Distribution and anti-HBV effects of antisense oligodeoxynu-cleotides conjugated to galactosylated p

来源 :World Journal of Gastroenterology | 被引量 : 0次 | 上传用户:shlchen
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AIM:To describe distribution of the phosphorothioatedantisense oligodeoxynucleotides (PS-asODNs) conjugatedto galactosylated poly-L-lysine (GaI-PLL) in mice,and toobserve their effects on expression of HBV gene in the 2.2.15 cells and transgenic mice.METHODS:According to the result of direct sequencingof PCR amplified products,a 16 mer phosphorothioateanalogue of the antisense oligodeoxynucleotides (PS-asODNs) directed against the HBV Us-like region wasconjugated to the hepatotropic GaI-PLL molecules.Itsdistribution was demonstrated using asODNs labeled with~(32)p at the 5’ terminus with a T4-polynucleotide Kinase.Itsinhibition effect on HBV expression was observed in thetransfected 2.2.15 cells and transgenic mice.RESULTS:The GaI-PLL and asODNs could form stablecomplex at a molar ratio of 2:1.As shown in the HBV-transfected 2.2.15 cells,the inhibition effects of asODNsalone and asODNs conjugated to Gal-PLL,at 10 μmol/L forboth,on HBsAg and HBeAg production were different,theformer being 70 % and 58 %,respectively,and the latterbeing 96 % and 82 %,respectively.A more pronouncedreduction was also observed in viral DNA load in the culturesupernatant for the test with Gal-PLL-asODNs.Among manymouse organs,livers retained more asODNs molecules afteradministration.The preferential concentration in liver wasfound to be 52.14 % for GaI-PLL-asODNs,as high as 2.38-fold of that for asODNs (21.9%).Both elements decreasedgradually in liver,with 2.9 % of the former,5.99 % of thelatter retained 24 hours after the administration.Theinjection interval,therefore,was recommended to be24 hours.In the transgenic mice,serum HBsAg decreasedsignificantly (P<0.01) at the 12th day after administratingGaI-PLL- asODNs,the serum HBV DNA turned negative in4 of the 6 mice.CONCLUSION:Antisense oligodeoxynucleotidesconjugated to GaI-PLL can be concentrated in liver andintaked by hepatocytic cells.This may result in specificinhibition of expression and replication of HBV in vitroand in vivo. AIM: To describe distribution of the phosphorothioated antisense oligodeoxynucleotides (PS-asODNs) conjugated to galactosylated poly-L-lysine (GaI-PLL) in mice, and toobserve their effects on expression of HBV gene in the 2.2.15 cells and transgenic mice. METHODS: According to the result of direct sequencing of PCR amplified products, a 16 mer phosphorothioate analog of the antisense oligodeoxynucleotides (PS-asODNs) directed against the HBV Us-like region was conjugated to the hepatotropic GaI-PLL molecules. Itsdistribution was demonstrated using as 32) p at the 5 ’terminus with a T4-polynucleotide Kinase. Inhibitory effect on HBV expression was observed in the transfected 2.2.15 cells and transgenic mice .RESULTS: The GaI-PLL and asODNs could form stable complex at a molar ratio of 2: 1.As shown in the HBV-transfected 2.2.15 cells, the inhibition effects of asODNsalone and asODNs conjugated to Gal-PLL, at 10 μmol / L forboth, on HBsAg and HBeAg production were different, theformer be ing 70% and 58%, respectively, and the latter beings 96% and 82% respectively. A more pronouncedred was was also observed in viral DNA load in the cultures for test with Gal-PLL-asODNs. Among manymouse organs, livers retained more AsODNs molecules afteradministration. The preferential concentration in liver wasfound to be 52.14% for GaI-PLL-asODNs, as high as 2.38-fold of that for as ODNs (21.9%). Both elements decreasedgradually in liver, with 2.9% of the former, 5.99 % of thelatter was retained for 24 hours after the administration.Theinjection interval, therefore, was recommended to be24 hours.In the transgenic mice, serum HBsAg decreasedsignificantly (P <0.01) at the 12th day after administratingGaI-PLL-asODNs, the serum HBV DNA turned negative in 4 of the 6 mice. CONCLUSION: Antisense oligodeoxynucleotides conjugated to GaI-PLL can be concentrated in liver and inked by hepatocytic cells. This may result in specific inhibition and expression of HBV in vitro and in vivo.
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