UPLC-ESI-MS/MS strategy to analyze fatty acids composition and lipid profiles of Pacific saury (Cololabis saira).

The Pacific saury (Cololabis saira) is a highly nutritious deep-sea fish, rich in omega-3 polyunsaturated fatty acids (n-3 PUFAs). This study comprehensively investigated fatty acids composition and lipid profiles of different parts of Pacific saury based on an untargeted lipidomic strategy. Results suggested that the crude fat content of meat, head and viscera were 5.81%, 10.90%, and 19.46%, respectively. The contents of PUFAs were 41.08%, 34.96% and 33.14%, respectively. Among them, the n-3 PUFAs in the head (34.58%) were significantly higher than meat (29.40%) and viscera (27.95%). Moreover, 5752 lipid molecules were identified, where glycerophospholipids (GP) were the most numerous lipid type (45.58%), with phosphatidylcholine (PC) being main differential subclass. PC (20:3_22:6) was the most abundant molecule in the head (14.59%) and meat (19.60%). Head_vs_viscera group had higher characteristic PC abundance. This study will provide a theoretical basis for the physiological activity and lipid high-value utilization of Pacific saury.

The enzyme encoded by Myrmecia incisa, a green microalga, phospholipase A2 gene preferentially hydrolyzes arachidonic acid at the sn-2 position of phosphatidylcholine.

The enzyme phospholipase A2 (PLA2) plays a crucial role in acyl remodeling of phospholipids via the Lands' cycle, and consequently alters fatty acid compositions in triacylglycerol (TAG). In this study, a full-length cDNA sequence coding Myrmecia incisa phospholipase A2 (MiPLA2) was cloned using the technique of rapid amplification of cDNA ends. Comparison of the 1082-bp cDNA with its corresponding cloned DNA sequence revealed that MiPLA2 contained 3 introns. Mature MiPLA2 (mMiPLA2) had a conserved Ca2+-binding loop and a catalytic site motif that has been recognized in plant secretory PLA2 (sPLA2) proteins. Correspondingly, phylogenetic analysis illustrated that MiPLA2 was clustered within GroupXIA of plant sPLA2 proteins. To ascertain the function of MiPLA2, the cDNA coding for mMiPLA2 was subcloned into the vector pET-32a to facilitate the production of recombinant mMiPLA2 in Escherichia coli. Recombinant mMiPLA2 was purified and used for the in vitro enzyme reaction. Thin-layer chromatography profiles of the catalytic products generated by recombinant mMiPLA2 indicated a specificity for cleaving sn-2 acyl chains from phospholipids, thereby functionally characterizing MiPLA2. Although recombinant mMiPLA2 displayed a strong preference for phosphatidylethanolamine, it preferentially hydrolyzes arachidonic acid (ArA) at the sn-2 position of phosphatidylcholine. Results from the fused expression of p1300-sp-EGFP-mMiPLA2 illustrated that MiPLA2 was localized in the intercellular space of onion epidermis. Furthermore, the positive correlation between MiPLA2 transcription and free ArA levels were established. Consequently, the role of mMiPLA2 in the biosynthesis of ArA-rich TAG was elucidated. This study helps to understand how M. incisa preferentially uses ArA to synthesize TAG.

Circulating perturbation of phosphatidylcholine (PC) and phosphatidylethanolamine (PE) is associated to cardiac remodeling and NLRP3 inflammasome in cardiovascular patients with insulin resistance risk.

Lipidome perturbation occurring during meta-inflammation is associated to left ventricle (LV) remodeling though the activation of the NLRP3 inflammasome, a key regulator of chronic inflammation in obesity-related disorders. Little is known about phosphatidylcholine (PC) and phosphatidylethanolamine (PE) as DAMP-induced NLRP3 inflammasome. Our study is aimed to evaluate if a systemic reduction of PC/PE molar ratio can affect NLRP3 plasma levels in cardiovascular disease (CVD) patients with insulin resistance (IR) risk. Forty patients from IRCCS Policlinico San Donato were enrolled, and their blood samples were drawn before heart surgery. LV geometry measurements were evaluated by echocardiography and clinical data associated to IR risk were collected. PC and PE were quantified by ESI-MS/MS. Circulating NLRP3 was quantified by an ELISA assay. Our results have shown that CVD patients with IR risk presented systemic lipid impairment of PC and PE species and their ratio in plasma was inversely associated to NLRP3 levels. Interestingly, CVD patients with IR risk presented LV changes directly associated to increased levels of NLRP3 and a decrease in PC/PE ratio in plasma, highlighting the systemic effect of meta-inflammation in cardiac response. In summary, PC and PE can be considered bioactive mediators associated to both the NLRP3 and LV changes in CVD patients with IR risk.

Effect of cardiolipin on the lamellarity and elongation of liposomes hydrated in PBS.

Lamellarity and shape are important factors in the formation of vesicles and determine their role in biological systems and pharmaceutical applications. Cardiolipin (CL) is a major lipid in many biological membranes and exerts a great influence on their structural organization due to its particular structure and physico-chemical properties. Here, we used small-angle X-ray and neutron scattering to study the effects of CL with different acyl chain lengths and saturations (CL14:0, CL18:1, CL18:2) on vesicle morphology and lamellarity in membrane models containing mixtures of phosphatidylcholine and phosphatidylethanolamine with different acyl chain lengths and saturations (C14:0 and C 18:1). Measurements were performed in the presence of Phosphate Buffer Saline (PBS), at 37°C, to better reflect physiological conditions, which resulted in strong effects on vesicle morphology, depending on the type and amount of CL used. The presence of small quantities of CL (from 2.5%) reduced inter-membrane correlations and increased perturbation of the membrane, an effect which is enhanced in the presence of matched shorter saturated acyl chains, and mainly unilamellar vesicles (ULV) are formed. In extruded vesicles, employed for SANS experiments, flattened vesicles are observed partly due to the hypertonic effect of PBS, but also influenced by the type of CL added. Our experimental data from SAXS and SANS revealed a strong dependence on CL content in shaping the membrane microstructure, with an apparent optimum in the PC:CL mixture in terms of promoting reduced correlations, preferred curvature and elongation. However, the use of PBS caused distinct differences from previously published studies in water in terms of vesicle shape, and highlights the need to investigate vesicle formation under physiological conditions in order to be able to draw conclusions about membrane formation in biological systems.

Reprogramming of lipid metabolism in hepatocellular carcinoma resulting in downregulation of phosphatidylcholines used as potential markers for diagnosis and prediction.

BACKGROUND: Aberrant methylation and metabolic perturbations may deepen our understanding of hepatocarcinogenesis and help identify novel biomarkers for diagnosing hepatocellular carcinoma (HCC). We aimed to develop an HCC model based on a multi-omics. RESEARCH DESIGN AND METHODS: Four hundred patient samples (200 with HCC and 200 with hepatitis B virus-related liver disease (HBVLD)) were subjected to liquid chromatography-mass spectrometry and multiplex bisulfite sequencing. Integrative analysis of clinical data, CpG data, and metabolome for the 20 complete imputation datasets within a for-loopwas used to identify biomarker. RESULTS: Totally, 1,140 metabolites were annotated, of which 125 were differentially expressed. Lipid metabolism reprogramming in HCC, resulting in phosphatidylcholines (PC) significantly downregulated, partly due to the altered mitochondrial beta-oxidation of fatty acids with diverse chain lengths. Age, sex, serum-fetoprotein levels, cg05166871,cg14171514, cg18772205, PC (O-16:0/20:3(8Z, 11Z, 14Z)), and PC (16:1(9Z)/P-18:0) were used to develop the HCC model. The model presented a good diagnostic and an acceptable predictive performance. The cumulative incidence of HCC in low- and high-risk groups of HBVLD patients were 1.19% and 21.40%, respectively (p = 0.0039). CONCLUSIONS: PCs serve as potential plasma biomarkers and help identify patients with HBVLD at risk of HCC who should be screened for early diagnosis and intervention.

Insights into Q-markers and molecular mechanism of Sanguisorba saponins in treating ulcerative colitis based on lipid metabolism regulation.

BACKGROUND: Sanguisorba saponin extract (SSE) is the main active part of Sanguisorba officinalis with various pharmacological activities such as anti-inflammatory, anti-bacterial and anti-oxidant. However, its therapeutic role and underlying mechanisms for ulcerative colitis (UC) still need to be elucidated. PURPOSE: This study aims to explore the therapeutic effect, effectiveness-material basis-quality markers (Q-markers) and prospective mechanism of function of SSE on UC. METHODS: Fresh 2.5% dextran sulfate sodium salt (DSS) solution was placed in drinking bottles for 7 days to induce a mouse model of UC. SSE and sulfasalazine (SASP) were supplemented to mice by gavage for consecutive 7 days to investigate the therapeutic role of SSE on UC. Mouse monocyte macrophages (RAW264.7) and human normal colonic epithelial (NCM460) cells were treated with LPS to induce inflammatory responses, followed by pharmacodynamic examination with different concentrations of SSE. Hematoxylin-eosin (HE) and Alcian blue staining were conducted to evaluate the pathological damage of mice colon. Lipidomic technology was conducted to explore the differential lipids closely related to the disease process of UC. Quantitative PCR analysis, immunohistochemistry and ELISA kit were used to measure the expression levels of the corresponding proteins and pro-inflammatory factors. RESULTS: SSE treatment could effectively reduce the elevated expressions of pro-inflammatory factors in RAW264.7 and NCM460 cells due to LPS stimulation. Intragastric administration of SSE was found to significantly alleviate the symptoms of DSS-induced colon injury and low-polar saponins in SSE. Low polarity saponins, especially ZYS-II, were proved to be the main active substances of SSE in treating UC. In addition, SSE could significantly ameliorate the aberrant lipid metabolism in UC mice. The role of phosphatidylcholine (PC)34:1 in the UC pathogenesis has been fully verified in our previous studies. Herein, SSE-dosing effectively reversed the metabolic disorder of PCs in UC mice, and increased the PC34:1 level to normal via up-regulating the expression of phosphocholine cytidylyltransferase (PCYT1α). CONCLUSION: Our data innovatively revealed that SSE could significantly alleviate the symptoms of UC by reversing the disorder of PC metabolism induced by DSS modeling. SSE was proved for the first time to be a promising and effective candidate for UC treatment.

Effect of Four Extraction Processes with Acetone-Ethanol Protocols on the Properties of Egg Yolk Phosphatidylcholine and the Structure of Residual Protein.

In this study, four acetone-ethanol protocols were employed to investigate the effect of extraction processes on the yield and purity of phosphatidylcholine (PC) from dried egg yolk powder and fresh liquid egg yolk, as well as the cholesterol distribution between the oil and PC fraction. Furthermore, the physicochemical (thermo-stability, fatty acid composition, and molecular structure) and emulsifying (zeta potential, particle size, EAI, ESI, and creaming index) properties of the final PC product were also examined. In addition, the structural characteristics of the egg yolk residual protein were highlighted to promote its application in food industries. The results showed that de-oiling with acetone prior to ethanol extraction can achieve high yield (19.92%) and purity (68.62%) of the PC product with low cholesterol content (< 0.12%). The extraction processes exhibited a significant impact on the emulsifying properties of the PC product. The creaming index of PC emulsions was higher than that of egg yolk powder emulsions with high protein concentration, suggesting that PC plays a critical role in the emulsifying stability of egg yolk protein dispersion. The structural characteristics of residual protein, including free sulfhydryl groups and primary, secondary, and ternary structures, showed considerable differentiation related to extraction processes. These findings provide a powerful tool for the dietary utilization of egg yolk PC and protein in future.

Binding of Nanoparticles Harboring Recombinant Large Surface Protein of Hepatitis B Virus to Scavenger Receptor Class B Type 1.

(1) Background: As nanoparticles containing the hepatitis B virus (HBV) large (L) surface protein produced in yeast are expected to be useful as a carrier for targeting hepatocytes, they are also referred to as bio-nanocapsules (BNCs). However, a definitive cell membrane receptor for BNC binding has not yet been identified. (2) Methods: By utilizing fluorescence-labeled BNCs, we examined BNC binding to the scavenger receptor class B type 1 (SR-B1) expressed in HEK293T cells. (3) Results: Analyses employing SR-B1 siRNA and expression of SR-B1 fused with a green fluorescent protein (SR-B1-GFP) indicated that BNCs bind to SR-B1. As mutagenesis induced in the SR-B1 extracellular domain abrogates or attenuates BNC binding and endocytosis via SR-B1 in HEK293T cells, it was suggested that the ligand-binding site of SR-B1 is similar or close among high-density lipoprotein (HDL), silica, liposomes, and BNCs. On the other hand, L protein was suggested to attenuate an interaction between phospholipids and SR-B1. (4) Conclusions: SR-B1 can function as a receptor for binding and endocytosis of BNCs in HEK293T cells. Being expressed various types of cells, it is suggested that functions as a receptor for BNCs not only in HEK293T cells but also in other types of cells.

The neglected biliary mucus and its phosphatidylcholine content: a putative player in pathogenesis of primary cholangitis-a narrative review article.

Primary sclerosing cholangitis (PSC) is a rare progressive cholangitis resulting in cirrhosis and cholangiocellular carcinoma. The pathogenesis is unclear and an effective medical therapy is not available. It is highly associated to ulcerative colitis for which recently a disturbance of the tight junction (TJ) barrier has been claimed as etiologic feature. Genetic mouse models with intestinal TJ disruption showed a defective transport of phosphatidylcholine (PC) to intestinal mucus. Consequently, an ulcerative colitis phenotype developed. In the present study we evaluate whether there is also a paracellular transport of PC through TJ to the apical side of cholangiocytes. As in ulcerative colitis, a TJ defect could lead to deficient PC in biliary mucus. It would impair the protective barrier against aggressive bile acids in bile. Indeed with polarized biliary tumor cells a vectorial transport of PC from basal to luminal side was demonstrated using a transwell culture system. PC was not taken up by the cells but moved paracellularly via TJ to the apical side driven by luminal HCO3- generated by the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) and the anion exchange protein 2 (AE2). If such a TJ-mediated PC translocation to the apical surface of cholangiocytes could be disrupted in a genetic mouse model, a PSC phenotype would be expected. With such an experimental model functional operative therapies can be evaluated. We propose that disruption of TJ mediated paracellular transport of PC to the apical side of cholangiocytes could lead to biliary mucus PC depletion. This may be a pathogenetic factor for development of PSC.

In vitro evaluation of bone cements impregnated with selenium nanoparticles stabilized by phosphatidylcholine (PC) for application in bone.

One of the most common prophylactic techniques to solve prosthetic joint infection (PJI) is incorporation of antibiotics into acrylic bone cement to prevent bacterial colonization and proliferation by providing local antibiotic delivery directly at the implant site. Further, there has been a significant concern over the efficacy of commonly used antibiotics within bone cement due to the rise in multi-drug resistant (MDR) microorganisms. Selenium is an essential trace element that has multiple beneficial effects for human health and its chemotherapeutic action is well known. It was reported that nanostructured selenium enhanced bone cell adhesion and has an increased osteoblast function. In this context, we used the selenium nanoparticles (SeNPs) to improve antibacterial and antioxidant properties of poly (methyl methacrylate) (PMMA) and tri calcium phosphate (TCP)-based bone cements, and to reduce of the infection risk caused by orthopedic implants. As another novelty of this study, we proposed phosphatidylcholine (PC) as a unique and natural stabilizer in the synthesis of selenium nanoparticles. After the structural analysis of the prepared bone cements was performed, in vitro osteointegration and antibacterial efficiency were tested using MC3T-E1 (mouse osteoblastic cell line) and SaOS-2 (human primary osteogenic sarcoma) cell lines, and S. aureus (Gram positive) and E.coli (Gram negative) strains, respectively. More importantly, PC-SeNPs-reinforced bone cements exhibited significant effect against E. coli, compared to S. aureus and a dose-dependent antibacterial activity against both bacterial strains tested. Meanwhile, these bone cements induced the apoptosis of SaOS-2 through increased reactive oxygen species without negatively influencing the viability of the healthy cell line. Furthermore, the obtained confocal images revealed that PC-SeNPs (103.7 ± 0.56 nm) altered the cytoskeletal structure of SaOS-2 owing to SeNPs-induced apoptosis, when MC3T3-E1 cells showed a typical spindle-shaped morphology. Taken together, these results highlighted the potential of PC-SeNPs-doped bone cements as an effective graft material in bone applications.

Exogenous Liposomal Ceramide-C6 Ameliorates Lipidomic Profile, Energy Homeostasis, and Anti-Oxidant Systems in NASH.

In non-alcoholic steatohepatitis (NASH), many lines of investigation have reported a dysregulation in lipid homeostasis, leading to intrahepatic lipid accumulation. Recently, the role of dysfunctional sphingolipid metabolism has also been proposed. Human and animal models of NASH have been associated with elevated levels of long chain ceramides and pro-apoptotic sphingolipid metabolites, implicated in regulating fatty acid oxidation and inflammation. Importantly, inhibition of de novo ceramide biosynthesis or knock-down of ceramide synthases reverse some of the pathology of NASH. In contrast, cell permeable, short chain ceramides have shown anti-inflammatory actions in multiple models of inflammatory disease. Here, we investigated non-apoptotic doses of a liposome containing short chain C6-Ceramide (Lip-C6) administered to human hepatic stellate cells (hHSC), a key effector of hepatic fibrogenesis, and an animal model characterized by inflammation and elevated liver fat content. On the basis of the results from unbiased liver transcriptomic studies from non-alcoholic fatty liver disease patients, we chose to focus on adenosine monophosphate activated kinase (AMPK) and nuclear factor-erythroid 2-related factor (Nrf2) signaling pathways, which showed an abnormal profile. Lip-C6 administration inhibited hHSC proliferation while improving anti-oxidant protection and energy homeostasis, as indicated by upregulation of Nrf2, activation of AMPK and an increase in ATP. To confirm these in vitro data, we investigated the effect of a single tail-vein injection of Lip-C6 in the methionine-choline deficient (MCD) diet mouse model. Lip-C6, but not control liposomes, upregulated phospho-AMPK, without inducing liver toxicity, apoptosis, or exacerbating inflammatory signaling pathways. Alluding to mechanism, mass spectrometry lipidomics showed that Lip-C6-treatment reversed the imbalance in hepatic phosphatidylcholines and diacylglycerides species induced by the MCD-fed diet. These results reveal that short-term Lip-C6 administration reverses energy/metabolic depletion and increases protective anti-oxidant signaling pathways, possibly by restoring homeostatic lipid function in a model of liver inflammation with fat accumulation.

Plasma Lipidomics of Coronary Heart Disease Patient with Syndrome of Intermingling of Phlegm and Static Blood Based on UPLC-Q/TOF-MS / 中国实验方剂学杂志

<b>Objective::To study on the plasma lipidomics characteristics of coronary heart disease (CHD) patients with syndrome of of intermingling of phlegm and static blood, and to find differential lipid metabolites between them and healthy volunteers. <b>Method::The plasma samples from CHD patients with syndrome of intermingling of phlegm and static blood and healthy volunteers of the same age were collected. The plasma lipidomics was carried out by UPLC-Q/TOF-MS. The plasma samples were detected under positive and negative ion modes, and the primary and secondary mass spectrometry datas were collected simultaneously, and the <italic>m</italic>/<italic>z</italic> ranges were 100-2 000 and 50-2 000, respectively. The lipidomics model was established by orthogonal partial least squares discriminant analysis (OPLS-DA). Differential lipid metabolites were identified based on multivariate statistics. <b>Result::OPLS-DA model could obviously distinguish CHD patients with syndrome of intermingling of phlegm and static blood and healthy volunteers. A total of 15 plasma differential lipid metabolites were identified, such as C16 sphinganine, phytosphingosine, <italic>N</italic>, <italic>N</italic>-dimethyl-safingol, 2-hydroxyphytanic acid, orotinichalcone, PC[18∶2(2<italic>E</italic>, 4<italic>E</italic>)/0∶0], PC(0∶0/16∶0), epitestosterone sulfate, etiocholanolone sulfate, PS[22∶1(11<italic>Z</italic>)/0∶0], PC[16∶0/20∶4(5<italic>E</italic>, 8<italic>E</italic>, 11<italic>E</italic>, 14<italic>E</italic>)], PC[19∶1(9<italic>Z</italic>)/17∶2(9<italic>Z</italic>, 12<italic>Z</italic>)], PC(16∶0/0∶0), PC(18∶0/0∶0), PS[15∶1(9<italic>Z</italic>)/22∶1(11<italic>Z</italic>)]. <b>Conclusion::There are significant differences in plasma lipid characteristics between CHD patients with syndrome of intermingling of phlegm and static blood and healthy volunteers. The plasma differential lipid metabolites are helpful for the accurate differentiation of CHD patients with syndrome of intermingling of phlegm and static blood.

Polymer-lipid hybrid nanoparticles as enhanced indomethacin delivery systems.

Non-steroidal anti-inflammatory drugs (NSAIDs), i.e. indomethacin used for rheumatoid arthritis and non-rheumatoid inflammatory diseases, are known for their injurious actions on the gastrointestinal (GI) tract. Mucosal damage can be avoided by using nanoscale systems composed by a combination of liposomes and biodegradable natural polymer, i.e. chitosan, for enhancing drug activity. Aim of this study was to prepare chitosan-lipid hybrid delivery systems for indomethacin dosage through a novel continuous method based on microfluidic principles. The drop-wise conventional method was also applied in order to investigate the effect of the two polymeric coverage processes on the nanostructures features and their interactions with indomethacin. Thermal-physical properties, mucoadhesiveness, drug entrapment efficiency, in vitro release behavior in simulated GI fluids and stability in stocking conditions were assayed and compared, respectively, for the uncoated and chitosan-coated nanoliposomes prepared by the two introduced methods. The prepared chitosan-lipid hybrid structures, with nanometric size, have shown high indomethacin loading (about 10%) and drug encapsulation efficiency up to 99%. TEM investigation has highlighted that the developed novel simil-microfluidic method is able to put a polymeric layer, surrounding indomethacin loaded nanoliposomes, thicker and smoother than that achievable by the drop-wise method, improving their storage stability. Finally, double pH tests have confirmed that the chitosan-lipid hybrid nanostructures have a gastro retentive behavior in simulated gastric and intestinal fluids thus can be used as delivery systems for the oral-controlled release of indomethacin. Based on the present results, the simil-microfluidic method, working with large volumes, in a rapid manner, without the use of drastic conditions and with a precise control over the covering process, seems to be the most promising method for the production of suitable indomethacin delivery system, with a great potential in industrial manufacturing.

Controlling insulin release from reverse hexagonal (HII) liquid crystalline mesophase by enzymatic lipolysis.

In the present study we aimed to control insulin release from the reverse hexagonal (HII) mesophase using Thermomyces lanuginosa lipase (TLL) in the environment (outer TLL) or within the HII cylinders (inner TLL). Two insulin-loaded systems differing by the presence (or absence) of phosphatidylcholine (PC) were examined. In general, incorporation of PC into the HII interface (without TLL) increased insulin release, as a more cooperative system was formed. Addition of TLL to the systems' environments resulted in lipolysis of the HII structure. In the absence of PC, the lipolysis was more dominant and led to a significant increase in insulin release (50% after 8h). However, the presence of PC stabilized the interface, hindering the lipolysis, and therefore no impact on the release profile was detected during the first 8h. Entrapment of TLL within the HII cylinders (with and without PC) drastically increased insulin release in both systems up to 100%. In the presence of PC insulin released faster and the structure was more stable. Consequently, the presence of lipases (inner or outer) both enhanced the destruction of the carrier, and provided sustained release of the entrapped insulin.

Protective effects of phosphatidylcholine on oxaliplatin-induced neuropathy in rats.

AIMS: The present study was designed to investigate the therapeutic potential of phosphatidylcholine (PC) on oxaliplatin-induced peripheral neuropathy. MAIN METHODS: Male Sprague-Dawley rats were randomly divided into three groups: the control group, the oxaliplatin group (4mg/kg, twice per week for 4weeks) and the oxaliplatin+PC (300mg/kg) group. To evaluate the effect of PC, we examined the thermal nociceptive threshold changes in oxaliplatin-induced peripheral neuropathy by conducting paw pressure, hot-plate and tail-flick tests. Additional experiments on the degree of oxidative stress in the sciatic nerves were performed by measuring the level of MDA, total glutathione (GSH), glutathione peroxidase (GPx) activity and superoxide dismutase (SOD) activity. We also used histopathological and immunohistochemical methods to observe neuronal damage and glial activation. KEY FINDINGS: PC attenuated oxidative stress by increasing antioxidant levels. In histopathological evaluation, the PC administrated group maintained normal morphologic appearance of sciatic nerves, similar to the control group. In spinal cords, however, no significant difference between the oxaliplatin-alone group and the oxaliplatin+PC group was observed. In the immunohistochemical evaluation, PC administration ameliorated oxaliplatin-induced microglial activation. SIGNIFICANCE: It is suggested that PC has a therapeutic potential against oxaliplatin-induced peripheral neuropathy due to its antioxidant property and modulation of microglial activities.

Phosphatidylcholine is transferred from chemically-defined liposomes to chloroplasts through proteins of the chloroplast outer envelope membrane.

Chloroplasts maintain their lipid balance through a tight interplay with the endoplasmic reticulum (ER). The outer envelope membrane of chloroplasts contains a large proportion of the phospholipid phosphatidylcholine (PC), which is synthesized in the ER and also a possible precursor for thylakoid galactolipids. The mechanism for PC transport from the ER to chloroplasts is not known. Using isolated chloroplasts and liposomes containing radiolabeled PC we investigated non-vesicular transport of PC in vitro. PC uptake in chloroplasts was time and temperature dependent, but nucleotide independent. Increased radius of liposomes stimulated PC uptake, and protease treatment of the chloroplasts impaired PC uptake. This implies that the chloroplast outer envelopes contains an exposed proteinaceous machinery for the uptake of PC from closely apposed membranes.