[Anti-tumor effect of Inonotus obliquus extract on 4T1 tumor-bearing mice].

OBJECTIVE

To explore the antitumor effect of Inonotus obliquus extract on 4T1 tumor-bearing mice in vivo and its possible mechanism.

METHODS

4T1 tumor-bearing mice model was established. After successful modeling, tumor-bearing mice were randomly divided into model control group, cyclophosphamide(CTX) positive group, and high, medium and low dose groups of Inonotus obliquus extract, with 10 mice in each group, which were administered continuously for 21 days. The weight change, tumor weight, organ index, expression of cell cycle-related proteins CyclinB1, CyclinD1 and CDK4 in mice were detected, the tumor inhibition rate was calculated, and histopathological observation was made.

RESULTS

On the 5th day of tumor cells inoculation, nodules could be felt at the inoculation site in both model group and each dose group, indicating that the tumor cells were successfully inoculated. Compared with the model group, CTX and Inonotus obliquus extract could reduce the tumor weight of tumor-bearing mice, and the tumor inhibition rate was between 16.0% and 51.4%. Compared with model group, medium and high dose groups significantly inhibited the growth of tumors(P<0.05 or P<0.01), and the tumor inhibition rate gradually increased with the dose of Inonotus obliquus extract, indicating that the tumor inhibition effect of Inonotus obliquus extract has a dose-response relationship. Compared with the model group, Inonotus obliquus extract could significantly increase the spleen index(P<0.05). Pathological analysis showed that Inonotus obliquus extract could inhibit the proliferation of tumor cells and cause tumor cell necrosis in mice. Compared with the model group, Inonotus obliquus extract could significantly down-regulate the expression levels of CyclinB1, CyclinD1 and CDK4, and there was a certain dose-response relationship.

CONCLUSION

Inonotus obliquus extract can inhibit tumor growth to some extent, and the mechanism may be related to the inhibition of cyclin expression.