Objective:

2

To explore the therapeutic effect of naringin on colorectal cancer (CRC) and the related mechanism.

Methods:

2

Cell counting kit-8 (CCK-8) assay and annexin V-FITC/PI assay were used to detect the effect of naringin (50–400 μg/mL) on cell proliferation and apoptosis of CRC cells

respectively. The scratch wound assay and transwell migration assay were used to assess the effect of naringin on CRC cell migration. Four-week-old male nude mice were injected with HCT116 cells subcutaneously to establish the tumor xenograft model. Naringin was injected intraperitoneally at 50 mg/(kg•d)

with solvent and 5-fluorouracil treatment as control. The width and length of the tumors were measured and recorded every 6 days

and tumor tissues were photographed and weighed on the last day of the 24-d observation period. Immunohistochemical staining for caspase-3

proliferating cell nuclear antigen and TUNEL assay were used to evaluate the effect of naringin on cell proliferation and apoptosis in tumor tissues. The body weight

food and water intake of mice were recorded

and the major organs in different treatment groups were weighed on the last day and stained with hematoxylin and eosin for histological analysis. Meanwhile

the routine blood indicators were recorded.

Results:

2

CCK-8 and annexin V-FITC/PI results confirmed that naringin (100

200

and 400 μg/mL) could inhibit proliferation and promote apoptosis. The scratch wound assay and transwell migration assay results confirmed the inhibitory activity of naringin against CRC cells migration.

In vivo

results demonstrated the inhibitory effect of naringin on tumor growth with good bio-compatibility.

Conclusion:

2

Naringin inhibited colorectal carcinogenesis by inhibiting viability of CRC cells.