Objective:To investigate the role of Kiwi essence in sensibilization of chemotherapeutics for allotransplantation tumors in mice with lung adenocarcinoma

and preliminarily discuss the related mechanism thereof. Method:Transplantation tumor models were established in mice with lung adenocarcinoma. 40 C57BL/6J mice bearing Lewis cells were randomized into five groups

n=8 in each group:normal group (normal saline)

K. essence group (K. essence 180 mg·kg-1)

chemotherapy group (cisplatin and gemcitabine)

60 mg·kg-1 K. essence combined with chemotherapy group

180 mg·kg-1 K. essence combined with chemotherapy group. After inoculated with adenocarcinoma cells for 4 days

corresponding drugs were given for intervention. Mice were sacrificed 20 days after tumor inoculation

and the subcutaneous tumors were stripped for histological examination. The expressions of excision repair cross-complementation groupl(ERCC1) and ribonucleotidereductase subunit M1(RRM1) for chemotherapy-related drug resistance genes were detected by Western blot assay and RT-PCR. Result:Compared with the normal group

the tumor growth of various drug intervention groups was inhibited significantly (P<0.05

P<0.01)

and the anti-tumor rate was 14.95%

41.77%

44.21%

59.68% respectively in various groups. Expression of ERCC1 gene was highest in normal group

and significantly decreased in various K. essence essence groups

with statistically significant difference (P<0.01). Expression of ERCC1 in K. essence groups and K. essence high dose+chemotherapy group was significantly lower than other groups(P<0.01)。ERCC1 mRNA expression and ERCC1 proteins expression were in consistency. Expression of RRM1 gene was highest in normal group

nd significantly decreased in various K. essence groups

with statistically significant difference (P<0.01

P<0.05). Expression of RRM1 in K. essence groups and K. essence high dose+chemotherapy group was significantly lower than other groups. Conclusion:K. essence could increase the ability of chemotherapeutics to inhibit tumor growth and transfer by reducing ERCC1 expression and increasing RRM1 expression.