OBJECTIVETo research the effect of Jianpi Jiedu decoction (JPJDT) to PTEN/ERK1 of athymic mice with hepatocellular carcinoma.

METHODN2 male BALB/c athymic mice models were built by Bel-7402 with an indirect method. After 24 h of postoperation, the 90 athymic mice were distributed randomly into JPJDT groups: A, B, C, D, E, F, G, NS, FT each group had 10 athymic mice. Another 10 male BALB/c athymic mice without HCC was treated by NS as normal control (DZ). Group A to G were treated by intragastric administration with JPJDT that had been deliquated into 7 kinds of density for 8 wk. Group NS were were treated by intragastric administration with Sodium Chloride for 8 wk. Group FT were were treated by intragastric administration with FT207 (tegafur) for 8 wk . At last, athymic mice were sacrificed. PTEN/ERK1 was detected in hepatic tissue, latero-cancer tissue and cancer tissue by immunohistochemistry (PowerVision two-step histostaining reagent).

RESULTThe expression intensity of PTEN: The result showed that the intensity of PTEN in the normal hepatic tissue was the highest, and then latero-cancer tissue, the lowest was cancer tissue. In the normal hepatic tissue, the intensity of PTEN in Group B, D, E was higher than the Group NS, Group FT, Group DZ (P < 0.05). In the latero-cancer tissue, the intensity of PTEN in Group D was higher than the Group NS (P < 0.05). In the cancer tissue, the intensity of PTEN in Group JPJDT was higher than the Group NS and Group FT (P < 0.05). The expression intensity of ERK1: The result showed that the intensity of PTEN in the cancer tissue was the highest, and then latero-cancer tissue, the lowest was normal hepatic tissue. In the latero-cancer tissue, the intensity of ERK1 in Group FT was higher than the Group NS and Group JPJDT (P < 0.05). In the cancer tissue, the intensity of PTEN in Group NS and Group FT was higher than the Group C, D, E, G, F (P < 0.05). The correlation between PTEN and ERK1: The result showed that there was inverse correlation between the expression intensity of PTEN and ERK1 in the cancer tissue (P < 0.01).

CONCLUSIONOne of mechanism of antitumous effect of JPJDT maybe up-regulate anti-oncogene PTEN, restrain the signal way of ERK1, suppress the proliferation of hepatoma carcinoma cell. The carcinogenesis of primary hepatic carcinoma may exist the deletion of PTEN. Owing to low expression or deletion of PTEN in the cancer tissue, ERK1 signal transduction pathway cannot be actively suppressed which was activated by carcinogenic factor. So hepatoma carcinoma cell multiplicated.