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These results suggest that SSM plays a protective role during the development of AP and pancreatitis associated lung injury via deactivating c-Jun NH2-terminal kinase, p38 and NF-κB.

Kyungohkgo (KOG) is an oriental herbal medicine that has been used for its various pharmacological effects, which include anti-oxidant, anti-inflammatory and immuno-regulation activities. But its effects and mechanisms of anti-atopic dermatitis (AD) have not been elucidated. HaCaT cells were pre-treated with KOG for 1 h and stimulated with tumor necrosis factor (TNF)-α and interferon (IFN)-γ (10 ng/ml each). After 24 h, cells were harvested to measure the production of reactive oxygen species (ROS) and chemokines such as regulated upon activation, normal T cell expressed and secreted (RANTES/CCL5), Thymus and activation-regulated chemokine (TARC/CCL17) and macrophage-deraived chemokine (MDC/CCL22). To investigate the regulatory mechanisms of KOG, we also assessed the phosphorylation of signal transducer and activator of transcription (STAT1) signaling pathways in HaCaT cells. Treatment of KOG decreased the ROS production and mRNA levels of RANTES, TARC, MDC with a concentration dependent manner. In addition, KOG significantly inhibited TNF-α and IFN-γ induced phosphorylation of STAT1. This could indicate that the KOG shows anti-AD activity mainly through STAT1. Thus, we propose that KOG may be a promising anti-AD skin protector, which could suggest the clinical basis for cosmetics development.

Objectives : Lonicerae Japonicae Flos (LJF) has been shown anti-oxidant, anti-inflammatory, anti-viral, anti-rheumatoid properties. However, it is still largely unknown whether LJF inhibits skin injury against oxidative stress in human keratinocyte, HaCaT cells. The purpose of this study was to evaluate the protective effects of LJF against hydrogen peroxide(H2O2)-induced oxidative stress in human keratinocytes, HaCaT cells. Methods : To evaluate out the protective effects of LJF on oxidative injury in HaCaT cells, an oxidative stress model of HaCaT cells was established under a suitable concentration (500 µM) hydrogen peroxide. HaCaT keratinocyte cells were pre-treated with LJF (0.1, 0.25 or 0.5 mg/ml), and then stimulated with H2O2. Then, the cells were harvested to measure the cell viability, DNA damage, and release of reactive oxygen species (ROS). Results : LJF (0.1, 0.25 or 0.5 mg/ml) itself did not show any significant toxicity in HaCaT cells. The treatment of H2O2 caused the oxidative stress, leading to the cell death, and DNA injury. However, pretreatment with LJF reduced cell death, and DNA injury. The stimulation of H2O2 on HaCaT cells resulted in excessive release of ROS, which is the main factor of oxidative stress. The excessive release of ROS was inhibited by LJF treatment significantly. Conclusions : These results could suggest that LJF exhibited the protective effects of HaCaT cells against H2O2-induced oxidative stress by inhibiting ROS release. It could be explained that LJF inhibit skin damages against oxidative stress. Thus, LJF would be useful for the development of drug or cosmetics treating skin troubles.