To investigate the underlying mechanisms of C18 fatty acids (stearic acid, oleic acid, linoleic acid and alpha-linolenic acid) on mast cells, we measured the effect of C18 fatty acids on intracellular Ca2+ mobilization and histamine release in RBL-2H3 mast cells. Stearic acid rapidly increased initial peak of intracellular Ca2+ mobilization, whereas linoleic acid and alpha-linolenic acid gradually increased this mobilization. In the absence of extracellular Ca2+, stearic acid (100 microM) did not cause any increase of intracellular Ca2+ mobilization. Both linoleic acid and alpha-linolenic acid increased intracellular Ca2+ mobilization, but the increase was smaller than that in the presence of extracellular Ca2+. These results suggest that C18 fatty acid-induced intracellular Ca2+ mobilization is mainly dependent on extracellular Ca2+ influx. Verapamil dose-dependently inhibited stearic acid-induced intracellular Ca2+ mobilization, but did not affect both linoleic acid and alpha-linolenic acid-induced intracellular Ca2+ mobilization. These data suggest that the underlying mechanism of stearic acid, linoleic acid and alpha-linolenic acid on intracellular Ca2+ mobilization may differ. Linoleic acid and alpha-linolenic acid significantly increased histamine release. Linoleic acid (C18:2: omega-6)-induced intracellular Ca2+ mobilization and histamine release were more prominent than alpha-linolenic acid (C18:3: omega-3). These data support the view that the intake of more alpha-linolenic acid than linoleic acid is useful in preventing inflammation.
alpha-Linolenic Acid ; Fatty Acids* ; Histamine Release* ; Inflammation ; Linoleic Acid ; Mast Cells ; Oleic Acid ; Verapamil

BACKGROUND: To investigate the effect of manganese on lipid peroxidation and compositional changes of fatty acids in hippocampus of rat brain. METHODS: Seven rats in experimental group were given with MnCl2 intraperitoneally for 4 weeks (4 mg/kg once daily, 5 days per week). Twenty four hours after the last injection, rats were decapitated and, hippocampus were separated from the rat brain. RESULT: In Mn-treated group, manganese concentrations increased significantly in the hippocampus by 222% compared with control group (P<0.01). MDA concentrations increased significantly by 149% compared with control group (P<0.05). Among fatty acids, total n-6 polyunsaturated fatty acids (PUFAs) increased significantly by 237% compared with control group (P<0.05). Linoleic acid (LA) and arachidonic acids (AA) increased by 213%, 238% (P<0.05, P<0.01, respectively). Among n-3 PUFAs except linolenic acids, eicosapentanoic acid(EPA) and docosahexanoic acids (DHA) decreased significantly by 70%, 50% respectively compared with control group (both P<0.01). CONCLUSION: Our results suggest that manganese may cause compositional changes of fatty acids in hippocampus of rat brain. Characteristics of fatty acids compositional changes by manganese were the decrease of EPAs and DHAs (n-3 PUFAs), and increase of AA and LA (n-6 PUFAs). These changes with the increase of MDA, suggest that manganese neurotoxicity is caused by lipid peroxidation.
alpha-Linolenic Acid ; Animals ; Arachidonic Acid ; Arachidonic Acids ; Brain* ; Fatty Acids* ; Fatty Acids, Omega-3 ; Fatty Acids, Unsaturated ; Hippocampus* ; Linoleic Acid ; Linolenic Acids ; Lipid Peroxidation* ; Malondialdehyde ; Manganese* ; Rats*

The chemical constituents in Urtica dioica fruits were investigated by silica gel chromatography, preparative HPLC, NMR, and HR-MS for the first time. As a result, 21 compounds were isolated from the fruits of U. dioica and identified 7R,8S,8'R-olivil(1), oleic acid(2), α-linoleic acid(3), palmic acid(4), methyl palmitate(5), α-linolenic acid(6), α-linolenic acid methyl ester(7), 5-O-caffeoyl-shikimic acid(8), vanillic acid(9), p-coumaric acid(10), 5-O-p-coumaroylshikimic acid(11), cinnamic acid(12), quinic acid(13), shikimic acid(14), ethyl caffeate(15), coniferyl ferulate(16), ferulic acid(17), caffeic acid(18), chlorogenic acid(19), pinoresinol(20), and quercetin(21). Compound 1 was a new compound and compounds 2-16 were isolated from U. dioica for the first time.
Chlorogenic Acid ; Fruit ; Linoleic Acid ; Oleic Acid ; Quercetin/chemistry* ; Quinic Acid ; Shikimic Acid ; Silicon Dioxide ; Urtica dioica/chemistry* ; Vanillic Acid ; alpha-Linolenic Acid

Evening primrose oil(EPO), which contains 72% cis-linoleic acid and 9% cisgamma linolenic acid, has been clinically used for treatment of number of diseases in human and animals. And it is also known to lower cholesterol(CHO) level of hypercholesterolaemic individuals. But the role of EPO as CHO-suppressant is controversial, and the relationship of EPO to CHO level in immune regulating activities is unclear at present. To evaluate the effect of evening primrose on the normal plasma CHO-levels, rabbits were fed with evening primrose seed(EPS) or injected with evening primrose seed-extract(EPE), and measured the plasma CHO-levels by duration of treatment. Both of EPS and EPE did not influence the plasma CHO-levels until 4 day treatment and thereafter the levels were significantly reduced. For the investigation of the EPE-effect on immune response to sheep erythrocytes(SRBC), mice were injected with EPE for 4 days before SRBC-sensitization or with CHO just before SRBC, Sensitization or with CHO in regulating effect of immune response was evaluated by the measuring the footpad swelling reaction and antibody response to SRBC. EPE itself did not influence Arthus reaction but it remarkable reduced delayed type hypersensitivity(DTH) and antibody production in comparison with control. CHO slightly increased Arthus reaction and DTH, but it somewhat decreased antibody responses. However, CHO significantly recovered the EPE-induced decrement of DTH and humoral immunity. There results led to that conclusion the evening primrose triggers the decrease of plasma CHO-levels and immune responses, and suggested that the mechanisms responsible for the nonspecific immune inhibitory effect of evening primrose might be partially due to the decrement of the CHO-levels.
alpha-Linolenic Acid ; Animals ; Antibody Formation ; Arthus Reaction ; Cholesterol* ; Erythrocytes* ; Humans ; Immunity, Humoral ; Mice ; Oenothera biennis ; Plasma* ; Primula* ; Rabbits ; Sheep*

Essential fatty acid (EFA) is known to be required for the body to function normally and healthily. However, the effect of EFA on glucose uptake in skeletal muscle has not yet been fully investigated. In this study, we examined the effect of two EFAs, linoleic acid (LA) and alpha-linolenic acid (ALA), on glucose uptake of C2C12 skeletal muscle cells and investigated the mechanism underlying the stimulatory effect of polyunsaturated EFAs in comparison with monounsaturated oleic acid (OA). In palmitic acid (PA)-induced insulin resistant cells, the co-treatment of EFAs and OA with PA almost restored the PA-induced decrease in the basal and insulin-stimulated 2-NBDG (fluorescent D-glucose analogue) uptake, respectively. Two EFAs and OA significantly protected PA-induced suppression of insulin signaling, respectively, which was confirmed by the increased levels of Akt phosphorylation and serine/threonine kinases (PKCtheta and JNK) dephosphorylation in the western blot analysis. In PA-untreated, control cells, the treatment of 500 microM EFA significantly stimulated 2-NBDG uptake, whereas OA did not. Phosphorylation of AMP-activated protein kinase (AMPK) and one of its downstream molecules, acetyl-CoA carboxylase (ACC) was markedly induced by EFA, but not OA. In addition, EFA-stimulated 2-NBDG uptake was significantly inhibited by the pre-treatment of a specific AMPK inhibitor, adenine 9-beta-D-arabinofuranoside (araA). These data suggest that the restoration of suppressed insulin signaling at PA-induced insulin resistant condition and AMPK activation are involved at least in the stimulatory effect of EFA on glucose uptake in C2C12 skeletal muscle cells.
Acetyl-CoA Carboxylase ; Adenine ; alpha-Linolenic Acid ; AMP-Activated Protein Kinases* ; Blotting, Western ; Fatty Acids, Essential* ; Glucose* ; Insulin ; Linoleic Acid ; Muscle, Skeletal* ; Oleic Acid ; Palmitic Acid ; Phosphorylation ; Phosphotransferases

PURPOSE: Citron seed oil (CSO) has been reported to have high antioxidant activity. However, the composition and other biologically activities of CSO have not been reported. In this study, we confirmed the fatty acid composition of CSO, which may be beneficial to vascular disease and obesity. METHODS: We investigated the oil composition of CSO using gas chromatography coupled with mass spectrometry (GC-MS) analysis, and cytotoxicity was confirmed by Cell Counting Kit-8 (CCK-8) assay. Nitric oxide (NO) production in human umbilical vein endothelial cells (HUVECs) was measured using Griess reagent, and lipid accumulation and leptin secretion in 3T3-L1 cells were measured by Oil-Red O staining and commercial ELISA kit, respectively. RESULTS: GC-MS analysis indicated that CSO contains several components, including linoleic acid, oleic acid, palmitic acid, stearic acid, linolenic acid, palmitoleic acid, and arachidic acid. In physiological activity analysis, CSO did not induce cytotoxic effects in HUVECs and 3T3-L1 cells. Further, CSO significantly induced nitric oxide and leptin secretion as well as inhibited lipid accumulation. CONCLUSION: CSO increased NO release, inhibited lipid accumulation, and induced leptin secretion, suggesting it may be useful for the management of vessels and weight gain. Although further studies are required to investigate the safety and mechanism of action of CSO, our results show that the composition and physiological activity of CSO are sufficient for its use as functional edible oil.
3T3-L1 Cells ; alpha-Linolenic Acid ; Cell Count ; Chromatography, Gas ; Enzyme-Linked Immunosorbent Assay ; Human Umbilical Vein Endothelial Cells ; Leptin* ; Linoleic Acid ; Mass Spectrometry ; Nitric Oxide* ; Obesity

Alpha-linolenic acid(ALA, C18:3delta9,12,15 ) is an essential fatty acid which has many sanitary functions to human. However, its contents in diets are often not enough. In plants, omega-3 fatty acid desaturases(FAD) catalyze linoleic acid(LA, C18:2delta9,12) into ALA. The seed oil of Glycine max contains high level of ALA. To investigate the functions of Glycine max omega-3FAD, the cDNA of GmFAD3 C was amplified by RT-PCR from immature seeds, then cloned into the shuttle expression vector p416 to generate the recombinant vector p4GFAD3C. The resulting vector was transformed into Saccharomyces cerevisiae K601 throuth LiAc method. The positive clones were screened on the CM(Ura-) medium and identified by PCR, and then cultured in CM (Ura-) liquid medium with exogenous LA in 20 degrees C for three days. The intracellular fatty acid composition of the engineering strain Kp416 and Kp4GFAD3C was analyzed by gas chromatography (GC). A novel peak in strain Kp4GFAD3C was detected,which was not detectable in control, Comparison of the retention times of the newly yielded peak with that of authentic standard indicated that the fatty acid is ALA. The content of ALA reached to 3.1% of the total fatty acid in recombinant strain, the content of LA correspondingly decreased from 22% to 16.2% by contrast. It was suggested that the protein encoded by GmFAD3 C can specifically catalyze 18 carbon PUFA substrate of LA into ALA by taking off hydrogen atoms at delta15 location. In this study, we expressed a Glycine max omega-3 fatty acid desaturase gene in S. cerevisiae; An efficient and economical yeast expressing system(K601-p416 system) which is suitable for the expression of FAD was built.
Chromatography, Gas ; Cloning, Molecular ; Fatty Acid Desaturases ; biosynthesis ; genetics ; Saccharomyces cerevisiae ; genetics ; metabolism ; Soybeans ; enzymology ; genetics ; alpha-Linolenic Acid ; analysis ; biosynthesis ; genetics

Exogenous lipid pneumonia is a rare disease resulting from the aspiration or inhalation of vegetable, animal, or mineral oils. In Korea, the most frequently implicated agent is squalen, which can be obtained from shark liver oil. Lipid pneumonia by aspiration of the vegetable oil is very rare. We experienced a 77-year-old man with a history of ingestion of green perilla oil. His clinical course was favorable; after exposure to the oil was stopped, the patient's symptoms improved.
Aged ; alpha-Linolenic Acid ; Animals ; Bronchoalveolar Lavage ; Eating ; Humans ; Inhalation ; Korea ; Liver ; Mineral Oil ; Perilla ; Plant Oils ; Pneumonia, Lipid ; Rare Diseases ; Sharks ; Vegetables

BACKGROUND: Several studies have been performed to evaluate the efficacy of dietary n-3 fatty acid for patients with renal dysfunction. While about 40% to 80% of patients with end-stage renal disease (ESRD) complain about pruritus and xerosis, there are few reports on the effects of topical n-3 fatty acid on these symptoms. OBJECTIVE: In order to investigate the possible beneficial effects of topical n-3 fatty acid, oils extracted from chia (Salvia hispanica) seed were formulated into topical products, the effects of which were measured. METHODS: Five healthy volunteers having xerotic pruritus symptoms and 5 patients with pruritus caused by either ESRD or diabetes were involved in this study. A topical formulation containing 4% chia seed oils were applied for an 8-week duration. Subjective itching symptoms were assessed on a 6-point scale, as were other skin functions, namely transepidermal water loss and skin capacitance. RESULTS: After the 8 weeks of application, significant improvements in skin hydration, lichen simplex chronicus, and prurigo nodularis were observed in all patients. A similar improvement was also observed among healthy volunteers with xerotic pruritus. Improvement of epidermal permeability barrier function and skin hydration, represented by trans-epidermal water loss and skin capacitance, respectively, were also observed. No adverse effects were observed in all the tested patients and volunteers. CONCLUSION: Chia seed oil can be used as an adjuvant moisturizing agent for pruritic skin, including that of ESRD patients.
alpha-Linolenic Acid ; Fatty Acids, Omega-3 ; Humans ; Kidney Failure, Chronic ; Methylmethacrylates ; Neurodermatitis ; Oils ; Permeability ; Polystyrenes ; Prurigo ; Pruritus ; Seeds ; Skin ; Water Loss, Insensible

Rheumatoid arthritis(RA), a chronic autoimmune disease, is featured by persistent joint inflammation. The development of RA is associated with the disturbance of endogenous metabolites and intestinal microbiota. Gardeniae Fructus(GF), one of the commonly used medicinal food in China, is usually prescribed for the prevention and treatment of jaundice, inflammation, ache, fever, and skin ulcers. GF exerts an effect on ameliorating RA, the mechanism of which remains to be studied. In this study, ultra-perfor-mance liquid chromatography-tandem mass spectrometry(UPLC-MS/MS)-based serum non-target metabolomics and 16S rDNA high-throughput sequencing were employed to elucidate the mechanism of GF in ameliorating RA induced by complete Freund's adjuvant in rats. The results showed that GF alleviated the pathological conditions in adjuvant arthritis(AA) rats. The low-and high-dose GF lo-wered the serum levels of interleukin(IL)-6, tumor necrosis factor-α(TNF-α), IL-1β, and prostaglandin E2 in the rats(P<0.05, P<0.01). Pathways involved in metabolomics were mainly α-linolenic acid metabolism and glycerophospholipid metabolism. The results of 16S rDNA sequencing showed that the Streptococcus, Facklamia, Klebsiella, Enterococcus, and Kosakonia were the critical gut microorganisms for GF to treat AA in rats. Spearman correlation analysis showed that the three differential metabolites PE-NMe[18:1(9Z)/20:0], PC[20:1(11Z)/18:3(6Z,9Z,12Z)], and PC[20:0/18:4(6Z,9Z,12Z,15Z)] were correlated with the differential bacteria. In conclusion, GF may ameliorate RA by regulating the composition of intestinal microbiota, α-linolenic acid metabolism, and glycerophospholipid metabolism. The findings provide new ideas and data for elucidating the mechanism of GF in relieving RA.
Rats ; Animals ; Chromatography, Liquid ; Gardenia ; Tandem Mass Spectrometry ; Gastrointestinal Microbiome ; alpha-Linolenic Acid ; Metabolomics/methods* ; Arthritis, Rheumatoid/drug therapy* ; Inflammation ; Glycerophospholipids