关键词: 胱硫醚β合成酶, 自噬相关蛋白5, 巯基化, 细胞自噬, 阿尔茨海默病

Abstract: Objective To explore the effect of CBS on Alzheimer's disease and its mechanism. Methods Western blot was used to detect the over-expression of CBS and its effect on amyloid precursor protein (APP), LC3 and P62. The effect of CBS on Aβ1-42 in cell supernatant was detected by ELISA. The formation of H2S was detected by methylene blue method; The sulfhydration of ATG5 by H2S was verified by biotin conversion experiment and Western blot experiment. CBS was overexpressed in mice by injection of plasmid into the lateral ventricle; Y-maze test was used to verify the effect of CBS on learning and memory ability in mice. Results CBS decreased the level of Aβ1-42 in the cell supernatant (P<0.05) and inhibited the expression of APP (P<0.05); CBS promoted the formation of H2S (P<0.01); CBS promotes sulfhydration of ATG5; CBS promoted the expression of LC3 and inhibited the expression of P62, CBS promoted the level of autophagy; CBS promotes learning and memory ability of Alzheimer's disease model mice (P<0.05). Conclusions CBS promotes the sulfhydration of cysteine at position 19 of ATG5 by promoting the formation of hydrogen sulfide, thereby promoting autophagy and alleviating Alzheimer's disease.

Key words: CBS, ATG5, sulfhydration, autophagy, Alzheimer's disease