{"title":"Magnesium-assisted hydrogen improves isoproterenol-induced heart failure.","authors":"Fengbao Chen, Ruimin Chen, Lili Yang, Bowen Shen, Yunting Wang, Yongfeng Gao, Rui Tan, Xiaomin Zhao","doi":"10.4103/mgr.MEDGASRES-D-24-00135","DOIUrl":"https://doi.org/10.4103/mgr.MEDGASRES-D-24-00135","url":null,"abstract":"<p><p>Heart failure (HF) is a leading cause of mortality among patients with cardiovascular disease and is often associated with myocardial apoptosis and endoplasmic reticulum stress (ERS). While hydrogen has demonstrated potential in reducing oxidative stress and ERS, recent evidence suggests that magnesium may aid in hydrogen release within the body, further enhancing these protective effects. This study aimed to investigate the cardioprotective effects of magnesium in reducing apoptosis and ERS through hydrogen release in a rat model of isoproterenol (ISO)-induced HF. Magnesium was administered orally to ISO-induced HF rats, which improved cardiac function, reduced myocardial fibrosis and cardiac hypertrophy, and lowered the plasma levels of creatine kinase-MB, cardiac troponin-I, and N-terminal B-type natriuretic peptide precursor in ISO-induced HF rats. It also inhibited cardiomyocyte apoptosis by upregulating B-cell lymphoma-2, downregulating Bcl-2-associated X protein, and suppressing ERS markers (glucose-related protein 78, activating transcription factor 4, and C/EBP-homologous protein). Magnesium also elevated hydrogen levels in blood, plasma, and cardiac tissue, as well as in artificial gastric juice and pure water, where hydrogen release lasted for at least four hours. Additionally, complementary in vitro experiments were conducted using H9C2 cardiomyocyte injury models, with hydrogen-rich culture medium as the intervention. Hydrogen-rich culture medium improved the survival and proliferation of ISO-treated H9C2 cells, reduced the cell surface area, inhibited apoptosis, and downregulated ERS pathway proteins. However, the protective effects of hydrogen were negated by tunicamycin (an inducer of ERS) in H9C2 cells. In conclusion, magnesium exerts significant cardioprotection by mitigating ERS and apoptosis through hydrogen release effects in ISO-induced HF.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"15 4","pages":"459-470"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144028123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medical Gas ResearchPub Date : 2025-12-01Epub Date: 2025-04-29DOI: 10.4103/mgr.MEDGASRES-D-25-00012
Aleksandr L Urakov, Mithun Rudrapal, Natalya A Urakova, Valentina I Martiusheva, Anatoly N Osipov
{"title":"Medical \"gas fuse\": quickly and gently eliminates cerumen.","authors":"Aleksandr L Urakov, Mithun Rudrapal, Natalya A Urakova, Valentina I Martiusheva, Anatoly N Osipov","doi":"10.4103/mgr.MEDGASRES-D-25-00012","DOIUrl":"https://doi.org/10.4103/mgr.MEDGASRES-D-25-00012","url":null,"abstract":"","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"15 4","pages":"552-553"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medical Gas ResearchPub Date : 2025-12-01Epub Date: 2025-04-29DOI: 10.4103/mgr.MEDGASRES-D-25-00027
Natalya A Urakova, Aleksandr L Urakov, Petr D Shabanov
{"title":"Intrapulmonary and intrabronchial oxygen-producing antihypoxants eliminate asphyxia and hypoxemia.","authors":"Natalya A Urakova, Aleksandr L Urakov, Petr D Shabanov","doi":"10.4103/mgr.MEDGASRES-D-25-00027","DOIUrl":"https://doi.org/10.4103/mgr.MEDGASRES-D-25-00027","url":null,"abstract":"","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"15 4","pages":"550-551"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144003981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Inhibition of hepatic gluconeogenesis in type 2 diabetes by metformin: complementary role of nitric oxide.","authors":"Arman Farahani, Aryan Farahani, Khosrow Kashfi, Asghar Ghasemi","doi":"10.4103/mgr.MEDGASRES-D-24-00100","DOIUrl":"https://doi.org/10.4103/mgr.MEDGASRES-D-24-00100","url":null,"abstract":"<p><p>Metformin is the first-line treatment for type 2 diabetes mellitus. Type 2 diabetes mellitus is associated with decreased nitric oxide bioavailability, which has significant metabolic implications, including enhanced insulin secretion and peripheral glucose utilization. Similar to metformin, nitric oxide also inhibits hepatic glucose production, mainly by suppressing gluconeogenesis. This review explores the combined effects of metformin and nitric oxide on hepatic gluconeogenesis and proposes the potential of a hybrid metformin-nitric oxide drug for managing type 2 diabetes mellitus. Both metformin and nitric oxide inhibit gluconeogenesis through overlapping and distinct mechanisms. In hepatic gluconeogenesis, mitochondrial oxaloacetate is exported to the cytoplasm via various pathways, including the malate, direct, aspartate, and fumarate pathways. The effects of nitric oxide and metformin on the exportation of oxaloacetate are complementary; nitric oxide primarily inhibits the malate pathway, while metformin strongly inhibits the fumarate and aspartate pathways. Furthermore, metformin effectively blocks gluconeogenesis from lactate, glycerol, and glutamine, whereas nitric oxide mainly inhibits alanine-induced gluconeogenesis. Additionally, nitric oxide contributes to the adenosine monophosphate-activated protein kinase-dependent inhibition of gluconeogenesis induced by metformin. The combined use of metformin and nitric oxide offers the potential to mitigate common side effects. For example, lactic acidosis, a known side effect of metformin, is linked to nitric oxide deficiency, while the oxidative and nitrosative stress caused by nitric oxide could be counterbalanced by metformin's enhancement of glutathione. Metformin also amplifies nitric oxide -induced activation of adenosine monophosphate-activated protein kinase. In conclusion, a metformin-nitric oxide hybrid drug can benefit patients with type 2 diabetes mellitus by enhancing the inhibition of hepatic gluconeogenesis, decreasing the required dose of metformin for maintaining optimal glycemia, and lowering the incidence of metformin-associated lactic acidosis.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"15 4","pages":"507-519"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medical Gas ResearchPub Date : 2025-12-01Epub Date: 2025-04-29DOI: 10.4103/mgr.MEDGASRES-D-24-00161
Yan Liu, Tianhao Shen, Qiuying Li, Xue Yu, Yu Liu, Cheng Zhou, Ji Han, Yongqiang Zhu
{"title":"Various gases for the treatment of neuropathic pain: mechanisms, current status, and future perspectives.","authors":"Yan Liu, Tianhao Shen, Qiuying Li, Xue Yu, Yu Liu, Cheng Zhou, Ji Han, Yongqiang Zhu","doi":"10.4103/mgr.MEDGASRES-D-24-00161","DOIUrl":"https://doi.org/10.4103/mgr.MEDGASRES-D-24-00161","url":null,"abstract":"<p><p>In recent years, medical gas therapy has emerged as a promising approach for treating neuropathic pain. This review article aimed to investigate the therapeutic effects of medical gas therapy on neuropathic pain and its underlying mechanisms, thereby providing a theoretical foundation for clinical practice. A literature search was conducted using the Web of Science Core Collection database. Co-occurrence analysis of keywords revealed that terms including \"neuropathic pain,\" \"nitric oxide,\" \"nitric oxide synthase,\" \"pain,\" and \"ozone\" frequently appeared. Cluster analysis grouped these keywords into four primary categories: intervertebral disc disease and gas therapy, mechanisms of neuropathic pain and gas interventions, the role of nitric oxide in modulating neuropathic pain and gas therapy, and the effects of gas therapy on mental disorders in the context of neuropathic pain treatment. The analysis of highly cited literature in the field of medical gas therapy for neuropathic pain emphasizes the crucial roles of nitric oxide and nitric oxide synthase in nerve injury and pain. Various types of gas therapy, including oxygen-ozone therapy and nitric oxide-related therapies, show promise in treating pain following peripheral nerve injury. Oxidative stress and nitric oxide are crucial regulatory factors in the pain signaling associated with trigeminal neuralgia. Ozone therapy alleviates trigeminal pain by inhibiting inflammatory responses, reducing oxidative stress, and modulating neurotransmitter release. Novel nanomaterials, such as manganese oxide nanoparticles, have also demonstrated potential in scavenging free radicals and alleviating sciatic nerve pain. Ozone therapy has shown good clinical efficacy in treating lumbar disc herniation and sciatica, whereas both ozone therapy and hyperbaric oxygen therapy have demonstrated effectiveness and safety in managing postherpetic neuralgia. In conclusion, medical gas therapy for neuropathic pain primarily includes oxygen-ozone therapy, nitric oxide-related therapies, hydrogen sulfide-related therapies, and hyperbaric oxygen therapy. While these therapies exhibit efficacy in managing neuropathic pain, further research is necessary to elucidate their mechanisms of action and safety profiles. Although hyperbaric oxygen therapy and ozone therapy have already been implemented in clinical research, other types of gas therapy are still in the animal testing phase. Therefore, future studies should focus on conducting more multicenter, large-sample randomized controlled trials to accelerate clinical translation and provide more effective treatment options for patients suffering from neuropathic pain.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"15 4","pages":"488-495"},"PeriodicalIF":3.0,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143990190","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medical Gas ResearchPub Date : 2025-09-01Epub Date: 2025-04-17DOI: 10.4103/mgr.MEDGASRES-D-24-00147
Liang Zhao, Zheng Hong Lee, Yatrik M Shah
{"title":"Ammonia as a critical metabolic modulator of anti-tumor immunity.","authors":"Liang Zhao, Zheng Hong Lee, Yatrik M Shah","doi":"10.4103/mgr.MEDGASRES-D-24-00147","DOIUrl":"https://doi.org/10.4103/mgr.MEDGASRES-D-24-00147","url":null,"abstract":"","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"15 3","pages":"446-447"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12054676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144009911","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medical Gas ResearchPub Date : 2025-09-01Epub Date: 2025-04-17DOI: 10.4103/mgr.MEDGASRES-D-24-00120
Claudio Ripa, Laveena Munshi, Wolfgang M Kuebler, Aurora Magliocca, Fabio S Taccone, Lorraine B Ware, Giuseppe Citerio, John G Laffey, Emanuele Rezoagli
{"title":"Oxygen targets in critically ill patients: from pathophysiology to population enrichment strategies.","authors":"Claudio Ripa, Laveena Munshi, Wolfgang M Kuebler, Aurora Magliocca, Fabio S Taccone, Lorraine B Ware, Giuseppe Citerio, John G Laffey, Emanuele Rezoagli","doi":"10.4103/mgr.MEDGASRES-D-24-00120","DOIUrl":"https://doi.org/10.4103/mgr.MEDGASRES-D-24-00120","url":null,"abstract":"<p><p>Oxygen supplementation is widely used to enhance oxygen delivery and to treat or prevent hypoxia; however, it requires careful management to avoid the harmful effects of excessive oxygen exposure. Both hyperoxia (inspiratory oxygen fraction exceeding 0.21) and hyperoxemia (arterial oxygen tension oxygen partial pressure [PaO2] > 100 mmHg) can contribute to lung injury, promote systemic vasoconstriction, and increase the production of reactive oxygen species, which can impair macromolecular and cellular functions. Conversely, in certain situations, hyperoxemia may provide benefits, such as hemodynamic stabilization in hyperdynamic shock, immunomodulation, and bactericidal effects. The literature presents conflicting evidence regarding the impact of different oxygen targets (i.e., PaO2 and/or peripheral saturation of oxygen [SpO2]) on both short- and long-term outcomes in patients with acute critical conditions, such as acute respiratory distress syndrome, sepsis, cardiac arrest, and acute central nervous system injuries. These discrepancies may stem from the small differences between the oxygenation targets used in randomized trials, the physiological limitations of PaO2 and SpO2 targets, which reflect blood oxygen content rather than oxygen delivery, the lack of measurements of microvascular function or oxygen delivery, and the heterogeneity in treatment response. Furthermore, advanced analytical methods (e.g., machine learning) are emerging as promising tools to implement population enrichment strategies. By refining patient sub-group identification, these approaches can significantly optimize precision medicine, enabling more personalized oxygen therapy tailored to individual patient characteristics.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"15 3","pages":"409-419"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12054680/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144035849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medical Gas ResearchPub Date : 2025-09-01Epub Date: 2025-04-17DOI: 10.4103/mgr.MEDGASRES-D-24-00107
Menglin Tian, Wenyin Du, Sen Yang, Qiwei Liao, Fuding Guo, Shaolong Li
{"title":"Application and progress of hyperbaric oxygen therapy in cardiovascular diseases.","authors":"Menglin Tian, Wenyin Du, Sen Yang, Qiwei Liao, Fuding Guo, Shaolong Li","doi":"10.4103/mgr.MEDGASRES-D-24-00107","DOIUrl":"https://doi.org/10.4103/mgr.MEDGASRES-D-24-00107","url":null,"abstract":"<p><p>Cardiovascular diseases remain the leading cause of death worldwide, underscoring the urgent need for additional therapeutic strategies to reduce their mortality rates. This review systematically outlines the historical development and recent advances of hyperbaric oxygen therapy in cardiovascular diseases, with a focus on its therapeutic mechanisms and clinical outcomes. Hyperbaric oxygen therapy enhances oxygen delivery to ischemic and reperfused tissues, promotes angiogenesis, and significantly suppresses oxidative stress, inflammatory cascades, and cardiomyocyte apoptosis, demonstrating multifaceted therapeutic potential in cardiovascular conditions. Specifically, hyperbaric oxygen therapy combined with reperfusion strategies has been shown to markedly improve left ventricular ejection fraction in acute myocardial infarction. In heart failure, it facilitates myocardial repair and enhances cardiac function. For arrhythmias, hyperbaric oxygen therapy effectively reduces the frequency and duration of premature ventricular contractions and paroxysmal tachycardia, while mitigating the risk of neurological complications following atrial fibrillation ablation. Furthermore, hyperbaric oxygen therapy preconditioning in cardiac surgery has demonstrated improvements in left ventricular stroke work, reductions in postoperative myocardial injury, and a decrease in related complications. Despite its promising applications, the widespread adoption of hyperbaric oxygen therapy remains hindered by the lack of standardized treatment protocols and high-quality evidence from rigorous clinical trials. In conclusion, this review underscores the potential value of hyperbaric oxygen therapy in the cardiovascular domain while highlighting the need for further optimization of therapeutic parameters and exploration of its synergistic effects with conventional therapies to provide clearer guidance for clinical implementation.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"15 3","pages":"427-434"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12054664/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144031798","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Dietary addition of magnesium hydride nanoparticles: a breakthrough in combating high-fat diet-induced chronic kidney disease.","authors":"Hongtao Lu, Wanqiu Chen, Yajing Ying, Deqian Gu, Rui Li, Xiangtong Li, Jin Cheng, Xuejun Sun, Yinyin Zhang, Wenrui Liu, Hui Shen","doi":"10.4103/mgr.MEDGASRES-D-24-00090","DOIUrl":"https://doi.org/10.4103/mgr.MEDGASRES-D-24-00090","url":null,"abstract":"<p><p>A substantial body of evidence indicates a positive correlation between dyslipidemia and an elevated risk of chronic kidney disease, with renal interstitial fibrosis frequently serving as a common pathway in the advanced stages of chronic kidney disease progression. Hydrogen has anti-inflammatory and antioxidant properties, and magnesium hydride nanoparticle is a material with high hydrogen storage capacity. Magnesium hydride -fortified feed is capable of releasing hydrogen gas steadily and continuously within the digestive tract. A 12-week high-fat diet significantly elevated the serum urea and creatinine levels in mice. In contrast, dietary addition of magnesium hydride demonstrated a notable protective effect against pathological conditions. Additionally, magnesium hydride -fortified feed was found to reduce renal fibrosis and thereby improve renal function. In support of these findings, an in vitro study utilizing human kidney cortical proximal tubule epithelial cells (HK-2 cells) exposed to palmitic acid under conditions mimicking a high-fat diet confirmed the renoprotective effects of magnesium hydride. Furthermore, the primary target phosphatase and tensin homologue deleted on chromosome 10 and the molecular mechanisms underlying the effects of magnesium hydride, specifically its ability to inhibit the transforming growth factor-beta -Smad family member 2 and 3 (Smad2/3) axis through downregulating the expression of phosphatase and tensin homologue deleted on chromosome 10, were elucidated. Additionally, overexpression of Hes family BHLH transcription factor 1 can negate the beneficial effects of magnesium hydride, suggesting that Hes family BHLH transcription factor 1 may serve as an upstream regulatory target in the context of the effects of magnesium hydride. In conclusion, this study demonstrated that magnesium hydride functions as a safe and effective hydrogen source capable of inhibiting the activation of the transforming growth factor-beta/Smad2/3 and protein kinase B/mechanistic target of rapamycin pathways by increasing the expression of phosphatase and tensin homologue deleted on chromosome 10. This mechanism counteracts the progression of high-fat diet-induced chronic renal damage.</p>","PeriodicalId":18559,"journal":{"name":"Medical Gas Research","volume":"15 3","pages":"374-382"},"PeriodicalIF":3.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12054669/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}