JA, a new type of XXXX isolated from Juglans mandshurica Maxim, limits the survival and induces apoptosis of heptocarcinoma cells.

@entity1 @entity5204 @entity3437 @entity10610 @entity522 @entity589 @entity1477 @entity5 @entity8189 @entity3544 @entity14544 @entity12982 @entity8187 @entity36828 @entity157
UNASSIGNED: Juglans mandshurica Maxim (Juglandaceae) is a famous folk medicine for @entity5 treatment and some natural compounds isolated from it have been studied extensively. Previously we isolated a type of   -9 @entity5204 (JA) from the bark of J. mandshurica, however little is known about its activity and the underlying mechanisms. In this study, we studied anti- @entity5 activity of JA on several @entity1 @entity5 cell lines. Results showed that JA is cytotoxic to HepG2, MDA-MB-231, SGC-7901, A549 and Huh7 cells at a concentration exerting minimal toxic effects on L02 cells. The selective toxicity of JA was better than other classical anti- @entity5 drugs. Further investigation indicated that JA could induce cell apoptosis, characterized by chromatin condensation, DNA fragmentation and activation of the apoptosis-associated proteins such as @entity522 and @entity12982 . Moreover, we investigated the cellular apoptosis pathway involved in the apoptosis process in HepG2 cells. We found that proteins involved in mitochondrion (cleaved- @entity8187 , @entity3437 , @entity36828 /Omi, @entity589 , and Mitochondrial @entity589 ) and endocytoplasmic reticulum (XBP-1s, @entity1477 , cleaved- @entity14544 and cleaved-Caspase-12) apoptotic pathways were up-regulated when cells were treated by JA. In addition, a morphological change in the mitochondrion was detected. Furthermore, we found that JA could inhibit DNA synthesis and induce G2/M cell cycle arrest. The expression of G2-to-M transition related proteins, such as @entity8189 and phosphorylated- @entity10610 , were reduced. In contrast, the G2-to-M inhibitor @entity3544 was increased in JA-treated cells. Overall, our results suggest that JA can induce mitochondrion- and endocytoplasmic reticulum-mediated apoptosis, and G2/M phase arrest in HepG2 cells, making it a promising therapeutic agent against @entity157 .
