The importance of forests continues to increase throughout the world, and one of the reasons is that a forest is a major place to emit terpenes, which have been reported to be beneficial to human health. In South Korea, forests occupy about 64% of the total land area and consist mainly of pine and oak trees. Since only a limited number of forests have been analyzed to date, a comprehensive understanding of terpenes emitted from regional forests remains in its infancy in Korea. Here, to gain insights into terpenes from regional forests located in South Korea, we review the characteristics of Korean forests and recent studies on major terpenes emitted from regional forests as well as from native trees dominant in South Korea. We also discuss meteorological factors that affect the terpene emissions in Korean forests. In conclusion, 18 types of terpenes were detected in Korean forests and their compositions in different forests are largely dependent on the dominant plant species in the forest. Moreover, terpene emissions in Korean forests are affected by various environmental factors, including temperature, amount and duration of daylight, season, and age of trees. To improve the understanding of the characteristics of terpene distribution, more studies are required on the terpene production of Korean forests in various regions.

Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease characterized by synovitis, hyperplasia, and the destruction of bone and cartilage. A variety of immunosuppressive biological agents have been developed because the pathogenesis of RA is related predominantly to the inflammatory response. However, rheumatoid arthritis fibroblast-like synovial cells (RAFLS), which are known to play an important role in RA progression, exhibit resistance to immunosuppressants through cancer-like properties. In this study, we identified a novel therapeutic compound for RA, which reduced inflammation and the abnormal proliferation of RAFLS in natural product library made from Korean native plants. Eupatorium japonicum Thunb. (EJT) extract, a component of the natural product library, most effectively reduced viability through the induction of ROS-mediated apoptosis in a dose-dependent manner. In addition, the increased ROS induced the expression of ATF4 and CHOP, key players in ER stress-mediated apoptosis. Interestingly, EJT extract treatment dose-dependently reduced the expression of IL-1β and the transcription of MMP-9, which were induced by TNF-α treatment, through the inhibition of NF-κB and p38 activation. Collectively, we found that EJT extract exerted apoptotic effects through increases in ROS production and CHOP expression and exerted anti-inflammatory effects through the suppression of NF-κB activation, IL-1β expression, and MMP-9 transcription.

Natural products are valuable sources for drug discovery because they have a wide variety of useful chemical components and biological properties. A quick reevaluation of the potential therapeutic properties of established natural products was made possible by the recent development of the methodology and improvement in the accuracy of an automated high-throughput screening system. In this study, we screened natural product libraries to detect compounds with anticancer effects using HeLa cells. Of the 420 plant extracts screened, the extract of Angelica gigas Nakai (AGN) was the most effective in reducing cell viability of HeLa cells. Markers of apoptosis, such as exposure of phosphatidylserine and cleavage of caspase-7 and PARP, were increased by treatment with the AGN extract. Treatment of the AGN extract increased expression of PKR as well as ATF4 and CHOP, the unfolded protein response genes. In addition, cotreatment of doxorubicin and the AGN extract significantly increased doxorubicin-induced apoptosis in HeLa cells. Decursin and decursinol angelate, which were known to have anticancer effects, were the main components of the AGN extract. These results suggest that the extract of AGN containing, decursin and decursinol angelate, increases doxorubicin susceptibility.

BackgroundReactive oxygen species (ROS) produce different lesions in DNA by ROS-induced DNA damage. Detection and quantification of 8-oxo-7,8-dihydroguanine (8-oxoG) within cells are important for study. Human ribosomal protein S3 (hRpS3) has a high binding affinity to 8-oxoG. In this study, we developed an imaging probe to detect 8-oxoG using a specific peptide from hRpS3. Transactivator (TAT) proteins are known to have cell-penetrating properties. Therefore, we developed a TAT-S3 probe by attaching a TAT peptide to our imaging probe.ResultsA DNA binding assay was conducted to confirm that our probe bound to 8-oxoG and apurinic/apyrimidinic (AP) sites. We confirmed that the TAT-S3 probe localized in the mitochondria, without permeabilization, and fluoresced in H2O2-treated HeLa cells and zebrafish embryos. Treatment with Mitoquinone (MitoQ), a mitochondria-targeted antioxidant, reduced TAT-S3 probe fluorescence. Additionally, treatment with O8, an inhibitor of OGG1, increased probe fluorescence. A competition assay was conducted with an aldehyde reaction probe (ARP) and methoxyamine (MX) to confirm binding of TAT-S3 to the AP sites. The TAT-S3 probe showed competitive binding to AP sites with ARP and MX.ConclusionsThese results revealed that the TAT-S3 probe successfully detected the presence of 8-oxoG and AP sites in damaged cells. The TAT-S3 probe may have applications for the detection of diseases caused by reactive oxygen species.

Background Detection and quantification of 8-oxo-7,8-dihydroguanine (8-oxoG) within cells are important for studying the molecular mechanisms of cancer. Human ribosomal protein S3 (hRpS3), which is involved in DNA repair, has a high binding affinity to 8-oxoG. We developed an imaging probe to detect 8-oxoG using a specific peptide from hRpS3. Transactivator (TAT) proteins are commonly known to have cell-penetrating properties. Therefore, we developed the TAT-S3 probe via attaching a TAT peptide to our imaging probe. Result A DNA binding assay was conducted to confirm that our probe bound to 8-oxoG and AP sites. We confirmed that the TAT-S3 probe is present in the mitochondria, without permeabilization, and the TAT-S3 probe also showed fluorescence in H2O2-treated HeLa cells and zebrafish embryos. Treatment with MitoQ, a mitochondria-targeted anti-oxidant, reduced TAT-S3 probe fluorescence. Additionally, treatment with O8, an inhibitor of OGG1, increased probe fluorescence. A competition assay was conducted to utilize an aldehyde reaction probe (ARP) and methoxyamine (MX) to confirm the binding of the TAT-S3 to the AP sites. The TAT-S3 probe showed binding to AP sites competitive with ARP and MX. Conclusion These results revealed that the TAT-S3 probe successfully detected the presence of 8-oxoG and AP sites in damaged cells. The TAT-S3 probe may have applications for the detection of diseases caused by reactive oxygen species (ROS).