Altered gene expression reveals molecular mechanisms underlying oridonin-induced apoptosis of multiple myeloma LP-1 cells

ObjectiveTo investigate the effect of oridonin on proliferation and invasion of human multiple myeloma LP-1 cells and the underlying mechanism.MethodsLP-1 cells in culture medium in vitro were treated with oridonin at the different concentration. Cell proliferation was measured by Microwave Theory and Techniques (MTT) assay and cell apoptotic rate was detected by flow cytometry. Morphology of cell apoptosis was observed by transmission electron microscope. Expressions of Bax, Bcl-2, Caspase-3, NF-κB as well as I-κB mRNA were detected by real-time PCR.ResultsThe MTT assays and flow cytometry revealed that oridonin could inhibit the growth of LP-1 cells and cause apoptosis significantly; the suppression was both in time-and dose-dependent manner. Marked morphological changes of cell apoptosis were found under a transmission electron microscope after the cells were treated with oridonin at 25 μmol/L for 24 h. Along with the apoptotic process, Bcl-2, Caspase-3, NF-κB gene expressions were down-regulated (P<0.05). On the contrast, the Bax and I-κB gene expressions were up-regulated (P<0.05).ConclusionOridonin could inhibit the proliferation of LP-1 cells via inducing apoptosis. We concluded that oridonin induces apoptosis in LP-1 cells via activation of caspase-3 as well as down-regulation of Bcl-2 and up-regulation of Bax expression. The results suggested that oridonin could induce apoptosis of LP-1 cells through mitochondria- and caspase3-dependent pathways. Meanwhile, the inhibition of NF-κB and the activation of I-κB indicate pro-apoptotic stimuli. In one word, oridonin might be an important potential anti-myeloma reagent.