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Objective: The aim of this study was to explore the lipidomic profiles of the CAL-27 human tongue cancer cell line and the human oral keratinocyte (HOK) cell line. Methods: The lipidomic differences between the CAL-27 and the HOK cell lines were investigated using non-targeted high-performance liquid chromatography–mass spectrometry lipidomic analysis. The resulting data were then further mined via bioinformatics analysis technology and metabolic pathway analysis was conducted in order to map the most affected metabolites and pathways in the two cell lines. Results: A total of 711 lipids were identified, including 403 glycerophospholipids (GPs), 147 glycerolipids, and 161 sphingolipids. Comparison of the enhanced MS (EMS) spectra of the two cell lines in positive and negative ionization modes showed the lipid compositions of HOK and CAL-27 cells to be similar. The expressions of most GP species in CAL-27 cells showed an increasing trend as compared with HOK, whereas a significant increase in phosphatidylcholine was observed (p < 0.05). Significant differences in the lipid composition between CAL-27 and HOK cells were shown as a heatmap. Through principal component analysis and orthogonal partial least squares discriminant analysis, noticeably clear separation trends and satisfactory clustering trends between groups of HOK and CAL-27 cells were identified. The numbers of specific lipid metabolites that could distinguish CAL-27 from HOK in positive and negative modes were 100 and 248, respectively. GP metabolism was the most significantly altered lipid metabolic pathway, with 4 metabolites differentially expressed in 39 hit products. Conclusion: This study demonstrated the potential of using untargeted mass spectra and bioinformatics analysis to describe the lipid profiles of HOK and CAL-27 cells. [ABSTRACT FROM AUTHOR]

ObjectiveThe aim of this study was to explore the lipidomic profiles of the CAL-27 human tongue cancer cell line and the human oral keratinocyte (HOK) cell line.MethodsThe lipidomic differences between the CAL-27 and the HOK cell lines were investigated using non-targeted high-performance liquid chromatography–mass spectrometry lipidomic analysis. The resulting data were then further mined via bioinformatics analysis technology and metabolic pathway analysis was conducted in order to map the most affected metabolites and pathways in the two cell lines.ResultsA total of 711 lipids were identified, including 403 glycerophospholipids (GPs), 147 glycerolipids, and 161 sphingolipids. Comparison of the enhanced MS (EMS) spectra of the two cell lines in positive and negative ionization modes showed the lipid compositions of HOK and CAL-27 cells to be similar. The expressions of most GP species in CAL-27 cells showed an increasing trend as compared with HOK, whereas a significant increase in phosphatidylcholine was observed (p < 0.05). Significant differences in the lipid composition between CAL-27 and HOK cells were shown as a heatmap. Through principal component analysis and orthogonal partial least squares discriminant analysis, noticeably clear separation trends and satisfactory clustering trends between groups of HOK and CAL-27 cells were identified. The numbers of specific lipid metabolites that could distinguish CAL-27 from HOK in positive and negative modes were 100 and 248, respectively. GP metabolism was the most significantly altered lipid metabolic pathway, with 4 metabolites differentially expressed in 39 hit products.ConclusionThis study demonstrated the potential of using untargeted mass spectra and bioinformatics analysis to describe the lipid profiles of HOK and CAL-27 cells.

Huanglian Jiedu decoction (HLJDD) has been used in the clinical treatment of inflammatory conditions. To clarify the mechanism of its comprehensive anti-inflammatory activities, the correlation between lipid homeostasis and the TLR4/MyD88 signaling pathway in zebrafish was established in the present study. In the lipopolysaccharide (LPS)-induced inflammation in zebrafish model, RT-PCR assays of five inflammatory cytokines and six targeted proteins were measured. Lipidomics analysis was conducted to identify potential lipid markers. HLJDD displayed strong efficacies, with a 61% anti-inflammatory rate at a concentration of 50 μg/mL. The activation of TLR4/MyD88 played an essential role in the inflammatory process. All protein indexes in the HLJDD group exhibited a tendency to reverse back to normal levels. Moreover, 79 potential pathological lipid biomarkers were identified. Compared with the model group, 61 therapeutic lipid biomarkers were detected in HLJDD group. Most perturbations of lipids were ameliorated by HLJDD, mainly through the glycerophospholipid metabolic pathway. In the visual network study, the corresponding lipoproteins such as PLA2, SGMS, and SMDP were observed as important intermediates between lipid homeostasis and the TLR4/MyD88 signaling pathway.

PurposeTo investigate the effects of endurance training on the content of ω-3 polyunsaturated fatty acids (PUFAs) and their distribution among lipid classes in skeletal muscle in middle aged, high-fat diet fed rats.MethodThirty 10-month old male Sprague Dawley (SD) rats were assigned to four groups. Two groups of rats remained sedentary and were fed chow diet (C group), or high-fat diet (H group), respectively. The other two groups of rats were subjected to endurance training while maintaining their chow diet (EC group), or high-fat diet (EH group). After 16 weeks endurance training and/or diet intervention, the content of ω-3 PUFAs and ω-3 PUFA-containing lipids in rat soleus muscle were analyzed by lipidomics.ResultsRats fed a high-fat diet exhibited decreased overall amount of ω-3 PUFAs in soleus muscle, while endurance training preserved the total amount of ω-3 PUFAs. Both the endurance training and high-fat diet alone changed the profiles of ω-3 PUFAs in different lipid classes. Specifically, the amount of triacylglycerol (TG), lysophosphatidylcholine (LPC), phosphatidylcholine (PC), and phosphatidylglycerol (PG) containing ω-3 PUFAs in soleus muscle was increased by endurance training, but the amount of lysophosphatidylenthanol (LPE), lysophosphatidylinositol (LPI), lysophosphatidylserine (LPS), cardiolipin (CL), phosphatidic acid (PA), and phosphatidylinositol (PI) was decreased. The high-fat diet induced a decrease of ω-3 PUFAs in TG, LPE, LPS, CL, platelet activating factor (PAF), PC, phosphatidylethanolamine (PE), and phosphatidylserine (PS), and an increase in LPC, LPI, PA, and PG. In addition, the effects of the endurance training on ω-3 PUFAs in skeletal muscle was also evident in high-fat diets fed rats, which counteracts the profiling changes caused by high-fat diet feeding.ConclusionThe beneficial effects of endurance training on skeletal muscle may be achieved to some extent through recovering the content of ω-3 PUFAs that has been decreased by high-fat diet feeding.

Huanglian Jiedu decoction (HLJDD) has been used in the clinical treatment of inflammatory conditions. To clarify the mechanism of its comprehensive anti-inflammatory activities, the correlation between lipid homeostasis and the TLR4/MyD88 signaling pathway in zebrafish was established in the present study. In the lipopolysaccharide (LPS)-induced inflammation in zebrafish model, RT-PCR assays of five inflammatory cytokines and six targeted proteins were measured. Lipidomics analysis was conducted to identify potential lipid markers. HLJDD displayed strong efficacies, with a 61% anti-inflammatory rate at a concentration of 50 μg/mL. The activation of TLR4/MyD88 played an essential role in the inflammatory process. All protein indexes in the HLJDD group exhibited a tendency to reverse back to normal levels. Moreover, 79 potential pathological lipid biomarkers were identified. Compared with the model group, 61 therapeutic lipid biomarkers were detected in HLJDD group. Most perturbations of lipids were ameliorated by HLJDD, mainly through the glycerophospholipid metabolic pathway. In the visual network study, the corresponding lipoproteins such as PLA2, SGMS, and SMDP were observed as important intermediates between lipid homeostasis and the TLR4/MyD88 signaling pathway. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the effects of endurance training on the content of ω-3 polyunsaturated fatty acids (PUFAs) and their distribution among lipid classes in skeletal muscle in middle aged, high-fat diet fed rats. Method: Thirty 10-month old male Sprague Dawley (SD) rats were assigned to four groups. Two groups of rats remained sedentary and were fed chow diet (C group), or high-fat diet (H group), respectively. The other two groups of rats were subjected to endurance training while maintaining their chow diet (EC group), or high-fat diet (EH group). After 16 weeks endurance training and/or diet intervention, the content of ω-3 PUFAs and ω-3 PUFA-containing lipids in rat soleus muscle were analyzed by lipidomics. Results: Rats fed a high-fat diet exhibited decreased overall amount of ω-3 PUFAs in soleus muscle, while endurance training preserved the total amount of ω-3 PUFAs. Both the endurance training and high-fat diet alone changed the profiles of ω-3 PUFAs in different lipid classes. Specifically, the amount of triacylglycerol (TG), lysophosphatidylcholine (LPC), phosphatidylcholine (PC), and phosphatidylglycerol (PG) containing ω-3 PUFAs in soleus muscle was increased by endurance training, but the amount of lysophosphatidylenthanol (LPE), lysophosphatidylinositol (LPI), lysophosphatidylserine (LPS), cardiolipin (CL), phosphatidic acid (PA), and phosphatidylinositol (PI) was decreased. The high-fat diet induced a decrease of ω-3 PUFAs in TG, LPE, LPS, CL, platelet activating factor (PAF), PC, phosphatidylethanolamine (PE), and phosphatidylserine (PS), and an increase in LPC, LPI, PA, and PG. In addition, the effects of the endurance training on ω-3 PUFAs in skeletal muscle was also evident in high-fat diets fed rats, which counteracts the profiling changes caused by high-fat diet feeding. Conclusion: The beneficial effects of endurance training on skeletal muscle may be achieved to some extent through recovering the content of ω-3 PUFAs that has been decreased by high-fat diet feeding. [ABSTRACT FROM AUTHOR]