Molecular and Neuromuscular Responses to Hyperbaric Oxygen Therapy Following Tourniquet-Induced Ischemia-Reperfusion Injury

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Abstract
Tourniquet-induced ischemia-reperfusion injury (tourniquet/IR) causes oxidative stress, inflammation, neuromuscular junction (NMJ) dysfunction, and motor functional impair-ment. Although hyperbaric oxygen therapy (HBOT) exerts anti-inflammatory and antiox-idant effects, its impact on inflammatory and redox-associated pathways after tourni-quet/IR remains unclear. This study investigated the effects of HBOT on NMJ integrity, functional outcomes, skeletal muscle morphology, inflammatory and redox signaling in a mouse model of 3-hour unilateral hindlimb tourniquet followed by 1 or 2 weeks of tourni-quet release. Tourniquet/IR induced NMJ and skeletal muscle structural damage and func-tional impairment. Tourniquet/IR also increased protein expression of IL-1β, TNF-α, NOX2, p67-phox, and p47-phox, and decreased mitochondrial complex I-III expression, while tourniquet/IR did not change antioxidation demonstrated by Mn-SOD and Cu/Zn-SOD. HBOT improved NMJ and skeletal muscle function in the tourni-quet/IR-injured hindlimb, but it did not significantly affect tourniquet/IR-induced inflam-mation and oxidative stress. These findings demonstrate that HBOT mitigates tourni-quet/IR-induced skeletal muscle remodeling and neuromuscular dysfunction, and its ben-efits are not linked to the evaluated markers of inflammation or oxidative stress. A longer follow-up is needed to determine whether the early benefits of HBOT can translate into the sustained functional recovery of the NMJ and skeletal muscle, and to clarify the cellular and molecular mechanisms underlying HBOT-mediated functional recovery.

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