Carnosine modulates Aβ-induced transcriptional aberrations in murine microglial cells.

Carnosine (β-alanyl-L-histidine) is an endogenous dipeptide known for its anti-inflammatory and antioxidant effects, making it a promising agent for neurodegenerative diseases like Alzheimer's disease (AD). Carnosine has shown protective effects against amyloid beta (Aβ)-induced oxidative stress and inflammation in murine microglial cells, yet its full immunomodulatory impact on these cells, particularly in terms of transcriptional regulation and cytokine interplay, remains underexplored. This study examined carnosine's effects on immune response markers in BV-2 cells exposed to Aβ oligomers. Specifically, gene expression changes in anti-inflammatory mediators (CXCL2 and IL-10) and phagocytic markers (CD11b, CD68, TNFα, IL-1β) were assessed. Notably, carnosine increased CXCL2 and IL-10 expression, promoting an anti-inflammatory response and enhancing microglial phagocytosis. Additionally, carnosine restored CX3CR1 expression, a receptor implicated in Aβ- effects in murine macrophages, and upregulated TGF-β1 and its receptor, supporting its neuroprotective role. These results underscore carnosine's potential to modulate immune responses, enhance microglial activity, and provide neuroprotection in Aβ-induced conditions. The findings highlight carnosine's therapeutic promise for AD treatment, offering a pathway for future research on its use in neurodegenerative disease interventions.