甘草甜素抑制致癌过程中对DNA损伤修复的影响

PROTECTIVE EFFECT OF GLYCYRRHIZIN ON DNA REPALR DURING ITS INHIBITION ON DEN-INDUCED HEPATOCARCINOGENESIS

本文检测外周淋巴细胞非程序ＤＮＡ合成（ＵＤＳ），探讨甘草甜素（ＧＬ）在抑制二乙基亚硝胺（ＤＥＮ）致肝癌前病变发生过程中，对ＤＮＡ损伤修复的影响。结果显示；大鼠腹腔注射ＤＥＮ(１００ｍｇ／ｋｇ）后５小时，ＵＤＳ值（１６８．５±３６．５ｃｐｍ／５×１０５ＬＣ）显著低于正常大鼠（２２６．７±４７．０）（Ｐ＜０．０５）；在加用ＧＬ的影响下，ＵＤＳ值（２１２．３±６９．２）显著提高，与正常者相接近（Ｐ＞０．０５）。在注射ＤＥＮ后４周，肝癌前病变的发生受到ＧＬ抑制，同时ＵＤＳ值（５０１．０±１４０．０）也显著高于不用ＧＬ者（３６７．０±３６．３）（Ｐ ＜０．０１），而与正常者（６０６．８±８３．８５）无明显差别(Ｐ＞０．０５）。提示ＧＬ抑制ＤＥＮ致肝癌作用与ＧＬ保护ＤＮＡ损伤修复有关。

By using unscheduled DNA synthesis(UDS) of peripheral lympho- cytes(LC), the effect of glycyrrhirin(GL) on DNA repair was investigated during the inhi bition of GL on DEN-induced hepatocarcinogenesis in rats. Results; At the 5th hour after DEN exposure(i.p. 100mg/kg), the UDS yalue(168.5± 36.5 cpm/5x 105LC) was much lower than that of normal control rats(226.7± 47.0)(p<0.05). By pretreated with GL, the UDS level increased significantly in the DEN+ GL group(212.7±69.2)(p <0.05) and showed no remarkable difference with normal controls(p>0.05). At the 4th week after DEN injec- tion, the occurrence of precancerous lesion in the liver was inhibited by GL. The UDS level of DEN+GL group(501.0±140.0) was much higher than that of DEN alone group (367.0±86.8)(p<0.01) and similar to the normal controls(606.8±83.85)(p>0.05). These results revealed that the inhibitory action of GL on the DEN-induced hepato-carcinoge- nesis correlated well with the protective effect of GL on the DNA damage and/or repair, suggesting that an increased efficiency of DNA repair by GL may play an important role in the inhibition of GL on hopatocarcinogenesis.