Magic™ Anti-8-OHdG monoclonal antibody, clone O56.2

We aimed to investigate the effects of photobiomodulation (PBM) on periodontitis. A periodontitis model was established via Porphyromonas gingivalis infection in beagles. Mandibular second and third premolars were removed, and implants were positioned immediately after tooth extraction. Left gingiva was irradiated with PBM (450 nm) as the LG group, and right side without irradiation was regarded as the CG (control) group. PBM treatment increased oxidative stress by increasing the levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS). The elevated levels of H2O2 (a biomarker of oxidative stress) and the free radicals (NO center dot and O-2(center dot-)) reduced the concentration of dominant pathogens and regulated ROS/RNS/AMP-activated protein kinase (AMPK)/mTOR pathway by affecting p-AMPK, Runt-related transcription factor 2 (RUNX2), p-c-Jun N-terminal kinase (JNK)/mammalian target of rapamycin (mTOR), and acetyl-CoA carboxylase 1 (ACC1). PBM therapy increased salivary levels of interleukin-1 receptor antagonist (IL-1ra), interleukin (IL)-10, total antioxidant capacity (TAC) and catalase (CAT), and reduced the levels of tumor necrosis factor (TNF)alpha terleukin (IL)-1 beta, malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) (p < 0.05). All the results contributed to preventing periodontitis infection. PBM therapy improved bone mineral density and implant osseointegration by controlling dominant pathogens invasion via the upregulation of salivary anti-inflammatory and antioxidant defense by affecting ROS/RNS/AMPK/mTOR signaling pathway.

Lung ischemia-reperfusion injury (LIRI) is a common clinical concern. As the injury occurs, the pulmonary afferent nerves play a key role in regulating respiratory functions under pathophysiological conditions. The present study was to examine the effects of inhibiting microRNA-155 on the levels of proinflammatory cytokines and products of oxidative stress in the pulmonary vagal afferent nerves and the commissural nucleus of the solitary tract (cNTS) after LIRI. A rat model of LIRI was used. ELISA method was employed to examine proinflammatory cytokines, namely, IL-1 beta, IL-6 and TNF-alpha; and key biomarkers of oxidative stress, 8-isoprostaglandin F2 alpha (8-iso PGF2 alpha) and 8-hydroxy-2 '-deoxyguanosine (8-OHdG). In results, in the process of LIRI, the levels of microRNA-155 were amplified in the vagal afferent nerves and cNTS, and this was accompanied with increases of IL-1 beta, IL-6 and TNF-alpha; and 8-iso PGF2 alpha and 8-OHdG. Application of microRNA-155 inhibitor, but not its scramble, attenuated the elevation of proinflammatory cytokines and amplification of 8-iso PGF2 alpha and 8-OHdG in those nerve tissues. In conclusion, we observed the abnormalities in the pulmonary afferent pathways at the levels of the peripheral nerves and brainstem, which is likely to affect respiratory functions as LIRI occurs. Our data suggest that blocking microRNA-155 signal pathways plays a beneficial role in regulating LIRI via inhibiting responses of neuroinflammation and oxidative stress signal pathways to LIRI.