Ｏｂｊｅｃｔｉｖｅ　To explore the protective effect and the mechanism of microRNA (miRNA)-30c-2-3p on anoxia/reoxygenation injury in rat cardiomyocytes.　Methods　After being cultured for 72 h, the newborn rat (SPF) cadiomyocytes seeded in 6-well plates at a density of 5×105 cells/ml were randomly divided into 3 groups according to a random number table (n=72, when detected each items, 6 wells per group, repeated 3 times): control group (Sham group), anoxia/reoxygenation group (AR group) and anoxia preconditioning group (PAR group). The cells in Sham group were cultured in a normal way while the cells in AR group were cultured in anoxia condition for 3 h followed by 6 h reoxygenation. The cells in PAR group were cultured in anoxia condition for 30 min followed by 30 min reoxygenation before AR (anoxia for 3 h by reoxygenation 6 h). Then lactate dehydrogenase (LDH) release rate was detected by colorimetric method. The cardiomyocyte apoptosis was detected by the dead cell apoptosis kit with Annexin V/propidine iodide (Annexin V/PI). The expression of miRNA-30c-2-3p and X-box binding protein-1(XBP1) mRNA were detected by real-time polymerase chain reaction (PCR) while the expression of XBP1s(during endoplasmic reticulum stress, XBP1 is cleaved and translated to form the transcripition factor XBP1) and binding immunoglobulin protein(BiP) proteins were detected by Western blot. The dura luciferase report gene detection was done to measure a direct interaction between miRNA-30c-2-3p and XBP1.　Results　Compared to Sham group, the LDH release rate, the proportion of apoptosis cells, the expression of miRNA-30c-2-3p, XBP1mRNA,XBP1s and BiP proteins were significantly increased in AR and PAR groups (P<0.05). Moreover, compared with AR group, LDH leakage rate, the rate of apoptosis cells and the expression of miRNA-30c-2-3p were significantly reduced(P<0.05). The expression of XBP1 mRNA, XBP1s and BiP proteins were increased in PAR group (P<0.05). The result of dura luciferase report gene detection showed XBP1 was a target gene of miRNA-30c-2-3p.　Conclusions　The anoxia preconditioning results in cardio protection by inhibiting miRNA-30c-2-3p and increasing XBP1. Alleviating the injury induced by anoxia/reoxygenation, BiP maybe one of the XBP1 downstream factors to protect cardiomyocytes from apoptosis.