Research on the Mechanism of LncMSTRG.5686.1/let‐7a‐5p Regulating Cognitive Function Alteration Induced by Neodymium Nitrate Exposure During Pregnancy and Lactation in Offspring Rats and Mediating Mitochondrial Apoptosis in SH‐SY5Y Cells

Long‐term exposure to rare earth elements has been shown to induce neurotoxicity; however, research on neurotoxicity during the early developmental stages is limited, and the underlying mechanisms remain poorly understood. This study investigated the effects of prenatal and lactational exposure to neodymium nitrate on hippocampal function in rat offspring. Through behavioral assessments, pathological staining methods, and analysis of apoptosis‐associated variables (Bax, Bcl‐2, Caspase‐3, and Cyt‐c) in the hippocampal tissue of the offspring, we elucidated the mechanisms underlying impaired learning and cognitive abilities. Furthermore, high‐throughput sequencing revealed the differential expression of long noncoding RNA gene LncMSTRG.5686.1 in the hippocampus of exposed offspring rats, providing insights into its regulatory role in hippocampal neuronal apoptosis following prenatal and lactational exposure to neodymium nitrate. In vitro experiments demonstrated a dose‐dependent upregulation of LncMSTRG.5686.1 expression in Nd (NO 3 ) 3 ‐treated SH‐SY5Y cells, accompanied by the induction of mitochondrial apoptosis. Fluorescence in situ hybridization localized LncMSTRG.5686.1 to the cytoplasm, suggesting its potential involvement in the competitive endogenous RNA network. Subsequent experiments revealed that LncMSTRG.5686.1 binds to and regulates let‐7a‐5p expression, which in turn modulates the mitochondrial apoptosis pathway in Nd (NO 3 ) 3 ‐treated SH‐SY5Y cells by competitive binding with LncMSTRG.5686.1.