PUFA) that cause more oxidation than monounsaturated and saturated fatty acids [17] and also increased oxidized lipid products. Decreasing CA and CL might be due to the hydrolysis of the ester bond and the oxidized lipid products that were produced by lipid peroxidation of CA and CL [15]. Furthermore, hemin causes undetectable α-tocopherol.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, the phenolic compound reduces Fe 2+ to Fe 3+ , which includes the Fenton reaction. Fe 3+ generates the toxic hydroxyl radical, which reacts with cholesteryl ester in hydrophobic core lipoprotein and initiates lipid peroxidation [15]. Hence, it could be possible that lusianthridin inhibited lipid peroxidation of LDL induced by hemin due to the reduction of Fe 3+ .…”

Section: Discussionmentioning

confidence: 99%

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Protective Effect of Lusianthridin on Hemin-Induced Low-Density Lipoprotein Oxidation

et al. 2021

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Oxidation of low-density lipoprotein (LDL) plays a crucial role in the pathogenesis of atherosclerosis. Hemin (iron (III)-protoporphyrin IX) is a degradation product of hemoglobin that can be found in thalassemia patients. Hemin is a strong oxidant that can cause LDL oxidation and contributes to atherosclerosis in thalassemia patients. Lusianthridin from Dendrobium venustrum is a phenolic compound that possesses antioxidant activity. Hence, lusianthridin could be a promising compound to be used against hemin-induced oxidative stress. The major goal of this study is to evaluate the protective effect of lusianthridin on hemin-induced low-density lipoprotein oxidation (he-oxLDL). Here, various concentrations of lusianthridin (0.25, 0.5, 1, and 2 µM) were preincubated with LDL for 30 min, then 5 µM of hemin was added to initiate the oxidation, and oxidative parameters were measured at various times of incubation (0, 1, 3, 6, 12, 24 h). Lipid peroxidation of LDL was measured by thiobarbituric reactive substance (TBARs) assay and relative electrophoretic mobility (REM). The lipid composition of LDL was analyzed by using reverse-phase HPLC. Foam cell formation with he-oxLDL in RAW 264.7 macrophage cells was detected by Oil Red O staining. The results indicated that lusianthridin could inhibit TBARs formation, decrease REM, decrease oxidized lipid products, as well as preserve the level of cholesteryl arachidonate and cholesteryl linoleate. Moreover, He-oxLDL incubated with lusianthridin for 24 h can reduce the foam cell formation in RAW 264.7 macrophage cells. Taken together, lusianthridin could be a potential agent to be used to prevent atherosclerosis in thalassemia patients.

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“…Hemin may appear in plasma because of intravascular hemolysis and ferric component of hemin can cause oxidation of LDL. Hemin can be detected in the serum of β-thalassemia/hemoglobin (β-thal/HbE) [6] and serum hemin catalyses rapidly free radical reaction and serves as pro-oxidant to induce LDL oxidation in in vivo and cause vascular complications [7]. The lipophilic antioxidants in LDL have the protective effect on LDL from oxidation [8].…”

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confidence: 99%

Protective effects of lusianthridin on hemin-induced low density lipoprotein oxidation and foam cell formation of raw 264.7 macrophage cells

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Oxidation of low-density lipoprotein (LDL) take parts in a crucial role in the pathogenesis of atherosclerosis. Hemin (iron (III)-protoporphyrin IX) is a degradation product of hemoglobin and cause oxidative stress-promoting vascular complications in thalassemia patients. Hemin was used as an oxidizing agent for LDL oxidation. Lusianthridin (LST) from Dendrobium venustum is a plant phenolic compound and possess antioxidant activity. The aim of this study is to evaluate the protective effect of lusianthridin on hemin-induced LDL oxidation (he-oxLDL) and foam cell formation in RAW 264.7 macrophage cell loaded with he-oxLDL treated with LST. Various concentrations of LST (0.25, 0.5, 1 and 2 µM) were preincubated with LDL for 30 min, then 5 µM hemin was added to initiate the oxidation and measured oxidative parameters at various times of incubation (0, 1, 3, 6, 12, 24 hr). Lipid peroxidation of LDL was measured by thiobarbituric reactive substance (TBARs) assay and relative electrophoretic mobility (REM). Lipid composition of LDL was analysed by using reverse phase HPLC. Foam cell formation with he-oxLDL in RAW 264.7 macrophage cells were detected by oil red O staining. The results demonstrated that LST at 1 and 2 µM were able to protect against lipid peroxidation in he-oxLDL by inhibition of TBARs formation, decreasing REM, preservation of cholesteryl arachidonate and cholesteryl linoleate level and decreased oxidized lipid products. In addition, exposure of he-oxLDL treated with 1 and 2 µM LST reduced the foam cell formation and decreased lipid content in macrophages significantly different from he-oxLDL untreated with LST (p<0.05 and p<0.0001, respectively). In conclusion, LST can protect LDL oxidation induced by hemin and showed the potential protective effect in foam cell formation in RAW 264.7 macrophage cell.

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Effects of turmeric extract on hemin-induced low-density lipoprotein oxidation

Cited by 9 publications

References 45 publications

In Vitro Hepatic Metabolism of Curcumin Diethyl Disuccinate by Liver S9 from Different Animal Species

In Vitro Hepatic Metabolism of Curcumin Diethyl Disuccinate by Liver S9 from Different Animal Species

Protective Effect of Lusianthridin on Hemin-Induced Low-Density Lipoprotein Oxidation

Protective effects of lusianthridin on hemin-induced low density lipoprotein oxidation and foam cell formation of raw 264.7 macrophage cells

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