자외선은 피부 광노화의 주요 요인이며, 효과적인 자외선 차단제가 피부의 건강과 아름다움을 위해 필요하다. 본 연구는 세포 실험을 통하여 자외선에 의해 유도된 세포 사멸, 산화적 스트레스, matrix metalloproteinase 1 발현에 미치는 죽여추출물의 영향을 알아보고자 수행하였다. HaCaT 인간 각질세포를 여러 농도의 죽여추출물 유무 조건에서 자외선을 조사하고 세포의 생존율과 생화학적 과정들의 변화를 분석하였다. 죽여추출물은 자외선을 조사한 세포의 생존율을 증진시켰고, procaspase 3가 활성화 형태로 절단되고, Bax/Bcl-2 비율이 증가하는 세포 자살 과정을 완화시켰다. 죽여추출물은 자외선에 노출된 세포에서 활성산소의 발생과 지질 과산화도 감소시켰다. 또한 죽여추출물은 자외선에 의해 자극된 matrix metalloproteinase 1의 발현과 c-Jun N-terminal kinase의 인산화를 억제하였다. 본 연구는 죽여추출물이 자외선에 의한 세포 사멸, 산화적 스트레스, 그리고 matrix metalloproteinase 1 발현을 억제함을 보여 주었으며, 이 추출물이 피부 광노화의 일부 현상을 억제하는 화장품 원료로 유용함을 시사하였다.

Ethanol treatment during the brain growth spurt period has been known to induce the death of Purkinje cells. The underlying molecular mechanisms and the role of reactive oxygen species (ROS) in triggering ethanol-induced Purkinje cell death are, however, largely unresolved. We undertook TUNEL staining, western blotting assay and immunohistochemistry for the cleaved forms of caspase-3 and -9, with calbindin D28K double immunostaining to identify apoptotic Purkinje cells. The possibility of ROS-induced Purkinje cell death was immunohistochemically determined by using anti-8-hydroxy-2'deoxyguanosine (8-OHdG), a specific cellular marker for oxidative damage. The results show that Purkinje cell death of PD 5 rat cerebellum following ethanol administration is mediated by the activation of caspase-3 and -9. However, unexpectedly, TUNEL staining did not reveal any positive Purkinje cells while there were some TUNEL-positive cells in the internal and external granular layer. 8-OHdG was detected in the Purkinje cell layers at 8 h, peaked at 12-24 h, but not at 30 h post-ethanol treatment. No 8-0HdG immunoreactive cells were detected in the internal and external granular layer. The lobule specific 8-OHdG staining patterns following ethanol exposure are consistent with that of ethanol-induced Purkinje cell loss. Thus, we suggest that ethanol-induced Purkinje cell death may not occur by the classical apoptotic pathway and oxidative damage is involved in ethanol-induced Purkinje cell death in the developing cerebellum.

Cerebral ischemia results from a transient or permanent reduction in cerebral blood flow that decreases oxygen and glucose supply. When the cellular oxygen supply is reduced to critical level, damage to cells and induction of cell death are occurred by excitotoxicity, oxidative stress and inflammation. Ischemia remains one of the leading causes of death, but there is no effective treatment that might protect neurons gainst ischemia by interrupting the cascade of cell death. In this study, human neuroblastoma SH-SY5Y cells are exposed to oxygen and glucose deprivation (OGD) followed by reoxgenation. OGD can mimic the acute restriction of metabolite and oxygen supply caused by ischemia and is widely used as a model of ischemic conditions. SH-SY5Y cells are treated samples at the commencement of OGD to achieve different final concentrations, and cell viabilities were quantified using the measurement of flow cytometry analysis. Of those tested, the extracts of Polygala tenuifolia (roots), Dictamnus dasycarpus (barks), Polygala tenuifolia (roots), Eucommia ulmoides (branches), Eucommia ulmoides (barks), Poria cocos (whole), Sophora flavescens (roots) showed neuroprotective effects, with EC50 values of 4.5±0.6, 7.9±1.5, 10.5±0.7, 18.4±1.9, 19.6±0.3, 21.6±1.9, and 30.7±3.9μg/ml, respectively.