Different in Vitro Wound Models for Studying Cell Salvage Effects of Concentrated Surfactant Gels
Background: Cell membrane damage is common in skin injury. Cell survival depends on the initiation of a rapid resealing to resume the structural integrity of the cell membrane to maintain homeostasis and protect intracellular organelles. In vitro and clinic studies have shown the effectiveness of using surfactant based wound dressing with or without antimicrobial agents in wound healing and pain reduction. However, fewer studies have discussed the mechanism of the interaction between concentrated surfactant gels and tissue/cells.
Purpose: We hypothesis that a concentrated surfactant-based gel (CSG) has the ability to reseal cell membranes to avoid further accumulation of cellular damage due to loss of lipid bilayer integrity to speed up wound healing.
Methods: In this study, plasma membrane disruption models by needle-scratch/ultrasonic/microwave were set up to study whether CSG has the ability to improve HaCaT cells, a spontaneously immortalized human keratinocyte line, and primary adult human dermal fibroblasts (HDFa) survival by resuming the structural integrity of cell plasma membranes to maintain homeostasis and protect intracellular organelles. Images of live/dead staining showed that dead cells decreased distinctly by CSG treatment for both HaCaT and HDFa compared to the DMEM control.
Results: The percentages of LDH in the supernatant of the CSG treatment were lower than the control group, which implied CSG treatment may have the ability to stabilize the membrane by resealing it. Compared to the no disruption control, HaCaT and HDFa in the control (DMEM medium) were elongated and showed actin rearrangement after the needle scratch; HaCaT and HDFa in the CSG treatment showed less morphological changes after the needle scratch.
Conclusion: All the results implied that non-ionic CSG increased HaCaT and HDFa viability by conferring significant protection to plasma membrane integrity which may be provided by non-ionic surfactant molecules inserting themselves into damaged membranes.