A new eremophilane glycoside from the fruits of Physalis pubescens and its cytotoxic activity.

Physalis pubescens L. has been used as a traditional folk medicine in China. Comprehensive studies aimed at identifying the bioactive constituents are still lacking. In the course of searching bioactive secondary metabolites from P. pubescens L., phytochemical investigation of the fruits of P. pubescens L. led to the isolation of one new eremophilane glycoside, 1ß,3α-dihydroxy-7α-eremophila-911-dien-3-O-[α-L-arabinopyranosyl-(l→6)]-ß-D-glucopyranoside (1), and six known glycosides (2-7). Their structures were established via extensive spectroscopic data including 1D and 2D NMR and HRESIMS. Cytotoxic effects against six human cancer cell lines (C4-2B, A375, A375-S2, 786-O, Caki-2, and ACHN) and one human normal hepatic cell line (L02) were evaluated and compounds 1 and 2 exhibited moderate cytotoxicity against C4-2B and A375 cell lines with IC50 values in the range of 6.78-28.3 µM. The study indicates that the fruits of P. pubescens L. have the potential to be used for drug discovery.

Physalin A induces G2/M phase cell cycle arrest in human non-small cell lung cancer cells: involvement of the p38 MAPK/ROS pathway.

Physalin A (PA) is an active withanolide isolated from Physalis alkekengi var. franchetii, a traditional Chinese herbal medicine named Jindenglong, which has long been used for the treatment of sore throat, hepatitis, and tumors in China. In the present study, we firstly investigated the effects of PA on proliferation and cell cycle distribution of the human non-small cell lung cancer (NSCLC) A549 cell line, and the potential mechanisms involved. Here, PA inhibited cell growth in dose- and time-dependent manners. Treatment of A549 cells with 28.4 µM PA for 24 h resulted in approximately 50 % cell death. PA increased the amount of intracellular ROS and the proportion of cells in G2/M. G2/M arrest was attenuated by the addition of ROS scavenger NAC. ERK and P38 were triggered by PA through phosphorylation in a time-dependent manner. The phosphorylation of ERK and P38 were not attenuated by the addition of NAC, but the use of the p38 inhibitor could reduce, at least in part, PA-induced ROS and the proportion of cells in G2/M. PA induces G2/M cell cycle arrest in A549 cells involving in the p38 MAPK/ROS pathway. This study suggests that PA might be a promising therapeutic agent against NSCLC.