Objectives: The existing inflammatory
models are concentrated in relatively complex medical fields, and most of them
use a single type of cell, and the induction conditions are not uniform, so the current LPS-induced inflammation model is less conducive to the study
of skin inflammation. The aim of this research is to enhance the existing
LPS-induced inflammation model and establish a skin inflammation model that is
suitable for the swift screening of anti-inflammatory agents in the cosmetics
industry. Methods: LPS was used to induce
inflammatory responses in KC and THP-1 cells. Enzyme-linked immunosorbent assay
(ELISA) was employed to assess the levels of IL-1α, IL-8, and TNF-α in the two cell types, while the DCFH-DA probe was utilized to label the
levels of reactive oxygen species (ROS) in both cell types. Results:In KC cells, 10 μg/mL of LPS induced a significant upregulation of IL-8
but did not result in elevated expression of IL-1α. However, at 100 μg/mL of LPS, both IL-8 and IL-1αwere highly expressed in KC cells. LPS concentrations ranging from 0.01
to 100 μg/mL failed to stimulate TNF-α production in KC cells but induced a gradient
increase in ROS levels. In THP-1 cells, LPS concentrations from 0.01 to 100
μg/mL did not induce IL-1αproduction but significantly elevated IL-8 and led to a gradient increase
in TNF-α and ROS. After treatment with 100 μg/mL of LPS, the cosmetic ingredient
Rucika KGM mitigated the elevated levels of IL-1α, IL-8, and ROS in LPS-induced KC cells and IL-8 and ROS in THP-1
cells. Conclusion:This study has successfully developed an
application-oriented
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