Effects of ursolic acid and oleanolic acid on human colon carcinoma cell line HCT15

来源 :World Journal of Gastroenterology | 被引量 : 0次 | 上传用户:lonlinyang
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AIM:Ursolic acid(UA)and oleanolic acid(OA)aretriperpene acids having a similar chemical structure and aredistributed wildly in plants all over the world.In recentyears,it was found that they had marked anti-tumor effects.There is little literature currently available regarding theireffects on colon carcinoma calls.The present study wasdesigned to investigate their inhibitory effects on humancolon carcinoma call line HCT15.METHODS:HCT15 calls were cultured with different drugs.The treated calls were stained with hematoxylin-eosin andtheir morphologic changes observed under a lightmicroscope.The cytotoxicity of these drugs was evaluatedby tetrazolium dye assay.Cell cycle analysis was performedby flow cytometry(FCM).Data were expressed as means±SEM and Analysis of variance and Student’ t-test forindividual comparisons.RESULTS:Twenty-four to 72 h after UA or OA 60 μmol/Ltreatment,the numbers of dead calls and call fragmentswere increased and most calls were dead at the 72 nd hour.The cytotoxicity of UA was stronger than that of OA.Seventy-eight hours after 50 μmol/L of UA or OA treatment,a number of calls were degenerated,but call fragments wererarely seen.The IC_(50)values for UA and OA were 30 and 60μmol/L,respectively.Proliferation assay showed thatproliferation of UA and OA-treated calls was slightlyincreased at 24 h and significantly decreased at 48 h and 60h,whereas untreated control calls maintained anexponential growth curve.Cell cycle analysis by FCMshowed HCT15 calls treated with UA 30 and OA 60 for 36 h and72 h gradually accumulated in G_0/G_1 phase(both drugs P<0.05 for 72 h),with a concomitant decrease of call populationsin S phase(both drugs P<0.01 for 72 h)and no detectableapoptotic fraction.CONCLUSION:UA and OA have significant anti-tumor activity.The effect of UA is stronger than that of OA.The possiblemechanism of action is that both drugs have an inhibitoryeffect on tumor call proliferation through call-cycle arrest. AIM: Ursolic acid (UA) and oleanolic acid (OA) aretriperpene acids having similar chemical structure and are distributed wildly in plants all over the world. Recentyears, it was found that they had marked anti-tumor effects. available regarding the effects of colon carcinoma calls. The present study was designed to investigate their inhibitory effects on human colon carcinoma call line HCT15.METHODS: HCT15 calls were cultured with different drugs. The treated calls were stained with hematoxylin-eosin and their morphologic changes observed under a light microscope . The cytotoxicity of these drugs was evaluated by tetrazolium dye assay. Cell cycle analysis was performed by flow cytometry (FCM). Data were expressed as mean ± SEM and Analysis of variance and Student ’t-test for independents comparisons .RESULTS: Twenty-four to 72 h after UA or OA 60 μmol / Ltreatment, the numbers of dead calls and call fragments were increased and most calls were dead at the 72 nd hour.The cyt otoxicity of UA was stronger than that of OA. Seventy-eight hours after 50 μmol / L of UA or OA treatment, a number of calls were degenerated, but call fragments wererarely seen. IC_ (50) values ​​for UA and OA were 30 and 60 μmol / L, respectively. Proliferation assay showed that profile of UA and OA-treated calls was slightly established at 24 h and significantly decreased at 48 h and 60 h, but untreated control calls maintained anexponential growth curve. Cell cycle analysis by FCMshowed HCT15 calls treated with UA 30 and OA 60 for 36 h and 72 h gradually accumulated in G_0 / G_1 phase (both drugs P <0.05 for 72 h), with a concomitant decrease of call populations in S phase (both drugs P <0.01 for 72 h) and no detectable apoptotic fraction.CONCLUSION: UA and OA have significant anti-tumor activity. The effect of UA is stronger than that of OA. The possible mechanism of action is that both drugs have an inhibitory effect on tumor call proliferation through call-cycle arrest.
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