Compound K (20-O-(β-D-glucopyranosyl)-20(S)-protopanaxadiol) is an active metabolite of ginsenosides and induces apoptosis in various types of cancer cells. This study investigated the role of autophagy in compound K-induced cell death of human HCT-116 colon cancer cells. Compound K activated an autophagy pathway characterized by the accumulation of vesicles, the increased positive acridine orange-stained cells, the accumulation of LC3-II, and the elevation of autophagic flux. Whereas blockade of compound K-induced autophagy by 3-methyladenein and bafilomycin A1 significantly increased cell viability. In addition, compound K augmented the time-dependent expression of the autophagy-related proteins Atg5, Atg6, and Atg7. However, knockdown of Atg5, Atg6, and Atg7 markedly inhibited the detrimental impact of compound K on LC3-II accumulation and cell vitality. Compound K-provoked autophagy was also linked to the generation of intracellular reactive oxygen species (ROS); both of these processes were mitigated by the pre-treatment of cells with the antioxidant N-acetylcysteine. Moreover, compound K activated the c-Jun NH2-terminal kinase (JNK) signaling pathway, whereas downregulation of JNK by its specific inhibitor SP600125 or by small interfering RNA against JNK attenuated autophagy-mediated cell death in response to compound K. Compound K also provoked apoptosis, as evidenced by an increased number of apoptotic bodies and sub-G1 hypodiploid cells, enhanced activation of caspase-3 and caspase-9, and modulation of Bcl-2 and Bcl-2-associated X protein expression. Notably, compound K-stimulated autophagy as well as apoptosis was induced by disrupting the interaction between Atg6 and Bcl-2. Taken together, these results indicate that the induction of autophagy and apoptosis by compound K is mediated through ROS generation and JNK activation in human colon cancer cells.

To investigate the relationship between the intestinal bacterial metabolism of kalopanaxsaponin B and H from Kalopanax pictus (Araliaceae), and their antidiabetic effect, kalopanaxsaponin B and H were metabolized by human intestinal microflora and the antidiabetic activity of their metabolites was measured. Human intestinal microflora metabolized kalopanaxsaponin B to kalopanaxsaponin A, hederagenin 3-O-alpha-L-arabinopyranoside and hederagenin. The main metabolites of kalopanaxsaponin B were kalopanaxsaponin A and hederagenin. Kalopanaxsaponin H was metabolized to kalopanaxsaponin A and I, hederagenin 3-O-alpha-L-arabinopyranoside and hederagenin. The main metabolites of kalopanaxsaponin H were kalopanaxsaponin I and hederagenin. Among kalopanaxsaponin B, H and their metabolites, kalopanaxsaponin A showed the most potent antidiabetic activity, followed by hederagenin. However, the main components, kalopanaxsaponin B and H, in K. pictus were inactive.

Background Inflammatory bowel disease (IBD) and psoriasis are chronic inflammatory diseases and have been reported to have an association between them. However, most of the patients included in the previous reports were adults. As both diseases are related to each other, special consideration is required in managing each disease, as there is a high possibility of co-occurrence. In this regard, to figure out the association between the two diseases in childhood and adolescence is needed. Methods A nationwide population-based retrospective cohort study was performed using the Korean National Health Insurance claims database. A birth cohort from January 2002 to December 2006. Claim data related to IBD and psoriasis was evaluated up to December 2019 and was analyzed to figure the association between the two diseases. Results The datasets contained a total of 2,347,591 individuals. A total of 2,444 IBD patients and 5,165 psoriasis patients were identified. Thirteen patients had both IBD and psoriasis. Compared to the age and sex-matched control group, IBD patients showed a higher association of psoriasis (Odd ratios (ORs), 2.476; 95% confidence interval (CI), 1.240–4.945). In contrast, psoriasis patients did not show a statistically significant association compared to the control group (ORs, 1.857; 95% CI, 0.962–3.585). However, the proportion of patients with severe IBD was significantly higher (ORs, 6.000; 95% CI, 1.003–35.908). Conclusion The association between IBD and psoriasis is observed in pediatric patients. Recognizing and early diagnosis of related diseases in children with IBD and psoriasis is necessary for better clinical outcomes