Effects Of Dihydroartemisinin On Ovarian Cancer HO-8910 Cells And Expression Of Akt

ObjectiveTo observe the effect of dihydroartemisinin（DHA）on the growth of human ovarian cancerHO-8910 cells and the expression of p-Akt,and study the mechanism.MethodsNude mouse model of tran- splanted ovarian cancer was established by injecting HO-8910cells into axillary fossa, and then Twenty - four model nude mice randomly divided into fourgroups, which include blank control group, positive control DDP group,dihydroartemisinin-high-dose group, dihydroartemisi- nin-low-do se group, each of which was composed of sixnude mice. Those in DDP control group intraperitoneal injected with DDP at a dosage of 2mg／kg body weight and received for 5 days . The mice in DHA-high-dose and DHA–low - dosegroups were gavage with DHA at dosages of 200 and 100 mg／kg body weight every other dayrespectively,and while those in blank control group gavage with saline,and continuously receivedfor 10 days in nude mice.Kill the mice on day 11 after treatment to observe the tumor growth andcomparison of tumor inhibitory rate after the intervention. The expression of p-Akt was determin-ed by immunohistochemical assay.Results①Pathological observation shows cells become large, and loose cytoplasm, nucleus deeplystained, pyknosis, nuclear dissolution, nuclear fragmentation, chromatin lumps also can befound,and cells have focal necrosis.②DHA showed significantly dosage-dependent inhibitoryeffect on the transplanted tumors of human ovarian cancer HO -8910 cells. The inhibitionrates of the DHA-low and high-dose groups and DDP group were 31.82 % , 46.21 % , and60.61% respectively. Compared with the saline group there were the statistically significantdifferences ( P < 0.05) . Inhibition rate of each experimental DHA groupwas compared withthe DDP , the difference was statisticallg significant ( P <0.05) .③Immunohisto- chemical assaydetection showed that the expression level of p- Akt decreased with the increasing dose ofDHA.ConclusionDHA has si- gnificant inhibition function on human ovarian cancer nude mice model tumorgrowth，through the mechanism of down-regulating the expression of p-Akt.