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Fig. 5 | Molecular Medicine

Fig. 5

From: The α7 nicotinic acetylcholine receptor agonist, GTS-21, attenuates hyperoxia-induced acute inflammatory lung injury by alleviating the accumulation of HMGB1 in the airways and the circulation

Fig. 5

Suggested pathways of GTS-21-mediated attenuation of HALI. In cells, including lung cells, HMGB1 shuttles between the nucleus and cytoplasm. Under room air, the rate of HMGB1 nuclear import exceeds that of re-diffusion plus export. Thus, HMGB1 appears predominantly or solely in the nucleus. The prolonged exposure to hyperoxia induces HMGB1 translocation from the nucleus to the cytoplasm. The α7nAChR agonist, GTS-21, inhibits hyperoxia-induced translocation and subsequent release of nuclear HMGB1, and its accumulation in the airways and the circulation. As a result, GTS-21 is efficacious in attenuating hyperoxia-induced infiltration of leukocytes, including neutrophils and inflammatory monocytes, into the airways, thereby significantly reducing hyperoxia-induced inflammatory lung injury

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