RB1 and ischemia: With the depletion of poly (A) tail, the protective effect of BBR on RB1 mRNA from degradation in the process of ischemia/reperfusion was also abolished, supporting the conclusion that the antagonist effect of BBR on Rb down-regulation in ischemia/reperfusion was due to its direct binding to the poly (A) tail of RB1 mRNA, which effectively stabilized the mRNA in this pathogenic process.