Hydrogenated soya phosphatidylcholines [97281-48-6]

Hydrogenated soya phosphatidylcholines are a type of phosphatidylcholine used to enhance the efficacy of oral administration of water-soluble drugs; they are extracted from natural soya lecithin and undergo a hydrogenation process. Hydrogenated soya phosphatidylcholines can increase drug loading and solubility, thereby prolonging the drug release time.

Method： Hydrogenated soya phosphatidylcholines (a hydrogenated soybean phospholipid mixture) was used to prepare cholesterol–phospholipid liposomal vesicles encapsulating natamycin by two techniques. For the proliposome method, 0.9 g Hydrogenated soya phosphatidylcholines, cholesterol (0.125 g), and natamycin (30 mg) were mixed with 1.5 mL ethanol, stirred at 45 °C, 400 rpm for ~30 min to evaporate solvent, then hydrated with 30 mL PBS (pH ~5.5) in portions and stirred 1 h at 800 rpm at room temperature. For the thin film method, 1 g Hydrogenated soya phosphatidylcholines, natamycin (30 mg), and cholesterol (0.150 mg) were dissolved in 5 mL chloroform:methanol (2:1), solvents evaporated under 100 mm Hg at 60 °C, 600 rpm for ~1 h to form a film, then hydrated with 30 mL PBS (pH ~5.5) for 1 h at 60 °C. Plain (drug-free) liposomes were prepared as controls. HaCaT human keratinocytes were exposed to these formulations, including free natamycin, and viability was quantified by MTT assay; the highest tested concentration corresponded to 10% liposomal sample, i.e., 100 µg/mL natamycin in loaded vesicles or solution. A non-treated negative control (100 ± 7.68% viability) was included. Statistical significance at 10% was assessed (**** p<0.0001).
Result： At 10% formulation (100 µg/mL natamycin), all liposomal formulations prepared with Hydrogenated soya phosphatidylcholines or Lipoid S100, with or without natamycin, and free natamycin reduced HaCaT viability, indicating a concentration-dependent inhibitory effect; all values remained above 80% viability. Free natamycin showed slightly higher cell viability than encapsulated forms at 100 µg/mL. Differences across formulations were significant at the 10% level (**** p<0.0001). ^[2]
Method： MCF-7 breast adenocarcinoma cells were treated with paclitaxel-loaded liposomes formulated from Hydrogenated soya phosphatidylcholines and cholesterol (HSPC:cholesterol:PCL = 7:2:0.1) prepared by thin-film hydration; cytotoxicity was assessed over 24 h and 48 h, and compared with free paclitaxel.
Result： Liposomal paclitaxel showed time-dependent cytotoxicity with IC₅₀ decreasing from 0.525 µg/mL at 24 h to 0.09 µg/mL at 48 h, which was 54% superior to free paclitaxel (IC₅₀ = 0.139 µg/mL). ^[4]
Method： Mechanistic assays in MCF-7 cells treated with paclitaxel-loaded Hydrogenated soya phosphatidylcholines liposomes evaluated cell-cycle distribution, caspase activation, cellular uptake, and anti-metastatic effects (migration and invasion).
Result： Compared with control, treatment induced 2.96-fold G2/M accumulation (63.23% vs. 21.38%, p<0.001), mitochondrial apoptosis with 2.8-fold caspase-3 and 3.1-fold caspase-9 activation, 4.2-fold enhanced cellular uptake, and anti-metastatic activity with 62% migration and 68% invasion inhibition. ^[4]
Method： High-molecular-weight hyaluronic acid was mixed with gel-phase hydrogenated soy PC (HSPC) to form HA-HSPC complexes, and surface force balance measurements were performed to quantify boundary lubrication friction under high pressure; additional assays assessed lipid assembly, phase transition temperature, and bilayer spreading upon interfacial contact, and examined disruption of the HA network and shear-thinning properties.
Result： HA binding to HSPC altered lipid assembly, increased phase transition temperatures, and promoted bilayer spreading upon interfacial contact; lipids disrupted the HA network and enhanced shear-thinning; surface force balance measurements showed ultralow friction μ ≈ 10^-5–10^-3 that remained robust under high pressure for the HA-HSPC complex. ^[5]

Method： Mice were intravenously injected with oxymatrine HSPC liposomes (50 mg/kg). Plasma samples were collected at various time points post-administration, extracted by solid-phase extraction, and analyzed by high-performance liquid chromatography for concentrations of oxymatrine and its metabolite matrine. Pharmacokinetic parameters were calculated using a non-compartmental model.
Result： The half-life of oxymatrine in the HSPC liposome group was 17.10 h, which was 6.6 times longer than that of the oxymatrine solution group (2.58 h). The AUC(0-∞) was 724.41 mg·h/mL, 11.5 times higher than the solution group (63.11 mg·h/mL). The MRT(0-8) of matrine reached 67.50 h, 14.3 times higher than the solution group (4.71 h) ^[6].
Method： Mice were intravenously injected with oxymatrine HSPC liposomes (50 mg/kg) and sacrificed at 0.083, 1.0, and 8.0 h post-administration. Liver, spleen, heart, and kidney tissues were collected, homogenized, extracted by solid-phase extraction, and analyzed by high-performance liquid chromatography for oxymatrine and matrine distribution. The AUC(0-8) of total alkaloids in the liver was calculated.
Result： The AUC(0-8) of total alkaloids in the liver for the HSPC liposome group was 553.55 mg·h/mL, which was 2.37 times that of the oxymatrine solution group (234.03 mg·h/mL) and 4.18 times that of the SPC liposome group (132.46 mg·h/mL), indicating that HSPC liposomes significantly enhanced hepatic targeting distribution and accumulation of the drug ^[6].
Method： CCl₄-induced acute liver injury mice were treated with oxymatrine HSPC liposomes by either oral gavage or tail vein injection (50 mg/kg). Liver tissues were collected at various time points for H&E staining histopathological examination, and serum ALT and AST activities were measured to evaluate the therapeutic effect of HSPC liposomes on liver injury.
Result： The HSPC liposome treatment group showed significantly improved focal necrosis and ballooning degeneration in the liver, with gradual restoration of damaged liver tissue. Serum ALT and AST levels at 36 h (the most severe phase of liver injury) were significantly lower than those in the oxymatrine solution group (P<0.01) ^[6].

Ethanol: 80 mg/mL

Chloroform: 40 mg/mL