Objective To investigate the effect and mechanism of oetreotide (OCT) on DENA related hepatoeareinogenesis in rats. Methods Fresh diethylnitrosamine (DENA) solution was given to induce the model of rat hepatoeellular carcinoma. The rats were divided randomly into two groups: OCT treatment group and control group. The survival rate and hepatoeareinogenesis rate were observed. SSTR2 mRNA and protein expression were measured. Results The survival rote of OCT treatment group (70.0%, 7/10) was significantly higher than that of control group (30.0%, 6/20) (X2 = 4.344, P<0.05). 16 weeks after DENA treatment, the difference of bepatoearcinogenesis rate between the two groups was not remarkable though the value of OCT treatment group (0%, 0/10) was lower than that of control groups (30.0%, 6/20)(X2 = 3.750, P＞0.05). However, 22 weeks after DENA treatment, hepatoeareinogenesis in control group (83.3%, 10/12) was markedly higher than that in OCT treatment group (22.2% , 2/9)(X2 =7.843, P<0.01). With liver cirrhosis progressing, the expressions of SSTR2 mRNA and protein increased, and reached the peak 16 weeks after DENA treatment, then began to decrease. The expressions of SSTR2 mRNA and protein in hepatocellular carcinoma were significantly lower than those in the liver 22 weeks after DENA treatment (F = 35.010 and 13. 386, P<0.01). The expression levels in OCT treatment group were similar to those in control group 8 and 16 weeks after DENA treatment. But the expression levels in OCT group 22 weeks after DENA treatment didn't lower markedly, and were higher significantly than those in control group (t = 2.806 and 4.498, P<0.05). Conclusion OCT can inhibit efficiently hepatocareinogenesis and reduce the mortality of rots treated with DENA possibly by a mechanism maintaining the expression levels of SSTR2.