• Journal of the Society of Cosmetic Scientists of Korea
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• v.47 no.1
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• pp.65-73
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• 2021

It is very important to control the inflammation of the skin because it can develop into diseases such as atopy as well as scarring and aging. In this work, we recently identified the in vitro synthesis of specialized pro-resolving mediators (SPMs) known to control inflammation in the human body and the applicability of cosmetics. Using recombinant protein of lipoxygenase from Glycine max, we succeeded to prepare mixtures of mono- or di-hydroxy DHA named as S-SPMs and used them for in vitro efficacy test. To investigate anti-inflammatory effect of S-SPMs, mRNA level of TNF-α and IL-6 were analyzed. Under UVB exposed condition, expression of both were decreased by S-SPMs treatment. And we observed reduced production of nitric oxide (NO) by S-SPMs application under the condition with diesel particulate matter (DPM). At the same experimental condition, malondialdehyde (MDA) production was decreased by S-SPMs, indicating the inhibitory effect of S-SPMs in lipid peroxidation. In addition, S-SPMs treatment resulted in reduction of matrix metalloproteinases-1 (MMP-1) expression and elevation of procollagen type I synthesis. Together with this, mRNA level of filaggrin and loricrin were increased by S-SPMs, indicating enhancement of skin barrier function. These results demonstrate that S-SPMs is a good candidate to develop as a cosmetic ingredient for anti-inflammation, anti-wrinkle, and improvement of skin barrier function.

• Biomolecules & Therapeutics
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• v.29 no.5
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• pp.455-464
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• 2021

Uncontrolled inflammation is considered the pathophysiological basis of many prevalent metabolic disorders, such as nonalcoholic fatty liver disease, diabetes, obesity, and neurodegenerative diseases. The inflammatory response is a self-limiting process that produces a superfamily of chemical mediators, called specialized proresolving mediators (SPMs). SPMs include the ω-3-derived family of molecules, such as resolvins, protectins, and maresins, as well as arachidonic acid-derived (ω-6) lipoxins that stimulate and promote resolution of inflammation, clearance of microbes, and alleviation of pain and promote tissue regeneration via novel mechanisms. SPMs function by binding and activating G protein-coupled receptors, such as FPR2/ALX, GPR32, and ERV1, and nuclear orphan receptors, such as RORα. Recently, several studies reported that SPMs have the potential to attenuate lipid metabolism disorders. However, the understanding of pharmacological aspects of SPMs, including tissue-specific biosynthesis, and specific SPM receptors and signaling pathways, is currently limited. Here, we summarize recent advances in the role of SPMs in resolution of inflammatory diseases with metabolic disorders, such as nonalcoholic fatty liver disease and obesity, obtained from preclinical animal studies. In addition, the known SPM receptors and their intracellular signaling are reviewed as targets of resolution of inflammation, and the currently available information on the therapeutic effects of major SPMs for metabolic disorders is summarized.

• The Korean Journal of Physiology and Pharmacology
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• v.24 no.2
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• pp.165-171
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• 2020

Ischemic and traumatic brain injuries are the major acute central nervous system disorders that need to be adequately diagnosed and treated. To find biomarkers for these acute brain injuries, plasma levels of some specialized pro-resolving mediators (SPMs, i.e., lipoxin A4 [LXA4], resolvin [Rv] E1, RvE2, RvD1 and RvD2), CD59 and interleukin (IL)-6 were measured at 0, 6, 24, 72, and 168 h after global cerebral ischemic (GCI) and traumatic brain injuries (TBI) in rats. Plasma LXA4 levels tended to increase at 24 and 72 h after GCI. Plasma RvE1, RvE2, RvD1, and RvD2 levels showed a biphasic response to GCI; a significant decrease at 6 h with a return to the levels of the sham group at 24 h, and again a decrease at 72 h. Plasma CD59 levels increased at 6 and 24 h post-GCI, and returned to basal levels at 72 h post-GCI. For TBI, plasma LXA4 levels tended to decrease, while RvE1, RvE2, RvD1, and RvD2 showed barely significant changes. Plasma IL-6 levels were significantly increased after GCI and TBI, but with different time courses. These results show that plasma LXA4, RvE1, RvE2, RvD1, RvD2, and CD59 levels display differential responses to GCI and TBI, and need to be evaluated for their usefulness as biomarkers.