We further found that Sirtinol, the Sirt1 inhibitor, reversed the protection of H2S against CRS-elicited oxdative stress, as evidenced by increase in MAD level and decreases in SOD activity and GSH level, ER stress, as evidenced by upregulation of GPR78, Chop and cleaved caspase-12 level, and apoptosis, as evidenced by increases in the number of Tunel positive cells and the expression of Bax as well as decrease in the expression of Bcl2 in the hippocampus of cotreatment with NaHS and CRS rats. This evidence concerns the gene SOD1 and congenital rubella syndrome.