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Abstract The growth of digital financial inclusion has provided new ways of providing financial services in rural areas, greatly affecting the quality of life and health of rural residents. Using data from the China Household Finance Survey, we examine how digital financial inclusion (DFI) impacts the health of rural residents. The results show that DFI can enhance residents' health. Notably, DFI positively impacts the health of rural residents by promoting commercial insurance, improving medical conditions, and enhancing agricultural production efficiency. Additionally, DFI has a more significant effect on improving the health of low-income residents and those in less-developed areas. This research provides compelling evidence to substantiate the assertion that DFI contributes to enhancing the health of rural residents. It offers empirical support and a basis for decision-making to realize the health benefits of digital financial inclusion.

Background: Hypoxia-induced M1 polarization of microglia and resultant inflammation take part in the damage caused by hypoxic-ischemic encephalopathy (HIE). Histone lactylation, a novel epigenetic modification where lactate is added to lysine residues, may play a role in HIE pathogenesis. This study investigates the role of histone lactylation in hypoxia-induced M1 microglial polarization and inflammation, aiming to provide insights for HIE treatment. Methods: In this study, we assessed the effects of hypoxia on microglial polarization using both an HIE animal model and an oxygen–glucose deprivation cell model. Histone lactylation at various lysine residues was detected by Western blotting. Microglial polarization and inflammatory cytokines were analyzed by immunofluorescence, qPCR, and Western blotting. RNA sequencing, ChIP-qPCR, and siRNA were used to elucidate mechanisms of H3K9 lactylation. Results: H3K9 lactylation increased due to cytoplasmic lactate during M1 polarization. Inhibiting P300 or reducing lactate dehydrogenase A expression decreased H3K9 lactylation, suppressing M1 polarization. Transcriptomic analysis indicated that H3K9 lactylation regulated M1 polarization via the TNF signaling pathway. ChIP-qPCR confirmed H3K9 lactylation enrichment at the TNFα locus, promoting OGD-induced M1 polarization and inflammation. Conclusions: H3K9 lactylation promotes M1 polarization and inflammation via the TNF pathway, identifying it as a potential therapeutic target for neonatal HIE.