Oil-bearing plants are important sources of edible oil and proteins; they have attracted attention recently because of their antioxidant, antimicrobial and anti-inflammatory properties. The objective of this work was to investigate the nature of phenolic compounds in oil-bearing plants and the effects of phenolic compounds on protein isolates from soybean and flaxseed. Proteins were isolated from full-fat and defatted soybean and flaxseed using sodium hydroxide extraction and isoelectric precipitation. Free phenolic compounds were extracted from the oil-bearing plants and protein isolates using methanol; for bound phenolic compounds the oil-bearing plants and proteins were subjected to basic and acidic hydrolysis followed by methanol extraction. Total free and bound phenolic compounds were determined by spectrophotometric analysis. Reversed phase-HPLC was used for separation of individual phenolic compounds, which were identified by mass spectrometry (MS). Molecular characteristics and biological properties of the protein isolates were studied using RP-HPLC, polyacrylamide gel electrophoresis (PAGE) and MS. Thermal and gelation properties of protein isolates were investigated using differential scanning calorimetry (DSC) and rheometry. Generally, bound phenolic compounds (20%-30% of total phenolic content) were higher in protein isolates from flaxseed than in protein isolates from soybean (10%-20% of total phenolic content). With flaxseed protein isolates, removal of phenolic compounds showed little effect on the electropherotic behavior of the proteins or the protein subunits. Native-PAGE. SDS-PAGE and RP-HPLC for the peptides profiles of hydrolyzed protein isolates from both full-fat and defatted soybean revealed the removal of free and bound phenolic compounds affect on the biological properties of protein isolates. Removal of free and bound phenolic compounds affected the thermal stability and gelation properties of protein isolates from flaxseed and soybean.

The impact of the source of n-3 fatty acids on cardiovascular disease has not been fully investigated. This study was carried out to investigate cardiovascular benefits of diets with a low ratio (2:1) of n-6:n-3 fatty acids from different sources, either fish or flaxseed oil, in C57BL/6 mice. Twenty-one mice were divided into 3 groups (n=7) and fed an atherogenic diet supplemented with either a fish or flaxseed oil-based ‘designer oil’ with low n-6:n-3 fatty acid ratio (treated groups) or safflower oil-based formulation with a high ratio (control group) for 16 weeks. Plasma cholesterol levels declined significantly in both treated groups, by greater than 30%, compared to those in control. The ratio of n-6:n-3 fatty acids in liver was significantly lower in fish and flax groups as compared to control. Our data suggest that lowering dietary ratio of n-6:n-3 fatty acids may significantly reduce cardiovascular risks regardless of the source of n-3 fatty acids.

Dietary flaxseed intake has exhibited both cardioprotective and anti-atherogenic properties. Regardless, it remains unclear whether these beneficial effects extent to the regression of atherosclerotic plaques or the resolution of cholesterol-induced vascular contractile dysfunction. In the present study, we intended to determine whether dietary flaxseed has the capacity to ameliorate vascular function abnormalities and induce atherosclerotic plaque regression. As results from previous studies using a nutritional intervention to induce atherosclerotic regression may have been confounded by premature initiation of the intervention, an appropriate feeding regimen was developed to adequately evaluate flaxseeds’ effects on atherosclerotic plaque regression. New Zealand white rabbits were utilized in two studies. To establish clear evidence of plaque growth stabilization, animals received 4 weeks of a 1% cholesterol-supplemented diet. An initial subset of animals was immediately examined. The remaining animals were fed regular rabbit chow and examined at intervals up to 28 weeks. To ascertain flaxseeds’ effects on atherosclerotic plaque regression and vascular contractile function, animals were randomly assigned to a control group fed a regular diet for 12 weeks (Group I) or an experimental group fed a 1% cholesterol-supplemented diet for 4 weeks followed by a regular diet for 8 weeks (Group II). The control and a subset of experimental animals were examined immediately afterwards. The remaining experimental animals were given an additional 8 or 14 weeks of either a regular diet (Group III and V, respectively) or a 10% flaxseed-supplemented diet (Group IV and VI, respectively) and were examined afterwards. Cholesterol feeding followed by 8 weeks of withdrawal from cholesterol not only resulted in the development and stabilization of atherosclerotic plaques but also impaired the maximum contraction caused by norepinephrine and the relaxation response to acetylcholine. An additional 14 weeks of regular diet reduced the amount of plaques on the aorta while flax-supplementation resulted in a further reduction in plaques. Nevertheless, both treatments were unable to achieve statistical significance. Flax- supplemented and regular diets improved vessel relaxation and contraction; however, negligible changes in the relaxation response induced by sodium nitroprusside were observed. Dietary flaxseed may accelerate the regression of atherosclerotic plaques. Moreover, the known beneficial effects of flaxseed do not extend to restoration of vascular function.

The impact of the source of n-3 fatty acids on cardiovascular disease has not been fully investigated. This study was carried out to investigate cardiovascular benefits of diets with a low ratio (2:1) of n-6:n-3 fatty acids from different sources, either fish or flaxseed oil, in C57BL/6 mice. Twenty-one mice were divided into 3 groups (n=7) and fed an atherogenic diet supplemented with either a fish or flaxseed oil-based ‘designer oil’ with low n-6:n-3 fatty acid ratio (treated groups) or safflower oil-based formulation with a high ratio (control group) for 16 weeks. Plasma cholesterol levels declined significantly in both treated groups, by greater than 30%, compared to those in control. The ratio of n-6:n-3 fatty acids in liver was significantly lower in fish and flax groups as compared to control. Our data suggest that lowering dietary ratio of n-6:n-3 fatty acids may significantly reduce cardiovascular risks regardless of the source of n-3 fatty acids.

Dietary flaxseed intake has exhibited both cardioprotective and anti-atherogenic properties. Regardless, it remains unclear whether these beneficial effects extent to the regression of atherosclerotic plaques or the resolution of cholesterol-induced vascular contractile dysfunction. In the present study, we intended to determine whether dietary flaxseed has the capacity to ameliorate vascular function abnormalities and induce atherosclerotic plaque regression. As results from previous studies using a nutritional intervention to induce atherosclerotic regression may have been confounded by premature initiation of the intervention, an appropriate feeding regimen was developed to adequately evaluate flaxseeds’ effects on atherosclerotic plaque regression. New Zealand white rabbits were utilized in two studies. To establish clear evidence of plaque growth stabilization, animals received 4 weeks of a 1% cholesterol-supplemented diet. An initial subset of animals was immediately examined. The remaining animals were fed regular rabbit chow and examined at intervals up to 28 weeks. To ascertain flaxseeds’ effects on atherosclerotic plaque regression and vascular contractile function, animals were randomly assigned to a control group fed a regular diet for 12 weeks (Group I) or an experimental group fed a 1% cholesterol-supplemented diet for 4 weeks followed by a regular diet for 8 weeks (Group II). The control and a subset of experimental animals were examined immediately afterwards. The remaining experimental animals were given an additional 8 or 14 weeks of either a regular diet (Group III and V, respectively) or a 10% flaxseed-supplemented diet (Group IV and VI, respectively) and were examined afterwards. Cholesterol feeding followed by 8 weeks of withdrawal from cholesterol not only resulted in the development and stabilization of atherosclerotic plaques but also impaired the maximum contraction caused by norepinephrine and the relaxation response to acetylcholine. An additional 14 weeks of regular diet reduced the amount of plaques on the aorta while flax-supplementation resulted in a further reduction in plaques. Nevertheless, both treatments were unable to achieve statistical significance. Flax- supplemented and regular diets improved vessel relaxation and contraction; however, negligible changes in the relaxation response induced by sodium nitroprusside were observed. Dietary flaxseed may accelerate the regression of atherosclerotic plaques. Moreover, the known beneficial effects of flaxseed do not extend to restoration of vascular function.

Interest in flaxseed and products derived from flaxseed has increased considerably in the past decade. In the development of nutraceutical foods, several flaxseed components including lignans and alpha-linolenic acid, have been recognized to have health benefits. There are many patents and health claims to these components; however, relatively little research and information is found on flaxseed proteins. The objective of the present study was to isolate and characterize flaxseed proteins from defatted flaxseed meal. / Proteins were extracted from defatted flaxseed meal with NaOH. NaCl and NaCl/Papain. Protein solubility with these extractants ranged from 18 to 25%. Proteins were precipitated from the extracts using one or more of the following precipitation techniques; isoelectric precipitation (IP) gave yields and protein contents ranging between 22--25% and 67--73% respectively. Co-precipitation with soy and whey proteins gave yields of 26.95 and 35.78% respectively for a NaOH extract. Chemical hydrolysis of flaxseed meal with NaOH, NaCl and NaCl/Papain extraction and IP increased protein solubilization (35--43%) and protein yields (19--37%). / Proteins in the extracts and isolates were characterized by polyacrylamide gel electrophoresis (PAGE). Proteins extracted with NaOH and NaCl gave two bands by native-PAGE with molecular weights (MW) of 320 and 514KDa; proteins extracted with NaCl/Papain gave a single band at 188KDa. SDS-PAGE of isolates extracted with NaOH, NaCl and NaCl/Papain gave subunits with MW ranging from 6.5 to 56KDa. The major fractions isolated from NaOH-IP by RP-HPLC showed subunits with MW ranging from 6.5 to 40.1KDa by SDS-PAGE and 5.9 to 42.5KDa by ESI-MS. Subunits characterized by ESI-MS have not been reported previously in the literature.

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Ischemic heart disease is the largest cause of death due to cardiovascular origins. A better understanding of the mechanisms responsible for ischemic heart disease increases the potential for therapies. This will lead to decreased mortalities in Canada and around the world. Nutritional interventions have gained increasing attention as causes or treatments for cardiovascular disease. For example, trans fats (TFAs) have both beneficial and deleterious effects on cardiovascular disease [1]. In this study, we would like to examine this phenomenon. We contrast the effects of two different TFAs on cardiomyocyte viability. We compare the industrially produced trans-fat elaidic acid (EA) and the ruminant trans-fat vaccenic acid (VA) on apoptotic and autophagic markers during non-ischemic (control), ischemic (ISCH) and ischemia/reperfusion (IR) conditions. Rat cardiomyocytes are exposed to medium containing fatty acids conjugated with bovine serum albumin for 24 hours. VA and EA have no significant effect on biomarkers of apoptosis or cell death. Interestingly, a similar effect is observed with autophagic and apoptotic markers of LDLr-/- mice whose diets were supplemented with VA or EA. Cells pre-treated with EA prior to 60 minutes of simulated ISCH and 120 minutes of IR increased cell death compared to control through augmented apoptosis. VA decreases the number of dead cells during ISCH and IR. However, the apoptotic parameters remain unchanged. We also observe that VA decreases oxidized phospholipid content in non-ischemic conditions. We conclude that not all TFAs are deleterious to the heart. EA is toxic to cardiomyocytes with or without ISCH or IR whereas VA is cardioprotective during IR and ISCH conditions. We believe VA decreases oxidized phospholipid content to produce this cardioprotective effect. For the purposes of comparison, we examined the effects of α-linolenic acid (ALA), an essential polyunsaturated fatty acid found in foods like flaxseed. Omega-3 fatty acids have been associated with improved cardiovascular outcomes. Here, isolated adult rat cardiomyocytes from male Sprague Dawley rats were exposed to medium containing ALA for 24 hours and then exposed control, ISCH or IR conditions. Cell death increases during ISCH and IR. An increase in DNA fragmentation and caspase-3 activity was observed in both the ISCH and IR conditions. Pre-treatment of the cells with ALA subsequently inhibits cell death during ISCH and IR challenge and significantly reduced both DNA fragmentation and caspase-3 cleavage during ISCH and IR. Cardiomyocyte resting Ca2+ increased and Ca2+ transients decreased during ISCH or I/R but ALA pre-treatment did not improve either parameter significantly. We hypothesize that apoptosis is initiated through phosphatidylcholine oxidation within the cardiomyocytes. Pre-treatment of cells with ALA resulted in a significant incorporation of ALA within cardiomyocyte phosphatidylcholine. Two pro-apoptotic oxidized phosphatidylcholine (OxPC) species, 1-palmitoyl-2-(5'-oxo-valeroyl)-sn-glycero-3-phosphocholine (POVPC) and 1-palmitoyl-2-glutaroyl-sn-glycero-3-phosphocholine (PGPC) were significantly increased during both ISCH and IR. ALA pre-treatment significantly decreased the production of POVPC and PGPC during ISCH and I/R. It is concluded that ALA protects the cardiomyocyte from apoptotic cell death during simulated ISCH and IR by inhibiting the production of specific pro-apoptotic OxPC species. In summary, we observe a differential effect of ALA, VA and EA on parameters of cardiomyocyte viability during ISCH or IR.

The development of the monograph of a commonly used Chinese medicine, Lini Semen, for the Hong Kong Chinese Materia Medica Standards (HKCMMS) was recorded. HKCMMS is a set of reliable and internationally recognized standards of Chinese medicine. The monograph of Lini Semen was proposed, endorsed, and under editorial phase for the publication of the 9th volume of HKCMMS. In the proposed HKCMMS monograph of Lini Semen, besides regular content such as macroscopic and microscopic identification, and TLC identification, a HPLC fingerprint method and two assay methods were developed. All methods were well-established and validated. TLC identification: Lini Semen n-hexane extract is identified on a HPTLC Silica gel RP-18 plate, with α-linolenic acid and linoleic acid as the markers. The developing system consisted of acetone, acetic acid and dichloromethane in the ratio of 5:4:2. The spraying reagent was 5% sulphuric acid - ethanol solution and the plate was observed under 366 nm. HPLC fingerprint: Fingerprint of Lini Semen was conducted on a HPLC system with a C8 column. Mobile phase consisted of (A) water and (B) acetonitrile and isopropanol (9:1). Six characteristic peaks, including α-linolenic acid and linoleic acid were detected under 210 nm. Assay: α-Linolenic acid and linoleic acid were detected from Lini Semen n-hexane extract under the same HPLC condition of the fingerprint of Lini Semen. The proposed total content of α-linolenic acid and linoleic acid was not less than 0.56%. Secoisolariciresinol diglucoside (SDG) was detected from hydrolysed Lini Semen extract by HPLC system with a C18 column. Mobile phase consisted of (A) water and (B) acetonitrile. The detection wavelength was 280 nm. The proposed content of SDG was not less than 0.81%. Conclusion: It is the first time to propose a HPLC fingerprint and introduce SDG as a assay marker of Lini Semen in a regional standard monograph. The established methods for TLC identification, HPLC fingerprint, assay of the total content of α-linolenic acid and linoleic acid, as well as assay for SDG were validated with in-house and inter-laboratory comparison to prove that the methods are reliable.