Pioglitazone combined with atorvastatin promotes plaque stabilization in a rabbit model

Vascular ◽  
2021 ◽  
pp. 170853812110409
Author(s):  
Xuehui Zhang ◽  
Xue Chen ◽  
Zhe Liang ◽  
Maoxiao Nie ◽  
Yunfeng Yan ◽  
...  
Keyword(s):  
Therapy Group ◽  
Rabbit Model ◽  
Density Lipoprotein ◽  
Atherosclerotic Plaques ◽  
Atorvastatin Group ◽  
Plaque Stabilization ◽  
Hs Crp ◽  
Pioglitazone Group ◽  
Area Percentage ◽  
Progression Of Atherosclerosis

Objective It is not yet clear whether plaque inflammation and cardiovascular events are reduced further when pioglitazone and atorvastatin are combined. Our study aimed to determine whether pioglitazone combined with atorvastatin can restrain the progression of atherosclerosis and promote plaque stabilization in a rabbit model Method and Result Thirty rabbits were randomly divided into an atherosclerosis group, an atorvastatin group, and an atorvastatin plus pioglitazone group. The atherosclerosis model was induced using balloon injury and feeding a high-fat diet. Plasma samples were then used to analyze glucose, triglycerides (TG), high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), high-sensitivity C-reactive protein (hs-CRP), and matrix metalloproteinase-9 (MMP-9). The area percentage of atherosclerotic plaques was analyzed by hematoxylin-eosin staining. The relative reductions in TG and LDL-C and the increase in HDL-C levels were significantly greater in the combination therapy group than in the atorvastatin monotherapy group (TG: −33.60 ± 7.17% vs −24.16 ± 8.04%, p < 0.001; LDL-C: −42.89 ± 1.63% vs −37.13 ± 1.35%, p < 0.001; and HDL-C: 25.18 ± 5.53% vs 10.43 ± 6.31%, p < 0.001). The relative reductions in hs-CRP and MMP-9 levels were significantly greater in the combination therapy group than in the atorvastatin monotherapy group (−69.38 ± 1.06% vs-53.73 ± 1.92%, p < 0.001; −32.77 ± 2.49% vs −13.36 ± 1.66%, p < 0.001). The area percentage of atherosclerotic plaques was significantly smaller in the atorvastatin group (47.75%, p < 0.05) and in the atorvastatin plus pioglitazone group (22.57%, p < 0.05) than in the atherosclerosis group (84.08%, p < 0.05) Conclusion We can thus conclude that the combination treatment of atorvastatin and pioglitazone provided additive benefits on inflammatory parameters and lipid metabolism. Pioglitazone combined with atorvastatin can further restrain the progression of atherosclerosis and promote plaque stabilization in a rabbit model.

Negatively-charged liposome nanoparticles can prevent dyslipidemia and atherosclerosis progression in the rabbit model

2021 ◽  
Vol 19 ◽  
Author(s):  
Amir Abbas Momtazi-Borojeni ◽  
Elham Abdollahi ◽  
Mahmoud R. Jaafari ◽  
Maciej Banach ◽  
Gerald F. Watts ◽  
...  
Keyword(s):  
Rabbit Model ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Saline Control ◽  
Control Group ◽  
High Cholesterol Diet ◽  
Mean Values ◽  
Atherosclerotic Lesions ◽  
The Impact ◽  
Progression Of Atherosclerosis

Background and Aim: Negatively charged nanoliposomes have a strong attraction towards plasma lipoprotein particles and can thereby regulate lipid metabolism. Here, the impact of such nanoliposomes on dyslipidaemia and progression of atherosclerosis was investigated in a rabbit model. Methods: Two sets of negatively-charged nanoliposome formulations including [hydrogenated soy phosphatidylcholine (HSPC)/1,2-distearoyl-sn-glycero-3- phosphoglycerol (DSPG)] and [1,2-Dimyristoyl-sn-glycero-3-phosphorylcholine (DMPC)/1,2-Dimyristoyl-sn-glycero-3-phosphorylcholine (DMPG)/Cholesterol] were evaluated. Rabbits fed a high-cholesterol diet were randomly divided into 3 groups (n=5/group) intravenously administrated with HSPC/DSPG formulation (DSPG group; 100 mmol/kg), DMPC/DMPG formulation (DMPG group; 100 mmol/kg), or the normal saline (control group; 0.9% NaCl) over a 4-week period. The atherosclerotic lesions of the aortic arch wall were studied using haematoxylin and eosin staining. Results: Both DSPG and DMPG nanoliposome formulations showed a nano-sized range in diameter with a negatively-charged surface and a polydispersity index of <0.1. After 4 weeks administration, the nanoliposome formulations decreased triglycerides (-62±3% [DSPG group] and -58±2% [DMPG group]), total cholesterol (-58±9% [DSPG group] and -37±5% [DMPG group]), and low-density lipoprotein cholesterol (-64±6% [DSPG group] and -53±10% [DMPG group]) levels, and increased high-density lipoprotein cholesterol (+67±28% [DSPG group] and +35±19% [DMPG group]) levels compared with the controls. The nanoliposomes showed a significant decrease in the severity of atherosclerotic lesions: mean values of the intima to media ratio in DMPG (0.96±0.1 fold) and DSPG (0.54±0.02 fold) groups were found to be significantly lower than that in the control (1.2±0.2 fold) group (p<0.05). Conclusion: Anionic nanoliposomes containing [HSPC/DSPG] and [DMPC/DMPG] correct dyslipidaemia and inhibit the progression of atherosclerosis.

scholarly journals Comparing efficacy and safety of plasmapheresis versus atorvastatin in pathological progression of atherosclerosis in a rodent model

2021 ◽  
Vol 20 (11) ◽  
pp. 2347-2353
Author(s):  
Jun Zhang ◽  
Huawei Tian ◽  
Yuping Li
Keyword(s):  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Low Density ◽  
Adult Rats ◽  
Male Adult ◽  
Atorvastatin Group ◽  
Anti Oxidant ◽  
Group 2 ◽  
Composition I ◽  
Progression Of Atherosclerosis

Purpose: To evaluate the effect of plasmapheresis versus atorvastatin in pathological progression of atherosclerosis in a rodent model.Method: A total of 90 male adult rats of up to 300 g were randomly distributed in three groups (n = 30): group 1 (plasmapheresis up to 1.5 ml daily); group 2 (atorvastatin 0.1 mg/kg per day), and group 3 (hypercholesteremic rats). The following variables were assessed for 24 weeks: plasma and hepatic lipid and anti-oxidant profiles; atherosclerotic abrasions/lesions; coronary atherosclerosis/coronary stenosis score (CSS), composition of atherosclerotic lesions, incidence of xanthoma, arch and thoracic surface involvement including arch and thoracic area occupied by lesion; and thoracic aorta (I/M) ratio.Results: Compared to rats administered with atorvastatin, the rats treated with plasmapheresis had significantly greater improvement in levels of triglycerides (132 vs 124 mg/dl, p < 0.05), total cholesterol (201 vs 189 mg/dl, p < 0.05)), low-density lipoproteins (134 vs 123 mg/dl, p < 0.05)), very-low-density lipoprotein (11 vs 9 mg/dl, p < 0.05)) and high-density lipoprotein (36 vs 39 mg/dl, p < 0.05) levels. Plasmapheresis after 24 weeks of treatment improve CSS in all coronary arteries than atorvastatin (22 vs 24 respectively; p < 0.05. Furthermore, lesioned composition, I/M ratio and xanthoma incidence were significantly lower in plasmapheresis group than in atorvastatin group (p < 0.05).Conclusion: Plasmapheresis is a better alternative than atorvastatin in preventing pathological progression of atherosclerosis.

scholarly journals Idebenone protects against atherosclerosis in apolipoprotein E-deficient mice via activation of the Sirt3-SOD2-mtROS pathway

2020 ◽  
Author(s):  
Wei Jiang ◽  
Hongzhi Geng ◽  
Xiaoqing Lv ◽  
Jing Ma ◽  
Pengfei Lin ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Apolipoprotein E ◽  
Cell Damage ◽  
Density Lipoprotein ◽  
Control Group ◽  
Atherosclerotic Plaques ◽  
High Dose ◽  
Protective Agent ◽  
Deficient Mice ◽  
Progression Of Atherosclerosis

Abstract Background: Atherosclerosis, which is a form of chronic aortic disease, results from the accumulation and aggregation of oxidized low density lipoprotein（LDL）in the vessel walls, the development of neointima, the formation of a fibrous cap, and the migration of immune cells to the damaged vascular endothelium. Recent studies have shown that mitochondrial function is closely associated with the development and progression of atherosclerosis. Idebenone functions as an electron carrier and antioxidant, and previous studies have shown that it effectively clears oxygen-free radicals. In the current study, we demonstrate that idebenone could protect against atherosclerosis using apolipoprotein E-deficient mice. Methods: High-fat diet（HFD）and idebenone treatment with apolipoprotein E-deficient mice . A total of 60 mices were randomized into the following four groups: (1) HFD (2) idebenone-low dose (3) idebenone-medium dose and (4) idebenone-high dose for 16 weeks. The HUVECs were pretreated with endothelial cell medium in the presence or absence of 0.2 mM idebenone working solution for 3 h followed by exposure to 10 μM cholesterol for 24 h. Proteomics analysis was performed between the HFD group (n=3) and the high-dose idebenone group (n=3, concentration = 400 mg/kg/d).Results: Compared with the HFD group, Idebenone can suppresses the formation of atherosclerotic plaques and increases the stability of atherosclerotic plaques in apoE-/- mice; Compared with the control group, Idebenone can protects against endothelial cell damage and inhibits the production of mtROS in cholesterol mediated HUVECs; Idebenone could effectively inhibit the development and progression of atherosclerosis and the injury of endothelial cells through the SIRT3-SOD2-mtROS pathway.Conclusions: We showed that idebenone could act as a mitochondrial protective agent during the development and progression of atherosclerosis by inhibiting the activation of NLPR3 via the SIRT3-SOD2-mtROS pathway. Idebenone may be a promising therapy for patients with atherosclerosis in the future, as it can improve mitochondrial dysfunction and inhibit oxidative stress.

scholarly journals Prediction of subclinical coronary atherosclerosis in patients with high and very high cardiovascular risk

2021 ◽  
Vol 28 (Supplement_1) ◽  
Author(s):  
N Pogosova ◽  
NP Kachanova ◽  
YM Yufereva ◽  
OY Sokolova ◽  
IE Koltunov ◽  
...  
Keyword(s):  
Family History ◽  
Ct Angiography ◽  
Coronary Atherosclerosis ◽  
Subclinical Atherosclerosis ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Diagnostic Model ◽  
History Of ◽  
Hs Crp ◽  
Very High

Abstract Funding Acknowledgements Type of funding sources: None. Background Coronary atherosclerosis has a long subclinical period. It’s early detection may offer a possibility of timely initiation of preventive interventions Purpose To develop a diagnostic rule for detection of patients (pts) with high probability of subclinical atherosclerosis among those with high or very high cardiovascular (CV) risk. Methods This cross-sectional study enrolled 52 pts (32 men [62%]), aged 40 to 65 years [mean age 54.6 ± 8.0]) with high or very high CV risk (5-9 and ≥10% by The Systematic Coronary Risk Estimation Scale [SCORE], respectively). All participants underwent cardiac computed tomography (CT) angiography and calcium scoring. Traditional risk factors (RFs) (family history of premature CVD, smoking, overweight/obesity and abdominal obesity, hypertension, type 2 diabetes mellitus, lipids parameters (total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides) and lipids-related markers (apolipoprotein A1, apolipoprotein B, ApoB/ApoA1 ratio), biomarkers of inflammation (high-sensitivity C-reactive protein [hs CRP], fibrinogen), indicator carbohydrate metabolism (glucose),  ankle-brachial index,  stress-test, carotid plaques according to ultrasound were evaluated in all pts. Psychological RFs were evaluated using Hospital Anxiety and Depression Scale and DS-14 for type D personality. Results All pts were divided into 2 groups according to the CT angiography results: pts in the main group (n = 21) had any non-obstructive lesions or calcium score &gt;0, pts in the control group (n = 31) had intact coronary arteries. The groups did not differ in age or gender. 26 multiple linear logistic models for any subclinical atherosclerosis were developed based on obtained diagnostic features. Taking into account R-square = 0.344 (p = 0.0008), the best fitting model was follows:  subclinical coronary atherosclerosis= -1.576 + 0.234 x SCORE ≥5%  + 0.541 x hs CRP &gt;2 g/l + 0.015 x heart rate  (bpm) + 0.311 family history of premature CVD.  The developed algorithm had sensitivity of 63% and  specificity of 80%. Conclusions The created diagnostic model diagnostic model suggests the presence of subclinical coronary atherosclerosis in patients with high / very high CV risk with a high degree of probability. This easy-to-use method can be used in routine clinical practice to improve risk stratification and management choices in high-risk pts.

Abstract 3372: The Ratio Of Apolipoprotein B-100 And A-i And Risk Of Intracranial Artery Stenosis In Acute Ischemic Stroke

Stroke ◽  
2012 ◽  
Vol 43 (suppl_1) ◽  
Author(s):  
Hyun-Ji Cho ◽  
Yong Jae Kim
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Reference Group ◽  
Previous History ◽  
Density Lipoprotein ◽  
Intracranial Artery ◽  
Intracranial Artery Stenosis ◽  
History Of ◽  
Statin Medication ◽  
Hs Crp

Background and Object: Intracranial artery stenosis (ICAS) is a common cause of acute ischemic stroke and has characteristics of poor prognosis and high recurrence. The role of plasma lipid level as risk factors for ICAS, still has controversy. So we investigated the relationship between the levels of the major lipids, apolipoproteins (Apo), lipoprotein (LP) and ICAS in acute ischemic stroke patients. Method: We assessed the clinical data of 881 consecutive patients from the stroke registry who were admitted due to TIA or acute ischemic stroke between November 2007 and January 2011. The major lipid levels [total cholesterol (TC), low density lipoprotein cholesterol (LDL-C), high density lipoprotein cholesterol (HDL-C)], the levels of Apo B100, Apo A-I and lipoprotein A [Lp (a)] and the level of high sensitivity C reactive protein (Hs-CRP) and were measured within three days after admission. The arterial segments were classified as normal, < 50 % stenosis or ≥ 50% stenosis on magnetic resonance angiography. ICAS was defined when at least one artery had ≥ 50% stenosis. Results: Of the total 881 patients, ICAS was found in 422 patients (31.0%, mean age: 66.17 ± 11.79 year old, males: 307), and 460 (55.7%) patients without ICAS were analyzed as a reference group. Compared with the reference group, the patients with ICAS were older (P < 0.001) and they had a greater prevalence of hyperlipidemia (p=0.002), a previous history of stroke (P =0.004) and no statin medication history (P < 0.001). The serum concentration of Hs-CRP was significantly higher in the patients with ICAS. (P < 0.001) The level of TC, LDL-C, HDL-C, Apo B100, Apo A-I, ratio of Apo B100/A-I and Lp (a) showed no significant difference between the two groups. But with adjustment of age, hypertension, diabetes mellitus, smoking, a previous history of stroke and statin medication, the ratio of Apo B100/ Apo A-I was significant for ICAS, (p=0.010) and was also the level of Hs- CRP (P=0.023). The odds ratios (ORs) for the presence of ICAS for those patients in the top, second, third quartiles were 2.054 (95% CI, 1.218-3.464), 1.721(95% CI, 1.033-2.868), and 1.667(95% CI, 1.008-2.757) sequentially for the ratio of Apo B100/ Apo A-I . Conclusions: Our study showed that the ratio of Apo B100/ Apo A-I was independently associated with presence of ICAS.

scholarly journals KORELASI KADAR HIGH SENSITIVITY C-REACTIVE PROTEIN DENGAN KADAR LOW DENSITY LIPOPROTEIN PADA PENYANDANG OBES

2020 ◽  
Vol 5 (3) ◽  
pp. 676
Author(s):  
Rama Dhanivita Djamin
Keyword(s):  
Interleukin 1 ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Sensitivity ◽  
Low Grade ◽  
Low Density ◽  
C Reactive Protein ◽  
Necrosis Factor Alpha ◽  
Reactive Protein ◽  
Hs Crp

<p><em>Obesitas terjadi karena akumulasi lemak berlebih di dalam tubuh. Akumulasi lemak menimbulkan low grade inflammation pada jaringan adiposa, menyebabkan peningkatan sitokin inflamasi seperti tumor necrosis factor-alpha, interleukin-1 beta, dan interleukin-6 (IL-6). Peningkatan sekresi IL-6 merangsang hepar meningkatkan produksi protein fase akut. High sensitivity C-reactive protein (hs-CRP) sebagai penanda inflamasi merupakan protein fase akut. Low density lipoprotein (LDL-kolesterol) adalah lipoprotein yang paling banyak mengandung kolesterol. Peningkatan kadar hs-CRP dan kadar LDL-kolesterol pada obesitas diidentifikasi sebagai faktor risiko aterosklerosis. Penelitian ini bertujuan menganalisis hubungan hs-CRP dengan LDL-kolesterol pada penyandang obes, merupakan penelitian analitik rancangan potong lintang dilakukan  September 2018 sampai Agustus 2019. Kadar hs-CRP diperiksa dengan metode enzyme linked immunoassay (ELISA), sedangkan kadar LDL-kolesterol dengan metode kalkulasi (rumus Friedewald). Uji korelasi Spearman digunakan untuk menganalisi data, jika didapatkan nilai p&lt;0,05 korelasi dinyatakan bermakna. Subjek penelitian berjumlah 26 penyandang obes terdiri dari 6 laki-laki (23,1%) dan 20 perempuan (76,9%). Rerata umur subjek penelitian adalah 36,46(7,68) tahun. Rerata kadar hs-CRP dan kadar LDL-kolesterol adalah 5,08(1,28) mg/L dan  154,69(45,8) mg/dL. Analisis korelasi menunjukkan korelasi positif lemah dan tidak bermakna secara statistik antara kadar hs-CRP dengan kadar LDL-kolesterol (r= 0,333, p=0,096). Simpulan: Terdapat korelasi positif lemah antara kadar hs-CRP dengan kadar LDL-kolesterol pada penyandang obes.</em></p><p><strong><em>Kata kunci</em></strong><em>: </em><em>Obesitas, High Sensitivity C-Reactive, Low Density Lipoprotein</em><em></em></p>

scholarly journals Therapeutic effect of Xuezhitong capsule on microvascular angina

2021 ◽  
Vol 20 (9) ◽  
pp. 1991-1997
Author(s):  
Xiaomei Ma ◽  
Dehui Yang ◽  
Weichun Shen ◽  
Wei Liang ◽  
Qian Lin
Keyword(s):  
Treatment Group ◽  
Therapeutic Effect ◽  
Conventional Treatment ◽  
Density Lipoprotein ◽  
Control Group ◽  
Vascular Endothelial ◽  
Beijing City ◽  
Microvascular Angina ◽  
Tnf Α ◽  
Hs Crp

Purpose: To determine the therapeutic effect of Xuezhitong capsule in patients with microvascular angina (MVA), and its impact on vascular endothelial function.Methods: In total, 172 MVA patients treated in Beijing City Fengtai District Nanyuan Hospital from September 2017 to September 2019 were selected and randomized into control group which received conventional treatment, and treatment group which received Xuezhitong capsules plus. There were 86 patients in each group. Therapeutic effect, levels of inflammatory factors, i.e., high-sensitivity C- reactive protein (hs-CRP), interleukin-(IL-6), tumor necrosis factor-α (TNF-α), and vascular endothelial factors such as nitric oxide (NO), thromboxane B2 (TXB2) and endothelin (ET), were determined.Results: Markedly higher total treatment effectiveness was observed in the treatment group than in the control group (89.53 % vs. 72.94 %; p < 0.05). In both groups, treatment reduced the levels of hs-CRP, IL-6, TNF-α, TXB2 and ET, but elevated NO, with better results for treatment group than the control group (p < 0.05). Better optimizations of total cholesterol (TC), triglycerides (TGs), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein (HDL) were observed in the treatment group, relative to the control group (p < 0.05). Patients in the treatment group experienced fewer (8.14%) adverse reactions than those in control group (21.18 %, p < 0.05).Conclusion: Xuezhitong capsule, when combined with conventional treatment, exerts high therapeutic effectiveness and safety in MVA patients by inhibiting inflammatory reactions, optimizing endothelialfunction, reducing blood lipid levels, and decreasing the incidence of cardiovascular adverse events. Thus, the combination therapy is a potentially superior therapeutic strategy to the conventional approach for the management of MVA patients.

scholarly journals Targeting macrophage necroptosis for therapeutic and diagnostic interventions in atherosclerosis

2016 ◽  
Vol 2 (7) ◽  
pp. e1600224 ◽  
Author(s):  
Denuja Karunakaran ◽  
Michele Geoffrion ◽  
Lihui Wei ◽  
Wei Gan ◽  
Laura Richards ◽  
...  
Keyword(s):  
Cell Death ◽  
Molecular Mechanisms ◽  
Plaque Rupture ◽  
Ex Vivo ◽  
Density Lipoprotein ◽  
Necrotic Core ◽  
Atherosclerotic Plaques ◽  
Core Formation ◽  
Macrophage Cell ◽  
Plaque Instability

Atherosclerosis results from maladaptive inflammation driven primarily by macrophages, whose recruitment and proliferation drive plaque progression. In advanced plaques, macrophage death contributes centrally to the formation of plaque necrosis, which underlies the instability that promotes plaque rupture and myocardial infarction. Hence, targeting macrophage cell death pathways may offer promise for the stabilization of vulnerable plaques. Necroptosis is a recently discovered pathway of programmed cell necrosis regulated by RIP3 and MLKL kinases that, in contrast to apoptosis, induces a proinflammatory state. We show herein that necroptotic cell death is activated in human advanced atherosclerotic plaques and can be targeted in experimental atherosclerosis for both therapeutic and diagnostic interventions. In humans with unstable carotid atherosclerosis, expression of RIP3 and MLKL is increased, and MLKL phosphorylation, a key step in the commitment to necroptosis, is detected in advanced atheromas. Investigation of the molecular mechanisms underlying necroptosis showed that atherogenic forms of low-density lipoprotein increase RIP3 and MLKL transcription and phosphorylation—two critical steps in the execution of necroptosis. Using a radiotracer developed with the necroptosis inhibitor necrostatin-1 (Nec-1), we show that 123I-Nec-1 localizes specifically to atherosclerotic plaques in Apoe−/− mice, and its uptake is tightly correlated to lesion areas by ex vivo nuclear imaging. Furthermore, treatment of Apoe−/− mice with established atherosclerosis with Nec-1 reduced lesion size and markers of plaque instability, including necrotic core formation. Collectively, our findings offer molecular insight into the mechanisms of macrophage cell death that drive necrotic core formation in atherosclerosis and suggest that this pathway can be used as both a diagnostic and therapeutic tool for the treatment of unstable atherosclerosis.

Identification of molecular species of oxidized triglyceride in plasma and its distribution in lipoproteins

2015 ◽  
Vol 53 (11) ◽  
Author(s):  
Rojeet Shrestha ◽  
Shu-Ping Hui ◽  
Yusuke Miura ◽  
Akiko Yagi ◽  
Yuji Takahashi ◽  
...  
Keyword(s):  
Molecular Species ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Healthy Human ◽  
Human Volunteers ◽  
Edta Plasma ◽  
Mass Spectrometric Approach ◽  
Mean Concentration ◽  
Progression Of Atherosclerosis

AbstractThe role of triglycerides carried in the triglyceride-rich lipoproteins (TRL) in the progression of atherosclerosis is uncertain. Identification of oxidized triglycerides and its possible association with atherosclerosis were largely ignored. Here we applied mass spectrometric approach to detect and identify triglyceride hydroperoxides (TGOOH) in human plasma and lipoproteins.EDTA plasma was collected from healthy human volunteers (n=9) after 14–16 h of fasting. Very low-density lipoprotein (VLDL)We identified 11 molecular species of TGOOH in either plasma or VLDL and IDL, of which TGOOH-18:1/18:2/16:0, TGOOH-18:1/18:1/16:0, TGOOH-16:0/18:2/16:0, TGOOH-18:1/18:1/18:1, and TGOOH-16:0/20:4/16:0 were most dominant. These TGOOH molecules are carried by TRL but not by LDL and HDL. Mean concentration of TGOOH in plasma, VLDL and IDL were, respectively, 56.1±25.6, 349.8±253.6 and 512.5±173.2 μmol/mol of triglycerides.This is the first report to identify several molecular species of oxidized triglycerides in TRL. Presence of oxidized triglyceride may contribute to the atherogenicity of TRL. Further work is needed to elucidate the association of the oxidized triglyceride in atherosclerosis.

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