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In this study, a novel method utilizing enzyme and involving simple solvent extraction steps, is developed to yield an extract with high content of steryl glucosides (SG) and acyl steryl glucosides (ASG) from soy lecithin – the by‐product of vegetable oil refining. Phospholipase A1 is used to convert phospholipids in soy lecithin into more hydrophilic hydrolysates, from which SG and ASG are separated by solvent extractions. A 3 × 3 full factorial design is employed to investigate the effects of two parameters (enzyme dose and reaction time) on three responses (yield of extract, SG/ASG content of extract, and recovery of SG/ASG). There are significant enzyme dose – reaction time interaction effects on all the responses, except for yield of extract. The highest SG (including ASG) content of more than 90% in the extract is achieved at enzyme dose of 0.03 g and reaction time of 16 h, where the yield of extract obtained is 1.43%. Practical Applications: Conventionally, steryl glucosides and acyl steryl glucosides are isolated from lipid extract and purified by chromatographic methods, which result in a small amount of high purity steryl glucosides and acyl steryl glucosides, and thus is not economic to scale up. The method revealed in this study employed an enzymatic reaction followed by simple solvent extractions, and can be easily scaled up to produce high purity steryl glucosides and acyl steryl glucosides, making them more affordable for researchers. In addition, the method also presents a new application for soy lecithin or lecithin of other plant origins, whose current applications are mostly related to the main component‐phospholipids. In this study, a novel method utilizing enzyme and involving simple solvent extraction steps is developed to yield an extract with high content of steryl glucosides (SG) and acyl steryl glucosides (ASG) from soy lecithin – the by‐product of vegetable oil refining. [ABSTRACT FROM AUTHOR]

As the first peripheral immune cells to enter the brain after ischemic stroke, neutrophils are important participants in stroke-related neuroinflammation. Neutrophils are quickly mobilized from the periphery in response to a stroke episode and cross the blood-brain barrier to reach the ischemic brain parenchyma. This process involves the mobilization and activation of neutrophils from peripheral immune organs (including the bone marrow and spleen), their chemotaxis in the peripheral blood, and their infiltration into the brain parenchyma (including disruption of the blood-brain barrier, inflammatory effects on brain tissue, and interactions with other immune cell types). In the past, it was believed that neutrophils aggravated brain injuries through the massive release of proteases, reactive oxygen species, pro-inflammatory factors, and extracellular structures known as neutrophil extracellular traps (NETs). With the failure of early clinical trials targeting neutrophils and uncovering their underlying heterogeneity, our view of their role in ischemic stroke has become more complex and multifaceted. As neutrophils can be divided into N1 and N2 phenotypes in tumors, neutrophils have also been found to have similar phenotypes after ischemic stroke, and play different roles in the development and prognosis of ischemic stroke. N1 neutrophils are dominant during the acute phase of stroke (within three days) and are responsible for the damage to neural structures via the aforementioned mechanisms. However, the proportion of N2 neutrophils gradually increases in later phases, and this has a beneficial effect through the release of anti-inflammatory factors and other neuroprotective mediators. Moreover, the N1 and N2 phenotypes are highly plastic and can be transformed into each other under certain conditions. The pronounced differences in their function and their high degree of plasticity make these neutrophil subpopulations promising targets for the treatment of ischemic stroke., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)