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Beneficial Effects Of Hydrogen Inhalation on Inflammation

Anti-inflammatory Effect

Inflammation is considered as an adaptive response of the body caused by infection of foreign pathogens or tissue damage, which can cause the aggregation of local neutrophils, monocytes, and other immune cells and release inflammatory cytokines. This process is manifested as lymphocytes and mononuclear phagocytes migrating from veins to the site of injury tissue and getting activated and differentiated into macrophages, in which phagocytes are the main source of growth factors and cytokines.

In addition, excess intracellular ROS can activate inflammatory transcription factors, such as nuclear factor radicals, and initiate apoptosis (cell death). Therefore, in the whole pathological process of oxidative stress, inflammation, cell damage, and apoptosis accompany each other and are mutually influenced.

At the early stage of inflammation, H2 can reduce the infiltration of neutrophils and macrophages by down-regulating the expression of intercellular adhesion molecules and chemokines, such as early proinflammatory cytokines, subsequently decreasing the inflammatory cytokines found that H2-rich saline inhibited the activation of crucial inflammatory signaling pathway and reduced serum levels, thus alleviating the airway inflammatory response caused by a burn. In addition, H2 can significantly reduce the expression of NF-κB in liver injury, hematencephalon, and skeletal muscle injury caused by acute sports, suggesting that molecular hydrogen can affect the inflammatory process by regulating nuclear transcription factors and downstream pro-inflammatory cytokines. Besides, for the treatment of diseases of inflammation dysfunction, the balance between anti-inflammation and pro-inflammation should be emphasized. H2 also displays an anti-inflammatory effect in cerebral injury or by up-regulating regulatory T cells, which exerts the immunosuppressive function and inhibits the expression of NF-κB.

Heme oxygenase-1 belongs to the heat-shock protein family, which is a rate-limiting microsomal enzyme involved in heme catabolism. The product, biliverdin, is rapidly reduced to bilirubin, a potent endogenous antioxidant. It could suppress the expression of IL-1β and NF-κB, limiting septic injury. Studies have demonstrated that H2 administration increased the HO-1 expression and the number of anti-inflammatory cytokines, IL-10, in human umbilical vein endothelial cells stimulated by LPS and lung tissue. Similarly, they found that pre-inhalation of H2 could prevent acute pancreatitis effectively by enhancing the expression of Hsp60 protein, a heat stress protein, that stimulated synthesis by high temperature to protect itself, in the early stage. Therefore, they believe that H2 can mobilize the body's defense response to play a prominent role in anti-inflammation.

Regulating Cell Death


Apoptosis is a type of programmed cell death characterized by cell atrophy, apoptotic body formation, and chromatin condensation. The result is clearing cells from the body and minimizing the damage to surrounding tissues, which plays a pivotal role in normal cell turnover and tissue homeostasis. Apoptosis can be induced by both intrinsic and extrinsic signals. The extrinsic apoptotic pathway is initiated by the death receptors on the cell surface, which interact with the tumor necrosis factor receptor and Fas, resulting in the activation of the downstream and subsequent apoptosis. The intrinsic apoptotic pathway is closely related to the antiapoptotic B-cell lymphoma 2 (Bcl-2) and proapoptotic Bax proteins. Both apoptotic pathways converge at a common end-point, leading to caspase-3 activation and DNA fragmentation. H2 may exert antiapoptotic effect through scavenging ROS or regulation of gene transcription, which may regulate endogenous apoptosis.


Autophagy can maintain the energy balance by degrading macromolecular substances, but excessive autophagy will aggravate the inflammation and damage of tissues and organs, such as in sepsis. Autophagy-related proteins play a pivotal role in autophagy detection, including light chain 3 protein. H2 saturated water significantly reduced the expression of autophagy-related proteins LC3 and Beclin-1 in LPS-induced lung injury, suggesting that H2 protected tissues from excessive autophagy. However, H2 could alleviate LPS-induced neuroinflammation by reducing the expression of mTOR in glial cells, increasing the LC3 II/LC3 I ratio, and promoting autophagy. This may be related to different severity of LPS-induced inflammation models.

In conclusion, they deemed that H2 has a bidirectional regulatory effect on autophagy when autophagy is hyperactivated during inflammation or/and can protect cells and tissues from damage.


Pyrolysis is a programmed death pathway of pro-inflammatory cells that protects monocytes, macrophages, and other invading pathogens. Although pyrolysis is usually beneficial to the host, excessive pyrolysis can lead to sepsis and septic shock. Caspase-1 is a vital factor in the activation of pyrolysis, and cytokines, are the main downstream inflammatory factors in the pyrolysis pathway.

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