• Natural Product Sciences
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• 제7권4호
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• pp.110-113
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• 2001

The lipid classes constituents; hydrocarbons, wax esters, sterol esters, triacylglycerols, free fatty acids, 1,3-diacylglycerols, 1,2-diacylglycerols, free sterols, 2-monoacylglycerols, 1-monoacylglycerols, phosphatidylethanolamines, phosphatidylcholines, lysophosphatidylethanolamines and phosphatidylinositols of Nicotiana tabacum L. seeds oil were investigated by thin layer and gas chromatography. Palmitic, oleic and linoleic acids were the major components in all lipid classes studied.

• Natural Product Sciences
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• 제9권3호
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• pp.200-203
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• 2003

Total lipids extracted from the powdered seeds of Carum roxburghianum were fractionated into hydrocarbons (0.30%), wax esters (0.30%), sterol esters (1.35%), triacylglycerols (72.41%), free fatty acids (6.06%), 1,3-diacylglycerols (4.60%), 1,2- diacylglycerols (0.64%), glycolipids (5.10%), sterols (1.20%), 2-monoacylgylcerols (3.18%), 1-monoacylglycerols (1.46%), phosphatidylethanolamines (1.08%) phosphatidylcholines (0.40%), lysophosphatidylethanolamines (1.48%) and phosphatidylinositols (0.44%) with the help of TLC. The fatty acid composition of all the lipid fractions was determined after converting them into their methyl esters with $BF_3-methanol$ reagent and then analyzing them by GC. Oleic acid was found as a major component in all the lipid classes, whereas palmitic, linoleic and linolenic acids were present in lesser quantities. Arachidic acid was identified as a minor component in only seven out of twelve lipid classes.

• Bulletin of the Korean Chemical Society
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• 제35권4호
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• pp.1133-1138
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• 2014

Ultrahigh performance liquid chromatography-electrospray ionization-tandem mass spectrometry (UPLC-ESI- MS/MS) provides a high-speed method to screen a large number of samples for small molecules with specific properties. In this study, UPLC-ESI-MS/MS with multiple reaction monitoring (MRM) was employed to screen urinary phospholipid (PL) content for biomarkers of prostate cancer. From lists of urinary PLs structurally identified using nanoflow LC-ESI-MS/MS, 52 PL species were selected for quantitative analysis in urine samples between 22 cancer-free urologic patients as controls and 45 prostate cancer patients. Statistical treatment of data by receiver operating characteristic (ROC) analysis yielded 14 PL species that differed significantly in relative concentrations (area under curve (AUC) > 0.8) between the two groups. Among PLs present at higher levels in prostate cancer urine, phosphatidylcholines (PCs) and phosphatidylinositols (PIs) constituted the major head group PLs (3 PCs and 7 PIs). For technical reasons, PL species of low abundance may be underrepresented in data from UPLC-ESI-MS/MS performed in MRM mode. However, the proposed method enables the rapid screening of large numbers of plasma or urine samples in the search for biomarkers of human disease.

• The Korean Journal of Physiology and Pharmacology
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• 제27권2호
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• pp.187-196
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• 2023

Transient receptor potential canonical (TRPC) channels are non-selective calcium-permeable cation channels. It is suggested that TRPC4β is regulated by phospholipase C (PLC) signaling and is especially maintained by phosphatidylinositol 4,5-bisphosphate (PIP₂). In this study, we present the regulation mechanism of the TRPC4 channel with PIP₂ hydrolysis which is mediated by a channel-bound PLCδ1 but not by the G_qPCR signaling pathway. Our electrophysiological recordings demonstrate that the Ca²⁺ via an open TRPC4 channel activates PLCδ1 in the physiological range, and it causes the decrease of current amplitude. The existence of PLCδ1 accelerated PIP₂ depletion when the channel was activated by an agonist. Interestingly, PLCδ1 mutants which have lost the ability to regulate PIP₂ level failed to reduce the TRPC4 current amplitude. Our results demonstrate that TRPC4 self-regulates its activity by allowing Ca²⁺ ions into the cell and promoting the PIP₂ hydrolyzing activity of PLCδ1.

• Journal of Microbiology and Biotechnology
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• 제26권10호
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• pp.1790-1799
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• 2016

Matrix assisted laser desorption ionization (MALDI)-time of flight/mass spectrometry (TOF/MS) was applied to investigate alterations in phospholipids in mitophagic cancer cells. Several phospholipids, including phosphatidylcholines (PCs), sphingomyelins (SMs), and phosphatidylinositols (PIs), were successfully analyzed in control and mitophagy-induced H460 cells in the positive and negative ion modes. Principal component analysis was applied to differentiate the two groups. The upregulated and downregulated phospholipid species in the mitophagic cells were also represented in a heatmap. In the volcano plot (fold change > 1.3 and p value < 0.01), individual species of seven PCs, two SMs, and three PIs were selected as differentially regulated phospholipids. In particular, almost all the molecular species of PC, SM, and PI were downregulated in the mitophagic cells. Quantification of these lipids indicated that mitophagy induces altered metabolism of phospholipids. Therefore, phospholipid alterations during the mitophagic process of lung cancer cells were well characterized by MALDI-TOF/MS.

• Journal of Gastric Cancer
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• 제21권4호
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• pp.439-456
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• 2021

Purpose: Gastric cancer (GC) has high morbidity and mortality and is a serious threat to public health. The flavonoid compound vitexin is known to exhibit anti-tumor activity. In this study, we explored the therapeutic potential of vitexin in GC and its underlying mechanism. Materials and Methods: The viability, migration, and invasion of GC cells were determined using MTT, scratch wound healing, and transwell assays, respectively. Target molecule expression was determined by western blotting. Tumor growth and liver metastasis were evaluated in vivo using nude mice. Protein expression in the tumor tissues was examined by immunohistochemistry. Results: Vitexin inhibited GC cell viability, migration, invasion, and epithelial-mesenchymal transition (EMT) in a dose-dependent manner. Vitexin treatment led to the inactivation of phosphatidylinositol-3-kinase (PI3K)/AKT/hypoxia-inducible factor-1α (HIF-1α) pathway by repressing HMGB1 expression. Vitexin-mediated inhibition in proliferation, migration, invasion and EMT of GC cells were counteracted by hyper-activation of PI3K/AKT/HIF-1α pathway or HMGB1 overexpression. Finally, vitexin inhibited the xenograft tumor growth and liver metastasis in vivo by suppressing HMGB1 expression. Conclusions: Vitexin inhibited the malignant progression of GC in vitro and in vivo by suppressing HMGB1-mediated activation of PI3K/Akt/HIF-1α signaling pathway. Thus, vitexin may serve as a promising therapeutic agent for the treatment of GC.