EFFECT OF EPIGALLOCATECHIN-3-GALLATE ON THE FORMATION OF REACTIVE OXYGEN AND NITROGEN SPECIES IN PERIODONTAL SOFT TISSUES AFTER EXPERIMENTAL TRAUMATIC BRAIN INJURY

Traumatic brain injury (TBI) is accompanied by the development of systemic pathophysiological alterations, among which oxidative and nitrosative stress play a key role, leading to damage of peripheral tissues, including the periodontium. A promising approach to correcting these disturbances involves the use of natural polyphenols, particularly epigallocatechin-3-gallate (EGCG), which is capable of modulating redox-sensitive signaling pathways. The aim of this study was to investigate the effect of EGCG on the formation of reactive oxygen and nitrogen species in periodontal soft tissues of rats following experimental traumatic brain injury. The study was conducted on Wistar rats (n = 21), divided into three groups: control (sham-injured animals), animals with experimental TBI, and animals with TBI treated with EGCG (1 mg/kg) administered intraperitoneally for 7 days. The production of the superoxide anion radical, nitric oxide synthase (NOS) activity and its isoforms, the coupling index of constitutive NOS (cNOS), and peroxynitrite levels were evaluated. It was found that TBI was associated with a significant increase in superoxide anion production and activation of nitrosative stress, as evidenced by increased total NOS activity and inducible NOS (iNOS), decreased cNOS activity and its coupling index, and accumulation of peroxynitrite. Administration of EGCG resulted in a significant reduction in superoxide production by mitochondria (–21.9%) and leukocyte NADPH oxidase (–20.1%), decreased total NOS activity (–33.5%) and iNOS (–41.6%), increased cNOS activity (+61.7%) and restoration of its coupling (+83.9%), as well as reduced peroxynitrite levels (–22.4%). Conclusions. Under experimental conditions, EGCG administration normalizes key parameters of the nitric oxide system in periodontal soft tissues, as evidenced by decreased total and inducible NOS activity, increased cNOS activity with restoration of its coupling, and reduced peroxynitrite levels, indicating attenuation of nitrosative stress. These findings suggest that EGCG contributes to the restoration of redox homeostasis in periodontal tissues following TBI, likely through modulation of redox-sensitive signaling pathways, including activation of the Nrf2/ARE pathway and inhibition of NF-κB–mediated inflammatory responses.