The present study was undertaken to observe the quality and quantity of lipids in the adult worms of Chinese liverfluke, Clonorchis sinensis. Lipid extraction was done by the methods of Folch et a1. (l957) and Kenny (1952), and then the extracted lipid fractions of the worm were separated by thin layer chromatography. Those fractions were also subjected to perform the quantitative analyses of glycerides, cholesterols and phospholipids. The results obtained were summarized as follows: Total amount of glyceride was 37.56 mg per gram of worm tissue and the amount of monoglyceride was 8.34 mg per gm; diglyceride, 15.46 mg per gm; and triglyceride, 12.86 mg per gm. Total amount of cholesterol was 3.30 mg per gm of worm tissue, and the esterified cholesterol (1.72 mg/gm) was a little more than that of free cholesterol (1.26 mg/gm). The following 8 phospholipids were detected in the worm tissue of C. sinensis, i.e., lysophosphatidylcholine, phosphatidylcholine, phophatidylinositol, sphingomyelin, phosphatidylglycerol, phosphatidylserine, phosphatidylethanolamine and an unknown phospholipid.
parasitology-helminth-trematoda ; Clonorchis sinensis ; biochemistry ; glyceride ; cholesterol ; phospholipid ; lipid ; lysophosphatidylcholine ; phosphatidylcholine ; phophatidylinositol ; sphingomyelin ; phosphatidylglycerol ; phosphatidylserine ; phosphatidylethanolamine

BACKGROUND: Impairment of relaxing response and augmentation of contractile response to vasoactive substances have been reported in atherosclerotic arteries. These alterations in vascular reactivity are considered as an underlying mechanism for the development of acute vasospasm in atherosclerotic coronary artery. Recently, it has been reported that lysophophatidylcholine (LPC), an oxidative metabolite of low density lipoprotein causes this functional abnormality. However, the precise mechanism of LPC induced change of vascular reactivity is still uncertain. METHOD: In this study, to elucidate the underlying mechanisms of abnormal vascular reactivity in atherosclerotic coronary artery, we examined the effect of LPC on whole cell K+current using patch clamping technique in rabbit coronary smooth muscle cells. RESULTS: Application of LPC(1microM) showed dual effect on whole cell outward current which depends on the magnitude of test potentials. At relatively high depolarizing test potentials (> 10 mV), LPC increased amplitude of outward current which was blocked by Gd3+ not by iberiotoxin (100 nM) and TEA (1 mM). Reversal potential of this Gd3+sensitive, LPC-induced current was -9.7 +/- 0.6 mV. At less depolarizing test potentials (< 10 mV), LPC decreased whole cell K+currents in a dose dependent manner (from 0.01 to 10 microM) in the range of -30 mV to +0 mV. Half maximal inhibition of K+current was 1.509 microM at 0 mV test potential (n =5). Depolarizing holding potential (0 mV) prevented this LPC-induced inhibition of K+current. Steady state activation and inactivation parameters of K+current were significantly shifted to the positive direction by application of LPC (p < 0.01, n =8). Pretreatment of staurosporine (100 nM), a blocker of protein kinase C partially blocked LPC-induced decrease of K+currents. CONCLUSION: LPC-induced inhibition of voltage dependent K+current may explain abnormal vascular reactivity in atherosclerotic coronary artery.
Arteries ; Constriction ; Coronary Vessels ; Lipoproteins ; Lysophosphatidylcholines* ; Muscle, Smooth* ; Myocytes, Smooth Muscle* ; Protein Kinase C ; Staurosporine ; Tea

BACKGROUND AND OBJECTIVES: Lysophosphatidylcholine (lysoPC), an atherogenic lysophospholipid, is known to induce the proliferation of vascular smooth muscle cells (VSMCs). Naringin is a flavonoid in grapes and grapefruits and has anti-inflammatory as well as antioxidative effects. We investigated whether naringin could protect VSMCs from the effect of lysoPC. Additionally, we investigated the changes of nuclear translocation of nuclear factor-kappa B (NF-kappa B). MATERIALS AND METHODS: VSMCs were prepared from the aorta of Sprague-Dawley rats. Near-confluent VSMCs were preincubated in media containing 0, 10, 100 micrometer naringin, and incubated with 0, 10, 20, 100 micrometer lysoPC. The degree of proliferation of VSMCs was evaluated with [H3]-thymidine incorporation and MTT assay. The changes of nuclear translocation of NF-kappa B in VSMCs were investigated with EMSA. RESULTS: LysoPC promoted the growth of VSMCs, whereas naringin inhibited the proliferative effect of lysoPC on VSMCs. MTT assay showed a 63+/-24% and 89+/-17% increase of cellular growth in the 10 and 20 micrometer lysoPC groups, respectively, as compared with the control group with media only (p<0.01). [H3]-thymidine incorporation assay also showed 61+/-25% and 92+/-25% increase in the 10 and 20 micrometer lysoPC groups, respectively (p<0.01). However, the growth of VSMCs was suppressed in the 100 micrometer lysoPC group (p<0.01). Naringin inhibited the proliferative effects of lysoPC on VSMCs by 34+/-5% (MTT assay) and 35+/-5% ([H3]-thymidine incorporation assay) in the 100 micrometer naringin group (p=0.01). The nuclear translocation of NF-kappa B was stimulated by lysoPC and suppressed by naringin. CONCLUSION: LysoPC promoted the growth of VSMCs, whereas naringin inhibited the proliferative effect of lysoPC on VSMCs. These effects of lysoPC and naringin are associated with the regulation of nuclear translocation of NF-kappa B.
Aorta ; Citrus paradisi ; Lysophosphatidylcholines ; Muscle, Smooth, Vascular* ; NF-kappa B ; Rats, Sprague-Dawley ; Vitis

G-protein-coupled receptors (GPCR) are the largest superfamily of receptors responsible for signaling between cells and tissues, and because they play important physiological roles in homeostasis, they are major drug targets. New technologies have been developed for the identification of new ligands, new GPCR functions, and for drug discovery purposes. In particular, intercellular lipid mediators, such as, lysophosphatidic acid and sphingosine 1-phosphate have attracted much attention for drug discovery and this has resulted in the development of fingolimod (FTY-720) and AM095. The discovery of new intercellular lipid mediators and their GPCRs are discussed from the perspective of drug development. Lipid GPCRs for lysophospholipids, including lysophosphatidylserine, lysophosphatidylinositol, lysophosphatidylcholine, free fatty acids, fatty acid derivatives, and other lipid mediators are reviewed.
Drug Discovery* ; Fatty Acids, Nonesterified ; Homeostasis ; Ligands ; Lysophosphatidylcholines ; Lysophospholipids ; Receptors, G-Protein-Coupled ; Sphingosine ; Fingolimod Hydrochloride

A lipidomic study on extensive plasma lipids in bacterial peritonitis (cecal ligation and puncture, CLP)-induced sepsis in mice was done at 24 h post-CLP. The effects of administration of lysophosphatidylcholine (LPC) and lysophosphatidic acid (LPA), compounds known to have beneficial effects in CLP, on the sepsis-induced plasma lipid changes were also examined. Among the 147 plasma lipid species from 13 lipid subgroups (fatty acid [FA], LPA, LPC, lysophosphatidylethanolamine [LPE], phosphatidic acid [PA], phosphatidylcholine [PC], phosphatidylethanolamine [PE], phosphatidylinositol [PI], monoacylglyceride [MG], diacylglyceride [DG], triacylglyceride [TG], sphingomyelin [SM], and ceramide [Cer]) analyzed in this study, 40 and 70 species were increased, and decreased, respectively, in the CLP mice. Treatments with LPC and LPA affected 14 species from 7 subgroups, and 25 species from 9 subgroups, respectively. These results could contribute to finding the much needed reliable biomarkers of sepsis.
Animals ; Biomarkers ; Ligation ; Lysophosphatidylcholines ; Mice* ; Peritonitis ; Phosphatidic Acids ; Phosphatidylcholines ; Phosphatidylinositols ; Plasma* ; Punctures ; Sepsis

Effects of oxidized low-density lipoprotein (ox-LDL), l-alpha-stearoyl-lysophosphatidylcholine (LPC), on intracellular Ca2+ concentration were examined in mouse endothelial cells by measuring intracellular Ca2+ concentration ([Ca2+]i) with fura 2-AM and reverse transcription-polymerase chain reaction (RT-PCR). LPC increased [Ca2+]i under the condition of 1.5 mM [Ca2+]o but did not show any effect under the nominally Ca2+-free condition. Even after the store depletion with 30microM 2,5-di-tert- butylhydroquinone (BHQ) or 30microM ATP, LPC could still increase the [Ca2+]i under the condition of 1.5 mM [Ca2+]o. The time required to increase [Ca2+]i (about 1 minute) was longer than that for ATP-induced [Ca2+]i increase (10-30 seconds). LPC-induced [Ca2+]i increase was completely blocked by 1microM La3+. Transient receptor potential channel(trpc) 4 mRNA was detected with RT-PCR. From these results, we suggest that LPC increased [Ca2+]i via the increase of Ca2+ influx through the Ca2+ routes which exist in the plasma membrane.
Adenosine Triphosphate ; Animals ; Cell Membrane ; Endothelial Cells* ; Lipoproteins ; Lysophosphatidylcholines* ; Mice ; RNA, Messenger

Objective: To investigate the relationship between serum lysophosphatidylcholine (LPC) level and the health index of the elderly. Methods: A total of 251 subjects were selected from the 2016 baseline survey of the Yongfu Longevity Cohort in Guangxi Province among whom 66, 63 and 122 were in the young and middle-aged group (≤59 years old), the young group (60-89 years old) and the longevity group (≥90 years old), respectively. Demographic data were collected and related indicators of height, weight, blood pressure and lipid metabolism were measured. The cognitive and physical functions of the elderly were assessed by the results of the simple mental state scale and the daily living activity scale to construct the health index of the elderly. The serum levels of LPC16∶0, LPC18∶0, LPC18∶1 and LPC18∶2 were determined by liquid chromatography-tandem mass spectrometry, and the differences among different ages and health status groups were compared. The logistic regression model was used to analyze the relationship between the serum LPC level and the health index of the elderly. Results: With the increase in age, the proportion of female subjects increased, and the rate of smoking and drinking decreased. BMI, TC, TG, LDL-C, diastolic blood pressure, and the four LPCs levels decreased with the increase of age, and systolic blood pressure levels increased with the increase of age (all P values<0.05). There was no significant difference in HDL-C levels among age groups (P>0.05). With the decline of health status in the elderly, serum levels of LPC16∶0, LPC18∶0, LPC18∶1 and LPC18∶2 showed a downward trend (all P values<0.001). After adjusting for age and gender, only LPC18∶0 was associated with the health status in old age [OR (95%CI): 0.48 (0.25-0.92)]. For every 1 standard deviation (16.87 nmol/L) increase in serum LPC18∶0 concentration, the risk of poor health status in old age decreased by 52%. Conclusion: Serum LPC18∶0 was associated with the health status in old age independent of age and sex.
Aged ; Middle Aged ; Humans ; Female ; Aged, 80 and over ; Lysophosphatidylcholines ; Risk Factors ; China ; Longevity ; Surveys and Questionnaires ; Triglycerides

OBJECTIVE: The aim of this study were to examine the serum level of estradiol, estriol, progesterone, oxidized LDL in preeclamtic patients and to evaluate the protective effects of estrogen and progesterone against lysophosphatidylcholine (LPC) induced cell death in Human umbilical vein endothelial cells (HUVECs). METHODS: We analysed the serum level of estradiol, estriol, progesterone, oxidized LDL in patients with preeclampsia and control. We used LPC to induce cell death in HUVECs. For cytotoxic assay, we did LDL assay for cell death and Resazurin assay for cell viability. HUVECs were exposed to various concentrations of LPC, LPC+estrogen, LPC+progesterone and we did cytotoxic assay. RESULTS: The serum estradiol, estriol were lower in the preeclamptic patients (P<0.05). Oxidized LDL were higher in the preeclamptic patients(P<0.05). LPC induced cell death in a concentration-dependant manner. Estrogen or progesterone inhibited LPC-induced cell death in a concentration-dependant manner (P<0.05). CONCLUSION: Estrogen and progesterone attenuated LPC-induced cytotoxicity. The results suggest that Oxidized LDL induced endothelial damage in preeclampsia may be induced by low serum estradiol, estriol and progesterone levels and prevented by estrogen and progesterone addition.
Cell Death ; Cell Survival ; Estradiol ; Estriol ; Estrogens* ; Human Umbilical Vein Endothelial Cells ; Humans ; Lysophosphatidylcholines ; Pre-Eclampsia ; Progesterone*

PURPOSE: Asthma is a chronic inflammatory disease of the airways, and is associated with upregulation of phospholipase A2 (PLA2), the enzyme that hydrolyzes phosphatidylcholine, producing lysophosphatidylcholine (LPC) and free fatty acids. LPC is a lipid mediator with known pro-inflammatory and pro-atherogenic properties, and is believed to be a critical factor in cardiovascular diseases. We postulate that asthmatic subjects have an elevated content of LPC in the lung lining fluids. METHODS: Eight non-asthmatic controls and seven asthmatic subjects were recruited for broncho-alveolar lavage fluids (BALF) collection for analysis of LPC by high performance liquid chromatography-tandem mass spectrometry. RESULTS: LPC16:0 and LPC18:0 were significantly elevated in the BALF of asthmatics with impaired lung function characteristic of moderate asthma, but not mild asthma. The increased LPC content in BALF was accompanied by increased PLA2 activity. Furthermore, qRT-PCR analysis of the BALF cell fraction indicated increased secretory PLA2-X (sPLA2-X). CONCLUSIONS: The increased LPC content in the lung lining fluids is a potential critical lipid mediator in the initiation and/or progression of airway epithelial injury in asthma.
Asthma ; Cardiovascular Diseases ; Fatty Acids, Nonesterified ; Lung* ; Lysophosphatidylcholines* ; Mass Spectrometry ; Phosphatidylcholines ; Phospholipases A2 ; Therapeutic Irrigation ; Up-Regulation

AIMTo observe the effect of LPC on the pacemaker current I(f) in ischemic myocardium and if the effect could be reversed by ISO.

METHODSBy using two microelectrode voltage clamp technique to measure and compare the amplitude of I(f) of ischemic myocardium in the presence of LPC and LPC add ISO.

RESULTSIschemia decreased the amplitude of I(f) at all membrane potential levels. Adding LPC 2 x 10(-5) mol/L to the ischemia-like solution, the amplitude of I(f) decreased further (n = 5, P < 0.05), it means that LPC aggravated the inhibitory effect of "ischemia" on the pacemaker activity. Adding LPC 2 x 10(-5) mol/L and ISO 1 x 10(-6) mol/L together to the ischemia-like solution, the amplitude of I(f) increased significantly at membrane potential -90 mV to - 120 mV (n = 8, P < 0.05) compared with ischemia condition, but still did not reach the levels before ischemia.

CONCLUSIONIn acute myocardial ischemia condition, toxic metabolite LPC accentuated its inhibitory effect on pacemaker current I(f), a local release and accumulation of catecholamine could not completely reverse their inhibitory effect.

Animals ; Isoproterenol ; metabolism ; Lysophosphatidylcholines ; pharmacology ; Membrane Potentials ; drug effects ; Microelectrodes ; Myocardial Ischemia ; metabolism ; physiopathology ; Myocardium ; Patch-Clamp Techniques ; Sheep