Ernst-Moritz-Arndt University, Institute of Pharmacy, Department of Pharmaceutical Biology, Friedrich-Ludwig-Jahn Strasse 15a, Greifswald, Germany.
J Dermatol Sci. 2013 Jun;70(3):173-81. doi: 10.1016/j.jdermsci.2013.01.012. Epub 2013 Feb 16.
The use of non-thermal atmospheric pressure plasma in dermatology to improve the healing of chronic wounds is a promising application. The antimicrobial properties of physical plasma offer on the one hand the killing of bacteria, which are often a problem in chronic wounds. On the other hand, plasma can activate cells which are involved in the wound closure.
To guarantee a safe application it is essential to understand basic interactions between physical plasma and human skin cells.
In our study, human keratinocytes (HaCaT cells) were directly plasma treated with a dielectric barrier discharge (DBD) plasma source and effects on viability, DNA, cell cycle, intracellular concentration of reactive oxygen species and induction of apoptosis were observed.
A treatment time-dependent loss of recovered adherent HaCaT cells after 24h and a linear increase of DNA damage were observed, which was no longer evident 24h after plasma stimulation, except for long treatment times. An accumulation of HaCaT cells in G2/M phase and a decrease in the G1 phase was caused by DBD plasma. The increasing formation of intracellular ROS is also attributed to plasma treatment. In contrast to other studies we did not find clear evidences for apoptosis in adherent HaCaT cells. A culture medium exchange subsequently after plasma treatment weakened the observed effects.
DBD plasma treatment resulted in oxidative stress in human keratinocytes which is related to deficient cell performance.
非热常压等离子体在皮肤科中用于改善慢性伤口愈合是一种很有前途的应用。物理等离子体的抗菌特性一方面提供了杀死细菌的能力，而细菌通常是慢性伤口的一个问题。另一方面，等离子体可以激活参与伤口闭合的细胞。
为了保证安全应用，了解物理等离子体与人体皮肤细胞之间的基本相互作用至关重要。
在我们的研究中，人角质形成细胞（HaCaT 细胞）直接用介质阻挡放电（DBD）等离子体源进行等离子体处理，观察对细胞活力、DNA、细胞周期、细胞内活性氧浓度和细胞凋亡诱导的影响。
在 24 小时后观察到经处理的贴壁 HaCaT 细胞的恢复性损失和随处理时间呈线性增加的 DNA 损伤，24 小时后除了长时间处理外，这些损伤不再明显。DBD 等离子体导致 HaCaT 细胞在 G2/M 期积累和 G1 期减少。细胞内 ROS 的形成增加也归因于等离子体处理。与其他研究不同，我们没有在贴壁 HaCaT 细胞中发现明显的凋亡证据。随后在等离子体处理后进行培养基交换会削弱观察到的效果。
DBD 等离子体处理导致人角质形成细胞氧化应激，这与细胞功能缺陷有关。
