Monocytes and macrophages are crucial elements of the immune system, having various roles in tissue balance, inflammation, and conditions like stroke. They exhibit significant functional diversity, particularly evident in the M1 and M2 phenotypes and their marker characteristics. The functions of monocytes and macrophages are crucial in stroke studies, notably those related to intracerebral hemorrhage (ICH). ICH is the most severe type of stroke, characterized by inflammation, oxidative stress, and neuronal death, significantly increasing patient mortality and morbidity. Monocytes and macrophages play key roles in the inflammatory processes following ICH, participating in hematoma clearance and tissue repair. Despite their potential dual roles in the pathophysiology of ICH, involving both harmful and protective effects, the specific mechanisms remain to be further elucidated. This review summarizes the latest research progress on monocyte and macrophage subsets, with a particular focus on their contributions to ICH. It covers the relationships and differences between monocytes and macrophages, the functional diversity of macrophages, cell phenotypes and functions, regulatory mediators, gene expression and transcriptome analysis, and the clinical prognosis associated with blood monocyte counts. These research advancements aim to provide new insights for improving the diagnosis and treatment strategies for ICH.

The cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB) is associated with multiple signaling pathways. The signaling pathways leading to epilepsy have been extensively studied and include the Ca²⁺/CaMKiV/CREB pathway, the MAPK/CREB pathway, and the PI3K/Akt/CREB pathway. The regulation of transcription in cells requires CREB phosphorylation and dephosphorylation. Based on a review of the relevant literature, we found that increasing evidence demonstrates that drug-resistant epilepsy might be closely related to the upregulation and phosphorylation of CREB. Previous studies have shown that the mechanisms of epileptogenesis are associated with the over-excitability and sudden synchronous discharge of neurons. In turn, we have learned that inflammation produces proinflammatory factors that damage the blood–brain barrier and activate microglia (MG) and astrocytes (AS). Activated MG and AS not only play neuroprotective roles, but also cause neuroinflammation, which in turn damages nerve cells through CREB-related signaling pathways, leading to reduced effectiveness of antiepileptic drugs and, ultimately, to drug resistance in patients with epilepsy. Therefore, we hypothesized that the formation of drug-resistant epilepsy is related to the regulation of CREB activation or phosphorylation in glial cells activated by chronic inflammation.