Different Concentrations Of Oridonin Research Articles

Oridonin promotes osteogenesis through Wnt/β-catenin pathway and inhibits RANKL-induced osteoclastogenesis in vitro

AimsTo study the molecular mechanism of oridonin (ORI) on osteoblast differentiation and osteoclast formation in vitro. Main methodsRat bone marrow mesenchymal stem cells (BMSCs) were treated with different concentrations of ORI in osteogenic medium (OM). CCK-8 assay and were used to detect the effect on BMSCs viability. Alizarin red staining and ALP activity were used to illuminate the effect of ORI on osteogenic differentiation. Expressions of osteogenic differentiation related genes were detected by real-time quantitative PCR (qRT-PCR), and expressions of osteogenic related proteins were detected by Western blot (WB) and immunofluorescence. Similarly, bone marrow mononuclear cells (BMMs) were treated with different concentrations of ORI. CCK-8 assay and Live/Dead staining were used to detect the effect of ORI on BMMs activity. TRAP staining was used to detect its effect on osteoclast differentiation. Expressions of osteoclast-related genes were detected by qRT-PCR, and expressions of osteoclast-related proteins were detected by WB and immunofluorescence. Key findings(1) ORI (2 μM) promoted the ALP activity of BMSCs differentiation into osteoblasts and increased the number of calcium nodules. (2) ORI stimulated the expressions of wnt1, β-catenin and Runx2, but with no significantly effect on p-GSK-3β and GSK-3β. (3) ORI promoted the expression of OPG and inhibited the expression of RANKL. (4) ORI directly/indirectly inhibited the osteoclast formation and expressions of osteoclast-related genes TRAP, NFATc1 and c-Fos. SignificanceORI may promote BMSCs differentiate into osteoblasts through the Wnt/β-catenin signaling pathway. At the same time, it may also inhibit the formation of osteoclasts mediated by RANKL.

Oridonin Sensitizes Hepatocellular Carcinoma to the Anticancer Effect of Sorafenib by Targeting the Akt Pathway.

BackgroundOridonin is the core bioactive component of Rabdosia rubescens, a traditional Chinese herbal medicine used in the treatment of hepatoma. Sorafenib, a targeted therapeutic agent for advanced hepatocellular carcinoma (HCC), has recently been shown to exert limited clinical effects. However, few studies have focused on the synergistic effect of these two drugs on hepatocellular carcinoma.MethodsWe treated different HCC cell lines with different concentrations of oridonin and sorafenib and assessed the viability by using MTT assays and examined proliferation, migration, invasion and apoptosis after cotreatment of HepG2 cells with 20 μM oridonin and 5 μM sorafenib via colony formation assays, Transwell assays and flow cytometry. Regulatory effects were measured by Western blotting. The in vivo synergistic effect was confirmed through xenograft tumor models, and tumor tissues were analyzed by immunohistochemistry.ResultsThe inhibitory effects of oridonin and sorafenib cotreatment on HCC cells were stronger than those of either drug alone. In addition, combined treatment with the two drugs synergistically inhibited epithelial–mesenchymal transition and the Akt pathway but not NF-κB or MAPK signaling. Akt phosphorylation by SC79 reversed the inhibitory effects of the combined treatment. Synergistic inhibition was equally observed in vivo.ConclusionOridonin combined with sorafenib synergistically inhibited proliferation, migration, invasion, and epithelial–mesenchymal transition and induced apoptosis by targeting the Akt pathway but not NF-κB or MAPK signaling.

Effect of dexamethasone combined with oridonin on proliferation and apoptosis of multiple myeloma cell line U266

Objective To investigate the effect of dexamethasone combined with oridonin on proliferation and apoptosis in multiple myeloma cells U266 and the related molecular mechanism. Methods Exponential phase of growth U266 cells were treated with different concentrations of oridonin combined with dexamethasone or alone. U266 cells treated by DMSO were taken as control group. The proliferation inhibitory ratios were measured by CCK-8 assay followed by 24 h, 48 h and 72 h. Apoptosis induction was assessed by using Annexin V-FITC kit. Real time PCR was used to examine the mRNA changes of Notch1, NF-κB/p65 and bcl-2. Western blot assay was applied to detect the protein expression of Notch1, cleaved Notch1, NF-κB/p65 and bcl-2. Results Compared with that in control group, proliferation in all the experimental groups was inhibited(P<0.05), and the apoptosis was promoted(P<0.05); especially the combination of dexamethasone and oridonin had a synergistic effect on the proliferation and apoptosis of U266 cells(P<0.05). The results of PCR and Western blot showed that after treatment of U266 cells with dexamethasone, the mRNA as well as their protein levels of NF-κB/p65 and bcl-2 were decreased compared with those in the control group(P<0.05). Moreover, the mRNA and protein expression of Notch1, cleaved Notch1, NF-κB/p65 and bcl-2 was obviously down-regulated in oridonin group and the combination group(P<0.05). Conclusion Combination of dexamethasone and oridonin can significantly increase the anti-tumor effect by inhibiting proliferation and inducing apoptosis of U266 cells, which may be related to the inhibition of the Notch1 pathway. Key words: Multiple myeloma; Oridonin; Dexamethasone; Proliferation; Apoptosis

Oridonin induces apoptosis in gastric cancer through Apaf-1, cytochrome c and caspase-3 signaling pathway

To investigate the effect and mechanism of oridonin on the gastric cancer cell line HGC-27 in vitro. The inhibitory effect of oridonin on HGC-27 cells was detected using the 3-(4, 5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay. After treatment with 10 μg/mL oridonin for 24 h and 48 h, the cells were stained with acridine orange/ethidium bromide. The morphologic changes were observed under an inverted fluorescence microscope. DNA fragmentation (a hallmark of apoptosis) and lactate dehydrogenase activity were examined using DNA ladder assay and lactate dehydrogenase-release assay. After treated with oridonin (0, 1.25, 2.5, 5 and 10 μg/mL), HGC-27 cells were collected for anexin V-phycoerythrin and 7-amino-actinomycin D double staining and tested by flow cytometric analysis, and oridonin- induced apoptosis in HGC-27 cells was detected. After treatment with oridonin for 24 h, the effects of oridonin on expression of Apaf-1, Bcl-2, Bax, caspase-3 and cytochrome c were also analyzed using reverse-transcript polymerase chain reaction (RT-PCR) and Western blotting. Oridonin significantly inhibited the proliferation of HGC-27 cells in a dose- and time-dependent manner. The inhibition rates of HGC-27 treated with four different concentrations of oridonin for 24 h (1.25, 2.5, 5 and 10 μg/mL) were 1.78% ± 0.36%, 4.96% ± 1.59%, 10.35% ± 2.76% and 41.6% ± 4.29%, respectively, which showed a significant difference (P < 0.05). The inhibition rates of HGC-27 treated with oridonin at the four concentrations for 48 h were 14.77% ± 4.21%, 21.57% ± 3.75%, 30.31% ± 4.91% and 61.19% ± 5.81%, with a significant difference (P < 0.05). The inhibition rates of HGC-27 treated with oridonin for 72 h at the four concentrations were 25.77% ± 4.85%, 31.86% ± 3.86%, 48.30% ± 4.16% and 81.80% ± 6.72%, with a significant difference (P < 0.05). Cells treated with oridonin showed typical apoptotic features with acridine orange/ethidium bromide staining. After treatment with oridonin, the cells became round, shrank, and developed small buds around the nuclear membrane while forming apoptotic bodies. Lactate dehydrogenase (LDH) release assay showed that after treated with 1.25 μg/mL and 20 μg/mL oridonin for 24 h, LDH release of HGC-27 caused by apoptosis increased from 22.94% ± 3.8% to 52.68% ± 2.4% (P < 0.001). However, the change in the release of LDH caused by necrosis was insignificant, suggesting that the major cause of oridonin-induced HGC-27 cell death was apoptosis. Flow cytometric analysis also revealed that oridonin induced significant apoptosis compared with the controls (P < 0.05). And the apoptosis rates of HGC-27 induced by the four different concentrations of oridonin were 5.3% ± 1.02%, 12.8% ± 2.53%, 28.5% ± 4.23% and 49.6% ± 3.76%, which were in a dose-dependent manner (P < 0.05). After treatment for 24 h, DNA ladder showed that oridonin induced a significant increase in DNA fragmentation in a dose-dependent manner. RT-PCR revealed that mRNA expression levels were up-regulated compared with the controls in caspase-3 (0.917 ± 0.103 vs 0.357 ± 0.019, P < 0.05), cytochrome c (1.429 ± 0.111 vs 1.002 ± 0.014, P < 0.05), Apaf-1 (0.688 ± 0.101 vs 0.242 ± 0.037, P < 0.05) and Bax (0.856 ± 0.101 vs 0.278 ± 0.027, P < 0.05) (P < 0.05), whereas down-regulated in Bcl-2 (0.085 ± 0.012 vs 0.175 ± 0.030, P < 0.05). Western blotting analysis also confirmed this result. Apoptosis of HGC-27 induced by oridonin may be associated with differential expression of Apaf-1, caspase-3 and cytochrome c, which are highly dependent upon the mitochondrial pathway.

Metastasis-inhibiting effect of Oridonin on PC-3 cells and its mechanism

Objective To determine metastasis-inhibiting capability of Oridonin on PC-3 cells and to explore its mechanisms.Methods After PC-3 cells were Incubated with different concentrations of Oridonin,the metastasis ability was analyzed through experiment of chemotaxic migration.The mRNA expression levels of vascular endothelial growth factor (VEGF),matrix metalloproteinase ( MMP)-2 and MMP-9 were detected by using fluorescent quantitative polymerase chain reaction (PCR).The expression levels of VEGF,MMP-2 and MMP-9 proteins were examined by using enzyme linked immunosorbent assay (ELISA).Results Oridonin effectively inhibited the metastasis of PC-3 cells in a concentration- and timedependent manner,and there was significant difference between 40 μmol/L group and other groups (P ＜0.01 ).Oridonin effectively inhibited the expression levels of VEGF and MMP-9 in a concentration- and time-dependent fashion ( P ＜ 0.01 ).Conclusion Oridonin can inhibit metastasis of PC-3 cells effectively in a concentration-dependent manner probably by down-regulating the expression of VEGF,MMP-2 and MMP-9. Key words: Oridonin; Prostate carcinoma; Proliferation; Metastasis

Oridonin induced the apoptosis of PC-3 cells and its mechanism.

To observe the proliferation inhibition and apoptosis promotion effect of oridonin on PC-3 cells. PC-3 cells were treated with different concentrations of oridonin. MTT assay and drug concentration-time survival curve were used to test the effect of oridonin on the PC-3 cells. The percentage of earlier apoptosis cells was analyzed by flow cytometry. The protein expression of caspase-3, Bcl-2, and Bax in the PC-3 cells was detected by Western blot. Oridonin effectively inhibited the proliferation of PC-3 cells in both concentration- and time-dependent manner, and the IC50 of PC-3 cells was 10.29 μmol/L. HochesT(3)3258 staining and flow cytometry deteced that oridonin induced the apoptosis of PC-3 cells in a concentration-dependent manner (P<0.05). Oridonin down-regulated Bcl-2, up-regulated Bax protein, and activated caspase-3 in a concentration-dependent manner in the PC-3 cells. The apoptosis of PC-3 cells induced by oridonin might be associated with the mitochondrial pathway.

Oridonin, An Ent-Kaurane Diterpenoid, Shows Antileukemic Effect and Enhances the Effect of Indarubicin on Human T-Cell Leukemia Cell Line

AbstractAbstract 4933 IntroductionAcute lymphoblastic leukemia (ALL) is the most common type of leukemia in young children, and also affects adults, especially those aged 65 years or older. Although the outcome of children with ALL has been improved dramatically with current chemotherapy strategy, adult patients still have a worse outcome and the incidence of relapse remains high either in children or adult patients. Furthermore, there has been very little progress in improving the outcome of patients who experience relapse. Oridonin, an ent-kaurane diterpenoid derived from the herbal Rabdosia rubescens, has been proved to have significant antitumor effect on a large variety of cancer cells. In this study, we aimed to assess whether oridonin had antileukemic effection and the possibility of combination effect with indarubicin (IDA), an important component commonly used in T-ALL induction regimen. MethodsHuman T-cell leukemia cell line Jurkat cells in culture medium were treated with different concentrations of oridonin (1umol/L~ 20umol/L) for 24h and 48h. Cell Counting Kit-8 (CCK8) assay was used to detect the cell growth inhibitory rate. Apoptosis was measured with flow cytometric (FCM) by staining cells with Annexin V-fluorescein-isothiocyanate(FITC) and propidium iodide (PI). Hoechst 33258 staining was used to observe the apoptotic morphology. The expression of caspase-3, caspase-8 and other apoptosis modulators, including Bcl-2 family members, was analyzed by western blotting. When the combination effect of oridonin and indarubicin was investigated, oridonin was given one hour before indarubicin. The calculation of combined effect was used Isobologram Analysis. ResultsCCK8 assay revealed that oridonin could significantly inhibit the growth of Jurkat cells in vitro. The suppression was both time- and dose-dependent. The concentration of oridonin lower than 5 umol/L showed little inhibitory effect, but it presented significant inhibition of the proliferation at a higher concentration, especially when the concentration was higher than 10 umol/L. The 50% inhibitory concentration (IC50) values for 24h and 48h were 9.44 and 9.06 umol/L respectively. After Jurkat cells were treated with higher than 5 umol/L of oridonin for 24–48h., the percentage of Annexin VFITC positive cells was gradually increased in a time and dose-dependent manner and the percentage of Annexin VFITC positive cells could reach 40% to 50% after 10 umol/L of oridonin treatment for 48h. Marked morphological changes of cell apoptosis including condensation of chromatin and nuclear fragmentation were observed using Hoechst 33258 stain after 48h. Western blotting analysis showed cleavage of the caspase-3 zymogen protein (32 kDa) with the appearance of its 20-kDa subunit when apoptosis occurred; Expression of Bcl-2 was downregulated significantly after the cells were treated with oridonin for 24 h. The expression of caspase-8 remained constant before and after apoptosis occurred. We therefore concluded that oridonin has significant antiproliferation effects on Jurkat cells by activation of caspase-3 as well as down-regulation of anti-apoptotic protein Bcl-2. The 24h IC50 of IDA for Jurkat cells was 25.85nmol/L. When combined with 1umol/L of oridonin, the IC50 of IDA decreased to 4.93nmol/L. The combine index was < 1, indicating the synergistic antitumor effect of IDA and oridonin. The data from FCM showed that 2.5 umol/L of oridonin could augment the apoptosis effect of 2.5nmol/L of IDA from 5.1% to 12.7%. During the experiment, we found that oridonin given one hour before IDA could make a better combination effect than given simultaneously. We also discovered that low dose oridonin (lower than 5 umol/L) had little inhibitory effect on normal bone marrow mononuclear cells. ConclusionsThe results showed oridonin could effectively induce ALL cells apoptosis, and in low dose showed a significant synergistic effect with IDA, indicating oridonin may serve as a potential and secure antileukemia reagent for ALL, especially in the combination chemotherapy. The underlying machanisms of the combination effect with anthracycline should be explored. Disclosures:No relevant conflicts of interest to declare.

Apoptosis inducing effects of oridonin on THP-1 cells and its mechanisms of action

Objective To investigate the apoptosis inducing effects of oridonin on leukemic THP-1 cells and its mechanisms of action. Methods THP-1 cells in culture medium in vitro were given different concentrations of oridonin (16～56 μmol/L) for 24, 48 and 72 h. The inhibitory rate of the cells were measured by MTT assay, apoptotic morphology was observed by Hoechst 33258 staining, and Annexin V/PI staining was used to detect cell apoptosis by flow cytometry (FCM). Caspase-3 and poly (ADP-ribose) polymerase (PARP) expression were detected by Western blotting. Results Oridonin (over 32 μmol/L) could inhibit the growth of THP-1 cells and cause apoptosis remarkably, the suppression was both in time-and dose-dependentmanner. Marked morphological changes of cell apoptosis such as condensation of chromatin was clearly observed by Hoechst 33258 staining, and Annexin V/PI staining showed that apoptotic cells gradually increased after the cells treated with oridinon. Western blotting showed cleavage of the caspase-3 zymogen protein (32×103), with the appearance of its 20×103 subunit, and a cleaved 89×103 fragment of 116×103 PARP was also found. Conclusion Oridonin can inhibit cell growth and induce apoptosis in THP-1 cells via activation of caspase-3. The results indicated that oridonin might be an important potential anti-leukemia reagent. Key words: Oridonin; THP-1 cell; Apoptosis

Oridonin inhibits cell growth by induction of apoptosis on human hepatocelluar carcinoma BEL-7402 cells

The present study was undertaken to investigate the mechanisms of oridonin induced apoptosis on human hepatocellular carcinoma BEL-7402 cells. BEL-7402 cells in culture medium in vitro were given different concentrations of oridonin. Cell proliferation was measured by MTT assay and [(3)H]-thymidine uptake, cell apoptotic rate was detected by flow cytometry (FCM), morphology of cell apoptosis was observed by Hoechst 33258 staining and DNA fragmentation. Caspase-3 as well as Bcl-2 and Bax expressions were detected by Western blotting. The results revealed that oridonin could inhibit the growth of BEL-7402 cells and cause apoptosis significantly, the suppression was both in time- and dose-dependent manner. Marked morphological changes of cell apoptosis were observed very clearly by Hoechst 33258 staining as well as DNA fragmentation analysis after the cells exposed to oridonin for 60h; Western blotting showed cleavage of the caspase-3 zymogen protein (32-kDa) with the appearance of its 20-kDa subunit; Along with the apoptotic process Bcl-2 expression was down-regulated and Bax expression up-regulated concurrently observed by Western blotting. We therefore conclude that oridonin can inhibit cell growth by induction of apoptosis in BEL-7402 cells via activation of caspase-3 as well as down-regulation of Bcl-2 and up-regulation of Bax expression. The results indicate that oridonin may be an important potential anti-hepatocellular carcinoma reagent.

Antiproliferation effects of oridonin on HPB-ALL cells and its mechanisms of action

Oridonin, an ent-kaurane diterpenoid derived from the herbal Rabdosia rubescens, has been recently reported to have antitumor effects on a large variety of cancer cells. The present study was undertaken to investigate the in vitro antiproliferation and apoptosis inducing effects of oridonin on HPB-ALL cell lines and its mechanisms of action. HPB-ALL cells in culture medium in vitro were treated with different concentrations of oridonin (16-56 micromol/L). MTT assay was used to detect the cell growth inhibitory rate, and the cell viability was assessed by the trypan blue dye-exclusion method. Cell apoptosis and the mitochondrial membrane potential (delta psi m) were investigated by flow cytometry (FCM), Hoechst 33258 staining, and DNA fragmentation analysis. The expression of caspase-3 and different apoptosis modulators, including Fas and Bcl-2 family members, was analyzed by Western blotting. The results revealed that oridonin could significantly inhibit the growth of HPB-ALL cells and cause apoptosis, and the suppression was both time- and dose-dependent. After treatment with oridonin for 48 hr, the percentage of disruption of delta psi m gradually increased in a dose-dependent manner along with marked changes of cell apoptosis, and necrotic cells increased remarkably after the cells were treated with oridonin for 72 hr; Western blotting showed cleavage of the caspase-3 zymogen protein (32 kDa) with the appearance of its 20-kDa subunit when apoptosis occurred; expression of Bcl-2 and Bcl-XL was downregulated remarkably while expression of Bax and Bid was upregulated concurrently after the cells were treated with oridonin for 24 hr. Of note, the expressions of Fas and other Bcl-2 family members including Bak and Bad remained constant before and after apoptosis occurred. We therefore conclude that oridonin has significant antiproliferation effects on HPB-ALL cells by induction of apoptosis as well as directly causing cell necrosis and that oridonin-induced apoptosis on HPB-ALL cells is mainly related to the disruption of delta psi m and activation of caspase-3 as well as downregulation of anti-apoptotic protein Bcl-2, Bcl-XL, and upregulation of pro-apoptotic proteins Bax and Bid. The results indicate that oridonin may serve as a potential antileukemia reagent.

Apoptotic effect of oridonin on NB4 cells and its mechanism

The anti-proliferation effects of oridonin on acute promyelocytic leukemia (APL) cells and its mechanisms were studied in vitro. NB4 cells as well as fresh leukemia cells obtained from APL patients in culture medium were treated with different concentrations of oridonin. Cell growth inhibition, apoptosis and related pathways were assessed by MTT assay as well as flow cytometry (FCM) and western blot analysis. The data revealed that oridonin (over 16 micromol/L) could inhibit the growth of NB4 cells by induction of apoptosis. Marked changes of cell apoptosis were observed very clearly by using electron microscopy and DNA fragmentation analysis after the cells exposed to oridonin for 48 h; Western blotting showed cleavage of the caspase-3 zymogen protein (32-kDa) with the appearance of its 20-kDa subunit as well as a cleaved 89-kDa fragment of 116-kDa PARP when apoptosis occurred. The expression of Bcl-2 was down-regulated remarkably accompanied by the disruption of the mitochondrial membrane potential (delta(psi)m). The anti-proliferative and apoptosis-inducing effects by oridonin in fresh APL cells were also found remarkably using Trypan Blue dye exclusion method and Wright's staining. We concluded that oridoning has significant anti-proliferative and apoptosis-inducing effects on NB4 cells by activation of caspase-3 and cleavage of PARP as well as by down regulation of Bcl-2 and disruption of the delta(psi)m. Furthermore, oridonin demonstrated apparent cell growth inhibition effects on fresh APL cells in vitro. The results indicated that oridonin may serve as a potential anti-leukemia reagent.

Oridonin-induced apoptosis of Jurkat cells and its mechanism

Jurkat cells in culture medium in vitro were exposed to different concentrations of oridonin. The proliferation rate of the cells was measured by MTT assay, cell apoptotic rate was detected by flow cytometry, morphology of cell apoptosis was observed by Hoechst 33258 fluorescence staining, DNA fragmentation was assayed by agarose gel electrophoresis, caspase-3 and poly(ADP-ribose) polymerase (PARP) expressions were detected by Western blotting using polyclonal anti-caspase-3 antibody and mouse anti-human PARP monoclonal antibodies, and caspase-3 activity was assayed with a colorimetric assay kit before and after apoptosis had occurred. Oridonin (over 32 μmol/l) inhibited the growth of Jurkat cells and caused significant apoptosis. The suppression was both time-dependent and dose-dependent. Marked morphological changes of cell apoptosis, including condensation of chromatin and nuclear fragmentation, were clearly observed by Hoechst 33258 fluorescence staining, as well as by agarose gel electrophoresis. Western blotting showed cleavage of the caspase-3 zymogen protein (32 kDa), with the appearance of its 17 kDa subunit, and a cleaved 89-kDa fragment of 116 kDa PARP was also found, together with a concurrent increase in caspase-3 apoptotic activity. Oridonin can induce apoptosis in Jurkat cells via activation of caspase-3; the results indicate that oridonin might be an important potential anti-leukaemia reagent.

Antiproliferation effects of oridonin on HL-60 cells.

The antiproliferation effects and inhibition of telomerase activity of oridonin on leukemic HL-60 cells were studied. HL-60 cells in culture medium were treated with different concentrations of oridonin. The inhibitory rate of the cells was measured by MTT assay. Cell apoptotic rate was detected by flow cytometry (FCM). Morphology of cell apoptosis was observed by Wright's stain. Reverse transcriptase polymerase chain reaction (RT-PCR) and PCR-enzyme-linked immunosorbent assay (ELISA) were used to detect hTERT mRNA expression and telomerase activity before and after apoptosis. Oridonin (over 8 micromol/l) could inhibit the growth of HL-60 cells and cause apoptosis significantly. The suppression was in both time-dependent and dose-dependent manner. Marked morphological changes of cell apoptosis including condensation of chromatin and nuclear fragmentation were observed clearly by Wright's stain especially after the cells were treated 48-60 h by oridonin. The expression of hTERT mRNA as well as activity of telomerase were decreased concurrently by treatment with oridonin in HL-60 cells. Oridonin can downregulate the hTERT mRNA expression and decrease the telomerase activity of HL-60 cells; it has apparent antiproliferation and apoptosis-inducing effects on HL-60 cells in vitro.

Inhibitory Effect of Oridonin on the Proliferation of NB4 Cells and Its Mechanism

To investigate the anti-proliferation effect of oridonin on leukemic NB4 cells and its mechanism. NB4 cells in culture medium in vitro were given different concentrations of oridonin. The inhibitory rate of the cells were measured by MTT assay, cell apoptotic rate was detected by flow cytometry (FCM), morphology of cell apoptosis was observed by hoechst 33258 fluorescence staining, and the activity of telomerase was detected using TRAP-PCR-ELISA before and after apoptosis occurred. Oridonin (over 8 μmol/L) could decrease the telomerase activity, inhibit the growth of NB4 cells and induce apoptosis significantly in a time- and dose-dependent manner. Marked morphological changes of cell apoptosis were observed by hoechst 33258 fluorescence staining especially after the cells treated by oridonin for 48—60 h. Oridonin could inhibit the proliferation and induce the apoptosis of NB4 cells in vitro. One of the mechanisms may be the decrease of the telomerase activity of NB4 cells.