摘要
Objective:To observe effect of Jingulian capsule on the proliferation of human breast cancer MDA-MB-231 cells and investigate its action mechanism against triple negative breast cancer (TNBC). Method:The ingredients of Jingulian capsule were identified by ultra-performance liquid chromatography-tandem mass spectrometry(UPLC-MS/MS). The inhibitory effect of Jingulian capsule at different doses (0.125,0.25,0.5,1,and 2 g·L<sup>-1</sup>) against the proliferation of MDA-MB-231 cells were detected by methyl thiazolyl tetrazolium (MTT) assay. After treatment for 24 h, the morphological changes in nuclear apoptosis of MDA-MB-231 cells were detected by Hoechst 33258 staining. The effect of different concentrations of Jingulian capsule on the apoptosis and cycle of MDA-MB-231 cells after different treatment time were determined by flow cytometry. The protein expression levels of Poly-ADP-ribose polymeras (PARP), proto-oncogene c-Myc, cyclin B<sub>1</sub>, and phosphorylated extracellular signal-regulated kinase (p-ERK) in each group were assayed by Western blot. Result:A total of 113 compounds in Jingulian capsule were identified by UPLC-MS/MS. As revealed by MTT assay,compared with blank group,Jingulian capsule (0.125,0.25,0.5,1,2 g·L<sup>-1</sup>) significantly inhibited viability of MDA-MB-231 cells (<italic>P</italic><0.01), with the half maximal inhibitory concentration ( IC<sub>50</sub>) of(0.13±0.02)g·L<sup>-1</sup>. According to flow cytometry,compared with the blank group,Jingulian capsule at 1 g·L<sup>-1</sup> significantly induced the apoptosis of MDA-MB-231 cells (<italic>P</italic><0.05)and Jingulian capsule at 0.5, 1 g·L<sup>-1</sup> obviously increased the number of MDA-MB-231 cells in S phase (<italic>P</italic><0.05,<italic>P</italic><0.01). The results of Western blotting demonstrated that the protein expression levels of PARP,c-Myc,and cyclin B<sub>1</sub> in 0.5, 1 g·L<sup>-1 </sup>Jingulian capsule groups were remarkably down-regulated as compared with those in the blank group(<italic>P</italic><0.01), and the protein expression level of p-ERK in 1 g·L<sup>-1 </sup>Jingulian capsule group was also down-regulated (<italic>P</italic><0.01). Conclusion:Jingulian capsule is able to inhibit the proliferation of MDA-MB-231 cells,induce S phase cell cycle arrest, and promote their apoptosis, which may be related to the inactivation of the MAPK signaling pathway.
摘要
In this study, three new germacranolide sesquiterpenes (1-3), together with six related known analogues (4-9) were isolated from the whole plant of Carpesium cernuum. Their structures were established by a combination of extensive NMR spectroscopic analysis, HR-ESIMS data, and ECD calculations. The anti-leukemia activities of all compounds towards three cell lines (HEL, KG-1a, and K562) were evaluated in vitro. Compounds 1-3 exhibited moderate cytotoxicity with IC
Subject(s)
Humans , Antineoplastic Agents, Phytogenic/pharmacology , Asteraceae/chemistry , Drug Screening Assays, Antitumor , K562 Cells , Phytochemicals/pharmacology , Sesquiterpenes, Germacrane/pharmacology摘要
Objective: To establish a model for the injury of human neuroblastoma cell (SH-SY5Y) induced by sodium glutamate, and to observe the protective effect of syringaresinol on cell damage from Viscum liquidambaricolum hayataon, and to explore its mechanism. Method: Construction of SH-SY5Y cell injury model using sodium glutamate.The experiment was divided into normal cell group, injury model group (sodium glutamate 50 mmol·L-1, sodium glutamate 50 mmol·L-1 + DMSO),syringaresinol experimental group (6.25, 12.5, 25 μmol·L-1), by cell counting, cell morphology observation, Annexin V-FITC/PI apoptosis detection, ROS reactive oxygen species detection, mitochondrial membrane potential, and Western blot, evaluation of syringaresinol on glutamate-induced neuronal excitability injury neuroprotective activity. Result: Compared with normal group, the cell survival rate of the model group was significantly decreased (PPPPP-1) showed a concentration-dependent increase in cells. Survival rate (PPPPPConclusion: Syringaresinol has significant protective activity against excitatory damage induced by sodium glutamate in SH-SY5Y neurons, the mechanism may be through anti-oxidative stress, repairing mitochondrial function and DNA damage to significantly reduce sodium glutamate-induced neuronal apoptosis.