Thymosin α1 Protects Dental Pulp Cells and Alleviates Pulpitis by Inhibiting Ferroptosis

Pulpitis, an inflammatory condition of the dental pulp, is a common cause of toothache and can lead to irreversible damage, often requiring root canal treatment or extraction. The underlying mechanisms of dental pulp cell death during inflammation are not fully understood, but ferroptosis (a distinct form of iron-dependent programmed cell death) has emerged as a potential contributor. This study addresses the critical knowledge gap regarding novel therapeutic strategies that specifically target ferroptosis to mitigate pulpitis. Current treatments primarily focus on symptom management and infection control, leaving a need for therapies that directly protect pulp vitality.

The study found that Thymosin α1 treatment led to a significant alleviation of pulpitis symptoms and a marked reduction in inflammatory cell infiltration in the animal model compared to the control group. In vitro, Thymosin α1 robustly protected dental pulp cells from inflammation-induced ferroptosis, demonstrating a substantial increase in cell viability and a dramatic decrease in cell death markers. Specifically, the peptide significantly reduced levels of lipid peroxidation (a hallmark of ferroptosis) and intracellular iron accumulation. The most critical finding is that Thymosin α1 directly inhibits ferroptosis in dental pulp cells, thereby preventing tissue damage and inflammation associated with pulpitis through a novel mechanism.