Experimental research on the mechanisms of human multiple myeloma LP-1 cell apoptosis induced by oridonin.
- Author:
Jing ZHAO
1
;
Mei ZHANG
;
Ying CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; drug effects; Apoptosis Regulatory Proteins; metabolism; BH3 Interacting Domain Death Agonist Protein; metabolism; Cell Line, Tumor; Cell Proliferation; drug effects; Diterpenes, Kaurane; pharmacology; Humans; Multiple Myeloma; pathology; NF-kappa B p50 Subunit; metabolism; Neoplasm Proteins; metabolism; Proto-Oncogene Proteins c-bcl-2; metabolism
- From: Chinese Journal of Integrated Traditional and Western Medicine 2012;32(12):1642-1646
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effects of oridonin (Ori) on human multiple myeloma (MM) cell line LP-1 apoptosis and its mechanisms.
METHODSThe human MM LP-1 cells were incubated in vitro by different concentrations of Ori. The proliferation activities of LP-1 cells were detected using MTT assay. The apoptosis rate of LP-1 cells was detected using Annexin V/PI double staining method. The ultrastructural changes of LP-1 cells were observed under transmission electron microscope (TEM) after they were treated with Ori. The mRNA expression of apoptosis correlated genes were detected using Real-time PCR.
RESULTSOri inhibited the proliferation of LP-1 cells in a dose- and time-dependent way. Results of Annexin V/PI double staining method showed that, along with increased drug concentration and prolonged drug action time, the apoptosis rate of LP-1 cells significantly increased. Under TEM, chromatin margination and mitochondrial swelling could be seen in LP-1 cells after they were treated by Ori. The mRNA expressions of PDCD5 and Bid were up-regulated, and those of Bcl-2 and NK-kappaB were down-regulated after action of Ori.
CONCLUSIONSOri induced cell apoptosis by up-regulating the mRNA expression of Bid and down-regulating the mRNA expression of Bcl-2 to decrease the mitochondrial membrane potential, trigger mitochondrial apoptosis way of LP-1 cells. Ori, also as the inhibitor of NF-kappaB activities, blocked the NF-kappaB activation, induced cell apoptosis, and inhibited the cell proliferation. Of them, it is necessary to further study the role of PDCD5 as an apoptosis promoter.
