Biochemistry and Biophysics Reports最新文献

{"title":"Unveiling ferroptosis genes and inhibitors in diabetic retinopathy through single-cell analysis and docking simulations","authors":"Md. Maqsood Ahamad Khan ,&nbsp;Ananya Ganguly ,&nbsp;Shubhrajit Barman ,&nbsp;Chirasmita Das ,&nbsp;Senthil Kumar Ganesan","doi":"10.1016/j.bbrep.2025.101932","DOIUrl":"10.1016/j.bbrep.2025.101932","url":null,"abstract":"<div><div>Diabetic retinopathy (DR) is a common microvascular complication of diabetes and a leading cause of vision loss worldwide. Although several mechanisms have been implicated in the pathogenesis of DR, emerging evidence suggests a link between ferroptosis and DR. Unfortunately, the exact mechanism underlying this connection is not clear. Therefore, investigating the role of ferroptosis in diabetic retinopathy holds promise for advancing our understanding of this complex disease and developing innovative treatments. We have identified differentially expressed genes (DEGs) and differentially expressed marker genes (DEMGs) from open-source single-cell RNA sequencing datasets by using in depth in silico approach. Subsequently, ferroptosis-associated DEGs (FA-DEGs), ferroptosis-associated DEMGs (FA-DEMGs), and ferroptosis-associated Hub Genes (FAHGs) were identified. The FDA-approved drugs for our target proteins were also identified, and their ADMET properties were assessed. Molecular docking and simulation were utilized to explore the interaction stability of the compounds with the target proteins. Overall, we identified 63 FA-DEMGs that were significantly enriched in Peroxiredoxin activity, Ferroptosis, Mitophagy, and Autophagy. Further analysis predicted that PRDX1 and UBC are candidate target proteins. Molecular docking results showed that dexamethasone has a high binding affinity for both PRDX1 and UBC. Additionally, molecular dynamics simulations revealed that dexamethasone (which showed the best hit in the docking analysis) exhibited a ‘stable effect’ on both PRDX1 and UBC. To summarize, this study showed that PRDX1 and UBC could be suitable therapeutic targets for dexamethasone, which might be helpful in the advance of DR treatments in the future.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101932"},"PeriodicalIF":2.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143993","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":"Effect of epigallocatechin-3-gallate (EGCG) on cognitive functioning and the expression of APP and BDNF in the hippocampus of rats with streptozotocin -induced Alzheimer-like disease","authors":"Farnaz Ghayour Babaei ,&nbsp;Ehsan Saburi ,&nbsp;Fatemeh Forouzanfar ,&nbsp;Mohadese Asgari ,&nbsp;Zakieh Keshavarzi ,&nbsp;Vahid Hajali","doi":"10.1016/j.bbrep.2025.101930","DOIUrl":"10.1016/j.bbrep.2025.101930","url":null,"abstract":"<div><div>We aimed to investigate the potential therapeutic effects of the active substance of green tea, epigallocatechin-3-gallate (EGCG), on behavioral phenotypes and markers of neurogenesis in an Alzheimer disease (AD) rat model. The groups included sham, AD, and three AD groups receiving orally EGCG with different doses of 25, 50, and 100 mg/kg. The AD model was induced by intracerebroventricular (icv) injection of streptozocin (STZ) at a dose of 3 mg/kg. Spatial learning and memory were evaluated in the Morris water maze (MWM) test. Real-time PCR assay was used for evaluating the expression of beta-amyloid precursor protein (APP) and brain-derived neurotrophic factor (BDNF) in the hippocampus of animals. STZ disrupted the function of animals in MWM acquisition phase by almost 65 % and all doses of EGCG could return the learning parameters to those of control animals. STZ also impaired the memory function (P &lt; 0.05) and a dose of 25 mg/kg EGCG could significantly return it to the control level (29 % vs 53 %, P &lt; 0.01). Hippocampal APP gene expression was increased in the AD group and EGCG with dose 25 mg/kg decreased it significantly (P &lt; 0.05). AD animals had decreased levels of hippocampal BDNF and treating with dose 25 mg/kg of EGCG could significantly increase it (P &lt; 0.05). EGCG with dose 25 mg/kg can improve spatial memory deficits in AD model rats. It may be due to the impact on the expression of hippocampal factors involved in AD pathology. These findings could provide a beneficial insight for developing novel, safe, and efficient natural compounds for preventing or alleviation AD symptoms in humans.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101930"},"PeriodicalIF":2.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143273","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":"Ganoderma lucidum polysaccharide attenuates retinal ischemia-reperfusion injury by regulating microglial M1/M2 polarization, suppressing neuroinflammation and inhibiting JAK2/STAT3 pathway","authors":"Guangyu Zhu ,&nbsp;Yujie Liu ,&nbsp;Shichun Luo ,&nbsp;Chao Tang ,&nbsp;Chunlin Zhao ,&nbsp;Xuejing Lu","doi":"10.1016/j.bbrep.2025.101926","DOIUrl":"10.1016/j.bbrep.2025.101926","url":null,"abstract":"<div><div>Retinal ischemia-reperfusion (RIR) injury is implicated in the pathogenesis of numerous retinal degenerative disorders, resulting in visual impairment or even blindness in millions of individuals worldwide. In recent years, targeting the suppression of microglia-mediated neuroinflammation has emerged as a principal therapeutic strategy for RIR. Ganoderma lucidum polysaccharide (GLP), a pivotal bioactive extract of Ganoderma lucidum, has been demonstrated to possess efficacious anti-neuroinflammatory properties, while the precise impact of it on RIR injury remains incompletely elucidated. In this study, the RIR model was induced in Sprague-Dawley rats by elevating the intraocular pressure to 80 mmHg for 60 min. Our findings revealed that GLP significantly alleviated inflammatory processes by impeding the secretion of pro-inflammatory cytokines while facilitating that of anti-inflammatory cytokines. Moreover, the administration of GLP also promoted the polarization of microglia from the M1 phenotype to the M2 phenotype. Further investigation of the treatment mechanism indicated that the regulatory effects of GLP were presumably mediated by the inhibition of the JAK2/STAT3 signaling pathway. To summarize, we provided a novel insight into the mechanisms by which GLP ameliorated RIR injury, thereby indicating that it could be identified as a promising candidate for the management of RIR-related diseases.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101926"},"PeriodicalIF":2.3,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143272","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":"Modified creatine greatly increases the performance of skeletal and smooth muscles","authors":"Anatoly Soloviev ,&nbsp;Vadym Kozlovsky ,&nbsp;Dmytro Nozdrenko ,&nbsp;Vadym Sydorenko ,&nbsp;Igor Monchak ,&nbsp;Natalia Vdovenko ,&nbsp;Olena Maidaniuk ,&nbsp;Volodymyr Fetyukhin","doi":"10.1016/j.bbrep.2025.101934","DOIUrl":"10.1016/j.bbrep.2025.101934","url":null,"abstract":"<div><div>Creatine is a nitrogen-containing carboxylic acid and a main component of phosphocreatine. In recent years, creatine is considered as a component of dietary nutrition, to improve the efficiency of physical activity and increase muscle mass of athletes and older people. Creatine has been shown to be able restore cardiac contractility impairment after myocardial infarction. However, as muscle cells do not synthesise creatine, the efficiency of creatine depends on its transmembrane transport.</div><div>In our study, we evaluated the effect of «ProCreatine» (ProCr), a novel membrane transporter-independent creatine modification on fatigability of the rat gastrocnemius muscle and portal vein smooth muscle using fatigue stimulation pools. Mechanokinetic and biomechanical markers of fatigue in muscles to maintain the level of isometric tension induced by field electrical stimulation were examined. The results indicate that administration of ProCr to skeletal muscle significantly increases maximal force output, integrated muscle contractile force and significantly increases muscle productivity. We observed positive changes in all studied biochemical indices of fatigue. In addition, ProCr increases the duration of sustaining a constant level of isometric contraction in portal vein smooth muscle caused by electrical stimulation by 6 fold. Regular creatine in the same dose had no significant effect on these parameters neither in skeletal nor in smooth muscles. The data obtained suggest the possibility of using ProCr as a therapeutic agent capable of reducing and correcting pathological conditions of the muscular system that arise during the processes of fatigue in skeletal muscles and smooth muscles of hollow organs.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101934"},"PeriodicalIF":2.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143274","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":"Melatonin ameliorates astrogliosis and microgliosis in a cuprizone demyelinating mouse model","authors":"Mehdi Alidadi ,&nbsp;Negar Omidi ,&nbsp;Mahdad Abdi ,&nbsp;Maryam Mohammadi ,&nbsp;Maryam Shabani ,&nbsp;Iraj Ragerdi Kashani","doi":"10.1016/j.bbrep.2025.101929","DOIUrl":"10.1016/j.bbrep.2025.101929","url":null,"abstract":"<div><h3>Background and purpose</h3><div>Several investigations have reported that melatonin is involved in the amelioration of the inflammatory process, improvement of myelin function, and regeneration in the central nervous system (CNS). The current study aimed to evaluate the protective effect of melatonin in cuprizone (CPZ)-induced myelin damage in the corpus callosum (CC) and explore the plausible underlying mechanisms of remyelination capacity and/or neuroprotection.</div></div><div><h3>Method</h3><div>We administered cuprizone in chow either alone daily for 6 weeks or combined with simultaneously applied melatonin intra-peritoneal injections. we studied demyelination by LFB staining, oligodendrocyte staining using anti-Olig2 or anti-APC antibodies. In addition, we visualized microgliosis and astrocytosis by staining with anti-Iba-1 and anti-GFAP antibodies. Furthermore, we study the effect of melatonin on mRNA expression of Musashi-1, Hes-1 and Notch-1 genes.</div></div><div><h3>Results</h3><div>Our data showed that cuprizone intoxication caused a significant oligodendrocyte loss, demyelination, and reactive gliosis in CC. Administration of melatonin prevented the demyelination in CC as determined by Luxol fast blue staining. Furthermore, we found that the melatonin significantly suppressed the cuprizone-induced microgliosis and astrocytosis. while the frequency of oligodendrocytes (Olig2+) was significantly enhanced in the CC after melatonin administration. In addition, melatonin significantly modulated Musashi1, Hes1, and Notch1 mRNA expression in the CC of mice.</div></div><div><h3>Conclusion</h3><div>These results provide evidence that melatonin abolishes destructive cuprizone effects in the mouse corpus callosum by restoring oligodendrocyte generation, remyelination, and decreasing astrogliosis and microgliosis.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101929"},"PeriodicalIF":2.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143347","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":"Renoprotective mechanisms of celastrol in high glucose-mediated HK-2 cell injury through inhibition of the PI3K/Akt/NF-κB signalling pathway","authors":"Xiaojuan Wang ,&nbsp;Mohamad Hafizi Abu Bakar ,&nbsp;Mohd Asyraf Kassim ,&nbsp;Khairul Anuar Shariff ,&nbsp;Mohamad Norisham Mohamad Rosdi","doi":"10.1016/j.bbrep.2025.101928","DOIUrl":"10.1016/j.bbrep.2025.101928","url":null,"abstract":"<div><div>Hyperglycemia-induced inflammation and fibrosis in renal tubular epithelial cells are critical factors driving the progression of diabetic nephropathy (DN). Celastrol, a bioactive compound derived from <em>Tripterygium wilfordii Hook.F</em>, is recognized for its anti-inflammatory and anti-fibrotic properties. This study aimed to investigate the renoprotective effects of celastrol against high glucose (HG)-induced damage in human kidney 2 (HK-2) cells. Briefly, HK-2 cells were exposed to high glucose and treated with celastrol. Cell viability and apoptosis were evaluated using CCK-8 assay kit and flow cytometry, respectively. The pro-inflammatory cytokines, oxidative stress markers, and fibrotic-related proteins were measured using ELISA and immunoblotting. To further confirm the mechanistic actions of celastrol, the PI3K/Akt/NF-κB pathway was examined, and HG-treated cells were co-incubated with the NF-κB inhibitor bortezomib. Our result revealed that celastrol at the moderate concentration of 50 nM mitigated HG-induced toxicity, suggesting an optimal therapeutic window. Celastrol improved cell viability and reduced apoptosis in HG-treated HK-2 cells. It significantly decreased levels of inflammatory cytokines such as IL-6, TNF-α, IL-1β, and MCP-1, while enhancing antioxidant activities of GSH-Px and SOD, and lowering MDA levels, indicating diminished oxidative stress. Mechanistically, these renoprotective effects of celastrol partly attributed via inhibition of the PI3K/Akt/NF-κB signalling pathway, as blocking NF-κB signalling by bortezomib resulted in similar inhibitory effects against inflammation and fibrosis. Collectively, celastrol acts as a renoprotective agent against renal inflammation, oxidative stress, and fibrosis, partly through the inhibition of the PI3K/Akt/NF-κB pathway, offering potential therapeutic benefits against hyperglycemia-induced renal injury in DN.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101928"},"PeriodicalIF":2.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143346","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":"Propofol reduces human TRPA1 activity in a warm environment","authors":"Chihiro Suda ,&nbsp;Yasunori Takayama ,&nbsp;Makoto Tominaga ,&nbsp;Tomoko Akase","doi":"10.1016/j.bbrep.2025.101918","DOIUrl":"10.1016/j.bbrep.2025.101918","url":null,"abstract":"<div><div>Propofol, an intravenous anesthetic, has a side effect of causing vascular pain at the injection site. However, no effective method to inhibit this vascular pain has been established. Propofol-induced vascular pain is caused by activation of transient receptor potential ankyrin1 (TRPA1), which is expressed in the sensory nerve endings distributed around blood vessels. TRPA1 exhibits temperature sensitivity, and the degree of its activation has been reported to change with temperature. However, whether the temperature of propofol influences human TRPA1 (hTRPA1) activation and regulates the extent of vascular pain has not been examined. We investigated hTRPA1 activity in HEK293T cells in response to cooled or heated propofol using the patch-clamp method. We found that hTRPA1 currents were smaller in a warm environment (&gt;35 °C) with heated propofol. Our results suggest that propofol should be kept above 35 °C to minimize hTRPA1 activation. Moreover, heating propofol decreased hTRPA1-mediated currents but did not alter activation of human GABA_A receptors. This finding suggest that heated propofol can inhibit hTRPA1 activation and reduce vascular pain without losing its anesthetic function.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101918"},"PeriodicalIF":2.3,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143345","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":"Vitamin D stimulates Il-15 synthesis in rodent muscle","authors":"Franz Ewendt ,&nbsp;Fabienne Drewitz ,&nbsp;Michael Althammer ,&nbsp;Cosima Eichler ,&nbsp;Corinna Brandsch ,&nbsp;Stefanie Brey ,&nbsp;Thomas H. Winkler ,&nbsp;Mirja R. Wilkens ,&nbsp;René St-Arnaud ,&nbsp;Marina Kreutz ,&nbsp;Gabriele I. Stangl","doi":"10.1016/j.bbrep.2025.101925","DOIUrl":"10.1016/j.bbrep.2025.101925","url":null,"abstract":"<div><div>Besides its classical skeletal function, vitamin D plays a critical role in both skeletal muscle and the immune system. Interleukin-15 (IL-15), which is highly expressed, and secreted complexed with its receptor, IL-15Rα, by skeletal muscle, stimulates the development of immune cells and affects myogenesis and muscle mass. However, little is known about possible regulators of this myokine. To test whether vitamin D could be a regulator of muscle IL-15 and IL-15Rα expression, C2C12 myotubes were treated with vitamin D₃ metabolites and analysis were performed in gastrocnemius muscles of rats treated with a single intraperitoneal dose of 1,25(OH)₂D₃. The role of VDR was investigated by siRNA technique in C2C12 myotubes and in gastrocnemius muscles of vitamin D receptor knockout (Vdr-KO) mice. Treatment of C2C12 myotubes with 1,25(OH)₂D₃ or 25(OH)D₃ increased <em>Il-15</em> gene expression in a dose-dependent manner and 1,25(OH)₂D₃ also moderately increased the relative Il-15 protein amount. Rats treated with a single dose of 1,25(OH)₂D₃ demonstrated a higher mRNA abundance of muscle <em>Il-15</em> than controls. The 1,25(OH)₂D₃ effect on <em>Il-15</em> was considerably weaker in C2C12 myotubes treated with <em>Vdr</em>-specific siRNA. Vdr-KO mice showed significantly lower muscle <em>Il-</em>15 mRNA than WT mice. <em>Il-15Ra</em> mRNA and Il-15/Il-15Rα protein abundance were unaffected by 1,25(OH)₂D₃-treatment or VDR functionality, and Cyp27b1 activity is not required for 25(OH)D₃-mediated <em>Il-15</em> gene expression.</div><div>The results provide evidence for a regulatory role of hydroxyvitamin D₃ metabolites on the Il-15 synthesis in skeletal muscle cells, which is largely mediated by the VDR.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101925"},"PeriodicalIF":2.3,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143143344","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":"Biochemical strategies for opioid-sparing pain management in the operating room","authors":"Fatemeh Hosseinzadeh ,&nbsp;Alireza Nourazarian","doi":"10.1016/j.bbrep.2025.101927","DOIUrl":"10.1016/j.bbrep.2025.101927","url":null,"abstract":"<div><div>The opioid epidemic has highlighted the increasing need for alternative pain relievers in surgical settings. This review explores non-opioid approaches for managing pain in the ever-changing operating room. The review examines the molecular basis of pain perception, with a focus on receptor-targeted treatments that offer effectiveness without the risks associated with opioids. Despite the demonstrated benefits and improved side effect profiles, our literature analysis reveals the challenges that hinder the integration of innovative pain relievers. We explore the potential of neuroimmune modulators, peptide disruptors, and new neurotransmitter analogs in the quest for effective pain relief, paving the way for a future of anesthesia without opioids.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101927"},"PeriodicalIF":2.3,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143144330","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":"A comprehensive review of molecular hydrogen as a novel nutrition therapy in relieving oxidative stress and diseases: Mechanisms and perspectives","authors":"Fatmanur Yıldız ,&nbsp;Tyler W. LeBaron ,&nbsp;Duried Alwazeer","doi":"10.1016/j.bbrep.2025.101933","DOIUrl":"10.1016/j.bbrep.2025.101933","url":null,"abstract":"<div><div>Oxidative stress is responsible for the pathogenesis of many diseases, and antioxidants are commonly included in their treatment protocols. Over the past two decades, numerous biomedical reports have revealed the therapeutic benefits of molecular hydrogen (H₂) in relieving oxidation-related diseases. H₂ has been found to have selective antioxidant properties against the most dangerous oxidants (hydroxyl radicals and peroxynitrite). H₂ demonstrates numerous biologically therapeutic properties, including anti-inflammatory, antioxidant, anti-cancer, anti-stress, anti-apoptotic, anti-allergic effects, signaling molecule functions, regulation of redox balance, modulation of antioxidant enzyme gene expression, improvement of blood vessel function, down-regulation of pro-inflammatory cytokines, stimulation of energy metabolism, and protection of the nervous system. Experimental and clinical studies have shown the potential use of hydrogen nutrition therapy for ameliorating various diseases, including cardiovascular, respiratory, and metabolic disorders, as well as obesity, gastrointestinal disorders, and brain and nervous system disorders. The administration methods of hydrogen include inhalation, hydrogen-rich water, hydrogen-rich saline, hydrogen-rich eye drops, and hydrogen-rich bathing. Hydrogen nutritional therapy can be applied to different diseases, and it offers a natural alternative to chemical and radiation therapies. This review covers the different administration methods and the latest experimental and clinical research on the potential applications of H₂ in nutritional therapy for different diseases.</div></div>","PeriodicalId":8771,"journal":{"name":"Biochemistry and Biophysics Reports","volume":"41 ","pages":"Article 101933"},"PeriodicalIF":2.3,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143144331","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}