H2 Protects Against Lipopolysaccharide-Induced Cardiac Dysfunction via Blocking TLR4-Mediated Cytokines Expression.

In The mRNA levels of ANP and BNP were examined by PCR in vitro, lPS induced cardiac dysfunction; hydrogen therapy improved cardiac function after LPS challenge. The authors concluded that implications: Hydrogen therapy prevents LPS-induced cardiac dysfunction in part via downregulation of TLR4-mediated pro-inflammatory cytokines expression. These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.

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Inhibitory Effects of Hydrogen on Proliferation and Migration of Vascular Smooth Muscle Cells via Down-Regulation of Mitogen/Activated Protein Kinase and Ezrin-Radixin-Moesin Signaling Pathways.

In a laboratory model, treatment with hydrogen reduced Ang II- or AAC-induced oxidative stress, which was reflected by diminishing the induction of reactive oxygen species (ROS) in Ang II-stimulated VSMCs, inhibiting the levels of 3-nitrotyrosine (3-NT) in vascular and serum malondialdehyde (MDA). The authors concluded that taken together, the authors' studies indicate that hydrogen prevents AAC-induced vascular hypertrophy in vivo, and inhibits Ang II-induced proliferation and migration of VSMCs in vitro possibly by targeting ROS-dependent ERK1/2, p38 MAPK, JNK and ERM signaling. These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.

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Hydrogen gas post-conditioning attenuates early neuronal pyroptosis in a rat model of subarachnoid hemorrhage through the mitoKATP signaling pathway.

In rats, hydrogen gas reduced brain swelling, improved neurological function, and lowered markers of oxidative stress and neuronal pyroptosis after subarachnoid hemorrhage. These results are preclinical and suggest molecular hydrogen's therapeutic potential in the condition studied. Further human research is needed to establish clinical effectiveness.

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Hydrogen gas inhalation protects against cigarette smoke-induced COPD development in mice.

In The inflammatory cells were counted and the levels of IL-6 and KC in BALF were assayed with ELISA, these changes were reduced by H₂ treatment. The authors concluded that these findings demonstrated that H₂ inhalation could inhibit CS-induced COPD development in mice, which is associated with reduced ERK1/2 and NF-κB-dependent inflammatory responses. These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.

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Hydrogen-rich saline protects against liver injury in rats with obstructive jaundice.

In male Sprague-Dawley rats, hydrogen-rich saline reduced levels of these markers and relieved morphological liver injury. These results are preclinical and suggest molecular hydrogen's therapeutic potential in the condition studied. Further human research is needed to establish clinical effectiveness.

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Hydrogen gas (H2) delivered by intraperitoneal injection alleviated methionine- and choline-deficient diet-induced metabolic dysfunction-associated steatotic liver disease in mice via inhibiting GSDMD- and GSDME-mediated pyroptosis.

In Moreover, hepatic protective effect and anti-pyroptosis effect of H₂ were further confirmed by H₂-rich DMEM-treated HepG2 cells in vitro, the anti-pyroptosis effects of H₂ in vitro were further confirmed by the reduced expression of inflammatory cytokines, the decreased full-length and cleaved forms of GSDMD and GSDME, and the reduced number of HepG2 cells with pyroptotic morphology. The authors concluded that H₂ is an anti-pyroptosis gas molecule, intraperitoneal injection of H₂ is a novel therapeutic strategy for MASLD that deserves further investigation. These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.

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Hydrogen-rich saline attenuates vascular smooth muscle cell proliferation and neointimal hyperplasia by inhibiting reactive oxygen species production and inactivating the Ras-ERK1/2-MEK1/2 and Akt pathways.

In In vitro effects of hydrogen on fetal bovine serum (FBS)-induced vascular smooth muscle cell (VSMC) proliferation were also investigated, hRSS significantly decreased the neointima area and neointima/media ratio in a dose-dependent manner. These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.

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Treatment of hydrogen molecule abates oxidative stress and alleviates bone loss induced by modeled microgravity in rats.

In Hindlimb suspension (HLS) and rotary wall vessel bioreactor were used to model microgravity in vivo and in vitro, respectively, treatment with molecular hydrogen alleviates microgravity-induced bone loss in rats. The authors concluded that treatment with molecular hydrogen alleviates microgravity-induced bone loss in rats. These findings come from a laboratory model and suggest molecular hydrogen's biological potential. Further research is needed to determine clinical relevance.

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