Mechanistic investigation of the ameliorative effect of crocin on arsenic trioxide-induced HT22 nerve cells injury based on network pharmacology and in vitro validation

BACKGROUND: This study aims to explore the protective effect of crocin on arsenic trioxide (ATO)-induced HT22 nerve cell damage and its molecular mechanism. Preliminary predictions from network pharmacology indicate that the neuroprotective effect of crocin involves a wide range of areas, including the regulation of oxidative stress, inhibition of inflammation, and intervention in apoptosis. METHODS: ), oxidative stress level, cell apoptosis rate, reactive oxygen species (ROS) production, inflammatory factor expression level, and the expression levels of Nrf2/HO-1 pathway-related proteins. RESULTS: level, oxidative stress degree, cell apoptosis rate, ROS production, and inflammatory factor levels in HT22 nerve cells were significantly reduced; Crocin treatment could effectively regulate the expression levels of Nrf2/HO-1 pathway-related proteins. CONCLUSION: Crocin has a significant neuroprotective effect on ATO-induced HT22 nerve cell damage. Its mechanism may involve anti-oxidative stress, anti-cell apoptosis, and inhibition of inflammatory response, and this protective effect is likely achieved by activating the Nrf2/HO-1 signaling pathway.