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Four Korea-native wild vegetables belonging to the Allium genus (Allium tuberosum Rottl., Allium senescens L., Allium thunbergii G. Don., and Allium sacculiferum Maxim.) were investigated for their antioxidant and anti-obesity potential, in order to promote the utilization of wild edible plants for the development of potential new crops. In this study, we compared the antioxidant activity of the plant extracts by ABTS+ and DPPH scavenging method. We then compared the anti-adipogenic effects of the extracts in adipocytes. We quantified the phenolics in the extracts using high-performance liquid chromatography (HPLC) to identify the bioactive compounds. A. tuberosum and A. sacculiferum had a higher total phenolic content (19.0 ± 0.3 and 19.6 ± 0.7 mg GA/g extract, respectively) than A. senescens and A. thunbergii (16.0 ± 0.2 and 14.5 ± 0.7 mg GA/g extract). Caffeic acid, an antioxidant and anti-adipogenic compound, was detected in A. tuberosum and A. sacculiferum, but not in A. senescens and A. thunbergii. A. tuberosum, and A. sacculiferum showed superior antioxidative and anti-adipogenic activities compared to A. senescens and A. thunbergii. Therefore, A. tuberosum and A. sacculiferum, both of which contain antioxidant and anti-adipogenic phenolics, such as caffeic acid, present a therapeutic potential against obesity. Various phenolic compounds, which have been found to differ among Allium spp., may partially account for differences among the Allium spp. with respect to their antioxidant and anti-obesity effects.

Sophora flavescens, also known as Kushen, has traditionally been used as a herbal medicine. In the present study we evaluated the ameliorative effects of kushenol C (KC) from S. flavescens against tBHP (tert-Butyl hydroperoxide)-induced oxidative stress in hepatocellular carcinoma (HEPG2) cells and acetaminophen (APAP)-induced hepatotoxicity in mice. KC pretreatment protected the HEPG2 cells against oxidative stress by reducing cell death, apoptosis and reactive oxygen species (ROS) generation. KC pretreatment also upregulated pro-caspase 3 and GSH (glutathione) as well as expression of 8-Oxoguanine DNA Glycosylase (OGG1) in the HEPG2 cells. The mechanism of action was partly related by KC’s activation of Akt (Protein kinase B (PKB)) and Nrf2 (Nuclear factor (erythroid-derived 2)-like 2) in the HepG2 cells. In in vivo investigations, coadministration of mice with KC and APAP significantly attenuated APAP-induced hepatotoxicity and liver damage, as the serum enzymatic activity of aspartate aminotransferase and alanine aminotransferase, as well as liver lipid peroxidation and cleaved caspase 3 expression, were reduced in APAP-treated mice. Coadministration with KC also up-regulated antioxidant enzyme expression and prevented the production of proinflammatory mediators in APAP-treated mice. Taken together, these results showed that KC treatment has potential as a therapeutic agent against liver injury through the suppression of oxidative stress.