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AIM:To explore the inhibition of conjugated linoleic acidisomers in different purity(75% purity c9,t11-,98% purityc9,t11-and 98% purity t10,c12-CLA)on the formation offorestomach neoplasm and cheopreventive mechanisms.METHODS:Forestomach neoplasm model induced by B(a)P in KunMing mice was established.The numbers of tumorand diameter of each tumor in forestomach were counted;the mice plasma malondialdehyde(MDA)were measuredby TBARS assay;TUNEL assay was used to analyze theapoptosis in forestomach neoplasia and the expression ofMEK-1,ERK-1,MKP-1 protein in forestomach neoplasm werestudied by Western Blotting assay.RESULTS:The incidence of neoplasm in B(a)P group,75 %purity c9,t11-CLA group,98 % purity c9,t11-CLA groupand 98% purity tl0,c12-CLA group was 100 %,75.0 %(P>0.05),69.2%(P<0.05)and 53.8%(P<0.05)respectivelyand the effect of two CLA isomers in 98% purity onforestomach neoplasia was significant;CLA showed noinfluence on the average tumor numbers in tumor-bearingmouse,but significantly decreased the tumor size,the tumoraverage diameter of mice in 75% purity c9,t11-CLA group,98% purity c9,t11-CLA group and 98 % purity U0,c12-CLAgroup was 0.157±0.047 cm,0.127±0.038 cm and 0.128±0.077 cm(P<0.05)and 0.216±0.088 cm in B(a)P group;CLA could also significantly increase the apoptosis cellnumbers by 144.00±20.31,153.75±23.25,157.25±15.95(P<0.05)in 75% purity c9,t11-CLA group,98% purity c9,t11-CLA group and 98% purity t10,c12-CLA group(30.88±3.72 in BP group);but there were no significant differencesbetween the effects of 75 % purity c9,t11-CLA and twoisomers in 98% purity on tumor size and apoptotic cellnumbers;the plasma levels of MDA in were increased by75 % purity c9,t11-CLA,98 % purity c9,t11-CLA and 98 %purity t10,c12-CLA.The 75% purity c9,t11-CLA showedstronger inhibition;CLA could also inhibit the expression ofERK-1 protein and promote the expression of MKP-1 protein,however no influence of CLA on MEK-1 protein was observed.CONCLUSION:Two isomers in 98% purity show strongerinhibition on carcinogenesis.However,the inhibitory mechanisms of CLA on carcinogenesis is complicated,whichmay be due to the increased mice plasma MDA,the inducingapoptosis in tumor tissues.And the effect of CLA on theexpression of ERK-1 and MKP-1 may be one of themechanisms of the inhibition of CLA on the tumor.
AIM: To explore the inhibition of conjugated linoleic acid isomers in different purity (75% purity c9, t11-, 98% purity c9, t11-and 98% purity t10, c12-CLA) on the formation of forepart neoplasm and cheopreventive mechanisms. METHODS: Forestomach neoplasm model induced by B (a) P in KunMing mice was established. The numbers of tumorand diameter of each tumor in forestomach were counted; the mice plasma malondialdehyde (MDA) were measured by TBARS assay; TUNEL assay was used to analyze theapoptosis in forestomach neoplasia and the expression ofMEK-1, ERK-1, MKP-1 protein in forestomach neoplasm were studied by Western Blotting assay.RESULTS: The incidence of neoplasm in B (a) P group, 75% purity c9, t11-CLA group, 98% purity c9, t11-CLA group and 98% purity tl0, c12-CLA group was 100%, 75.0% (P> 0.05), 69.2% in 98% purity onforestomach neoplasia was significant; CLA showed no affect on the average tumor numbers in tumor-bearing mouse, but significa The tumor volume, the tumoraverage diameter of mice in 75% purity c9, t11-CLA group, 98% purity c9, t11-CLA group and 98% purity U0, c12- CLAgroup was 0.157 ± 0.047 cm, 0.127 ± 0.038 cm P could also significantly increase the apoptosis cell numbers by 144.00 ± 20.31,153.75 ± 23.25,157.25 ± 15.95 (P <0.05) in 75 (P <0.05) and 0.216 ± 0.088 cm in B % purity c9, t11-CLA group, 98% purity c9, t11-CLA group and 98% purity t10, c12-CLA group (30.88 ± 3.72 in BP group); but there were no significant differences between the effects of 75% purity c9 , t11-CLA and twoisomers in 98% purity on tumor size and apoptotic cell nuclei; the plasma levels of MDA in were increased by 75% purity c9, t11-CLA, 98% purity c9, t11-CLA and 98% purity t10, c12- CLA. 75% purity c9, t11-CLA showedstronger inhibition; CLA could also inhibit the expression ofERK-1 protein and promote the expression of MKP-1 protein, however no influence of CLA on MEK-1 protein was observed. isomers in 98% pu rity shOf stronger inhibitory on carcinogenesis. Of the inhibitory mechanisms of CLA on carcinogenesis is yet complicated, which may be due to the increased mice plasma MDA, the inducingapoptosis in tumor tissues. And the effect of CLA on the expression of ERK-1 and MKP-1 may be one of themechanisms of the inhibition of CLA on the tumor.