【Abstract】 Objective To investigate the role of protein kinase C (Protein kinase C,PKC) and mitochondrial KATP (mito ATP-sensetive potassium channel ,mKATP) channels in 0.5MAC sevoflurane (1.15%) pretreatment preventing intestinal ischemia-reperfusion injury in rats. Materials and Methods 45 rats were randomly divided into five groups (n = 9): ① sham-operated group (Sham group); ② The intestinal ischemia-reperfusion group (II/R group); ③ 0.5MAC sevoflurane preconditioning group (APC group); ④ PKC nonspecific blocker Chelerythrine group (CHE group): Intraperitoneally inject CHE 5mg/kg 15min before 0.5MAC sevoflurane pretreatment; ⑤ mKATP channel blocker 5-Hydroxydecanoic group (5HD group): Intraperitoneally inject 5-HD 10mg/kg 15min before 0.5MAC sevoflurane pretreatment. Clip three pieces of intestinal tissue when reperfusion happened 120min to make HE staining tissue sections, observed the degree of pathological changes of its structure by improved Chiu's scale in the microscope, the expression of Caspase-3 activation was observed in the light microscope, and expression changes of Bcl-2 and Caspase-3 activation protein in intestinal tissues was detected by Western blot method. Results Chiu's pathological score of APC group（4.04±1.31） was significantly lower than that of II/R group（6.71±1.06）, CHE（6.84±1.07） and 5HD group （5.78±1.16）(P<0.01), the latter three groups showed no significant difference (P>0.05). Compared with Sham group, Bcl-2 and Caspase-3 expression levels of the other four groups were significantly increased (P<0.01). Compared with APC group, Bcl-2 expression levels of the CHE Group, 5HD group and II/R group were significantly decreased (P<0.05). Compared with Sham group, Caspase-3 expression levels of the other four groups significantly increased (P<0.01), the increased range of APC group is significantly less than CHE group, the 5HD group II/R group (P<0.01), the latter three groups showed no significant difference (P>0.05). Conclusion 0.5MAC sevoflurane pretreatment can protect agaist the intestinal IRI through the activeation of PKC and mKATP channel.