3 oktober 2022: zie ook deze artikelen: https://kanker-actueel.nl/waterstoftherapie-bewijst-meer-en-meer-waarde-bij-chronische-ziektes-en-ook-bij-vormen-van-kanker-bewijzen-studies-dat-kankerpatienten-profijt-kunnen-hebben-van-waterstofbehandelingen.html

Zie hier mijn verslag en hoe ik de waterstoftherapie heb ervaren.

3 oktober 2022: Bron:  2020 Apr-Jun; 10(2): 75–80. Published online 2020 Jun 5.

Uit een kleine gerandomiseerde studie bij totaal 58 patiënten met gevorderde niet-kleincellige longkanker verdeeld in drie groepen blijkt waterstoftherapie (H2) de ziekteprogressie onder controle te houden en de bijwerkingen van medicijnen te verlichten.

Na 16 maanden follow-up ( maximaal 5 maanden kregen de patiënten waterstof 4 tot 5 uur per dag) was de progressievrije overleving van de controlegroep beduidend lager dan die van de groep met alleen waterstof (H2) en statistisch significant lager dan die van groepen met waterstof (H2) + chemotherapie, waterstof  (H2) + gerichte therapie en waterstof (H2) + immuuntherapie.

In de groepen met gecombineerde behandelingen namen de meeste aan het gegeven geneesmiddel gerelateerde bijwerkingen geleidelijk af of verdwenen zelfs.

Tussen juni en september 2019 namen 58 patiënten met gevorderde niet-kleincellige longkanker (NSCLC) in het Fuda Cancer Hospital van de Jinan University deel aan het onderzoek.

  • Vierendertig patiënten ondergingen een operatie vóór inschrijving bij de studie en 24 patiënten waren in een vergevorderd stadium van de ziekte bij het stellen van de diagnose.
  • Immunohistochemische testen van de verhouding van geprogrammeerde celdood-1: geprogrammeerde celdood-1-liganden, tumormutatiebelasting en microsatelliet-instabiliteit in tumorspecimens werden uitgevoerd.
  • Op basis van die testresultaten kregen 10 patiënten immuuntherapie met een geneesmiddel toegediend op basis van antilichamen tegen geprogrammeerde celdood-1 (Nivolumab - Opdivo®, of Pembrolizumab Keytruda®).
  • Door detectie van genmutaties in tumorweefsel werden 18 patiënten geselecteerd om gerichte therapie te krijgen. Patiënten met een mutatie in het gen voor de epidermale groeifactorreceptor (EGFR) kregen Osimertinib , Gefitinib of Erlotinib toegediend.
  • Patiënten met een mutatie in het anaplastische lymfoomkinasegen of receptortyrosinekinase-1-gen kregen Crizotinib toegediend (Xalkori®).
  • Op basis van de gegevens van gevoeligheidstests voor geneesmiddelen kregen 10 patiënten chemotherapie (Cisplatin of Carboplatin).

De overige 20 patiënten die niet gevoelig waren voor gewone geneesmiddelen of die niet reageerden op behandeling met gewone geneesmiddelen, werden gelijkmatig verdeeld over de waterstof (H2) -monotherapiegroep of de controlegroep.
Drie groepen patiënten die een H2-behandeling kregen in combinatie met een andere behandeling (immuuntherapie, gerichte therapie of chemotherapie) begonnen met de therapie vóór deelname aan onze klinische studie.
De meeste van die patiënten ondervonden ernstige effecten op aan kanker gerelateerde longsymptomen na het nemen van combinatietherapie, maar er kwamen nieuwe geneesmiddelgerelateerde bijwerkingen naar voren.
Longsymptomen of geneesmiddelgerelateerde bijwerkingen werden vergeleken voor en na H2-behandeling. De vergelijking van longsymptomen vóór waterstofbehandeling en de veranderingen van tumor- of geneesmiddelgerelateerde symptomen in elke groep na waterstofbehandeling worden getoond in Figure 1.

Tekst gaat verder onder afbeelding:

An external file that holds a picture, illustration, etc.
Object name is MGR-10-75-g001.jpg


Figure 1

Symptom comparison of patients in each group before and after hydrogen treatment.

Waterstof (H2) inademing:

Waterstof (H2) werd geproduceerd door een H2-zuurstofvernevelaar (H2 66,7% en zuurstof 33,3%; maximale gasstroom, 3 L/min; AMS-H-03, Shanghai Asclepius Meditec, Shanghai, China).
De controlegroep onderging een placebo procedure (H2 0% en zuurstof 33,3%; maximale gasstroom 3 L/min; Shanghai Asclepius Meditec).
Ingeschreven patiënten inhaleerden het gasmengsel elke dag gedurende 4-6 uur en ondergingen elke maand beeldvormend onderzoek totdat de bestaande tumoren (laesies) significant groeiden of nieuwe uitzaaiingen verschenen. Progressievrije ziekte (PFS) werd berekend vanaf het begin van H2-inhalatie tot tumorprogressie.
Alle patiënten kregen elke maand computertomografie of een magnetische resonantie-onderzoek. Als de bestaande tumoren significant waren gegroeid of nieuwe metastasen zijn verschenen, wordt dit beschouwd als tumorprogressie.

Klinische gegevens van patiënten met gevorderde niet-kleincellige longkanker met H2-inhalatiebehandeling

Patiënten ondergingen H2-inhalatie per dag gedurende 5 maanden of stopten de inhalatie wanneer de kanker terugkwam. Er was geen significant verschil in de meeste patiëntkenmerken (bijv. Geslacht) tussen elke groep. De gerichte therapie-H2-therapiegroep had echter een hoger percentage tumorgenmutaties dan de andere vier groepen (P = 0,005; Zie  Table 1.

Vóór de start van de waterstoftherapie (H2) was er geen significant verschil in longfunctie of de KPS-score tussen de vijf groepen patiënten (Table 2). De prevalentie van de meeste longsymptomen (bijv. milde dyspneu, niet-cardiale pijn op de borst, pleurale effusie en bloedspuwing) was vergelijkbaar tussen de groepen. De prevalentie van de meeste longsymptomen in de controlegroep, H2-monotherapiegroep en immuuntherapie-H2-therapiegroep was hoger dan die in de doeltherapie-H2-therapiegroep en chemotherapie-H2-therapiegroep (P = 0,0137).

Resultaten:

Aan het begin van de waterstofbehandeling (H2) was de prevalentie van tumorgerelateerde symptomen in de controlegroep en de H2-monotherapiegroep vergelijkbaar (P = 0,9994).
Bij verlenging van de behandelingstijd namen in de controlegroep, de prevalentie van matige hoest (P = 0,0023), milde dyspneu (P = 0,0019), milde niet-cardiale pijn op de borst (P = 0,006), milde pleurale effusie (P = 0,0023 ), en milde bloedspuwing (P = 0,0028) significant toe (Figure 2A).
In de H2-monotherapiegroep was de prevalentie van matige hoest (P = 0,0014), milde dyspneu (P = 0,0247), milde niet-cardiale pijn op de borst (P = 0,0136), milde pleurale effusie (P = 0,0015) en milde bloedspuwing (P = 0,0048) juist aanzienlijk afgenomen. (Figure 2B).

An external file that holds a picture, illustration, etc.
Object name is MGR-10-75-g002.jpg

Figure 2

Tumor-associated symptoms varied with the inhalation time of hydrogen (H2).

Note: (A) Control group (inhalation of 33.3% oxygen gas and no H2 (n = 10). (B) H2 only group (inhalation of 66.7% H2 + 33.3% O2) (n = 10). Each tumor-associated symptom was compared using linear regression analysis.

Aan het begin van de H2-behandeling was de prevalentie van tumorgerelateerde symptomen in de drie groepen vergelijkbaar (P = 0,5120), maar de geneesmiddelgerelateerde symptomen in de drie groepen waren behoorlijk verschillend  (Figure 3). 
Met de verlenging van de behandelingstijd namen de prevalentie van hoesten en niet-cardiale pijn op de borst (P = 0,0013), maculopapulaire uitslag (P = 0,0021), lever- en galaandoeningen (P = 0,0064) en duizeligheid en hoofdpijn (P = 0,0111) significant af maar diarree niet (P = 0,4144) (Figure 3A).

In de waterstof (H2) therapiegroep waren de prevalentie van febriele granulocytopenie (P = 0,0026), misselijkheid en braken (P = 0,0051), maculopapulaire uitslag (P < 0,0001), slapeloosheid (P = 0,0144) en orale mucositis (P = 0.0007) aanzienlijk gedaald  (Figure 3B).
In de groep met chemotherapie en waterstoftherapie (H2) nam de prevalentie van febriele granulocytopenie (P = 0,0086), anemie en trombocytopenie (P = 0,0009), constipatie en diarree (P = 0,0053) en anorexia (P = 0,0129) significant af, maar bij misselijkheid en braken was er geen statistisch significant (P = 0,0720;  Figure 3C).

Na 16 maanden follow-up ontwikkelden alle 58 patiënten tumorprogressie. Progressievrije tijd (PFS) voor de controlegroep was mediaan 4,4 maanden (± 1,2 maanden), terwijl die voor de groep met alleen waterstof (H2) mediaan 7,9 maanden (± 2,2 maanden) was, de H2-immunotherapiegroep 10,1 maanden (± 2,6 maanden) was, de H2-gerichte therapiegroep 9,4 maanden (± 3,1 maanden) en H2-chemotherapie groep was 8,5 maanden (± 3,0 maanden).

Progressievrije tijd (PFS) van de vier behandelingsgroepen was langer dan die van de controlegroep en die van de drie H2-therapie-combinatiegroepen was statistisch significant verlengd. (Figure 4)

Het volledige studieverslag is gratis in te zien of te downloaden. Klik op de titel van het abstract:

Abstract

Chemotherapy, targeted therapy, and immunotherapy are used against advanced non-small cell lung cancer. A clinically efficacious method for relieving the adverse events associated of such therapies is lacking. Fifty-eight adult patients were enrolled in our trial to relieve pulmonary symptoms or the adverse events of drugs. Twenty patients who refused drug treatment were assigned equally and randomly to a hydrogen (H2)-only group and a control group. According to the results of tumor-gene mutations and drug-sensitivity tests, 10, 18, and 10 patients were enrolled into chemotherapy, targeted therapy, and immunotherapy groups in which these therapies were combined with H2-therapy, respectively. Patients underwent H2 inhalation for 4–5 hours per day for 5 months or stopped when cancer recurrence. Before study initiation, the demographics (except for tumor-mutation genes) and pulmonary symptoms (except for moderate cough) of the five groups showed no significant difference. During the first 5 months of treatment, the prevalence of symptoms of the control group increased gradually, whereas that of the four treatment groups decreased gradually. After 16 months of follow-up, progression-free survival of the control group was lower than that of the H2-only group, and significantly lower than that of H2 + chemotherapy, H2 + targeted therapy, and H2 + immunotherapy groups. In the combined-therapy groups, most drug-associated adverse events decreased gradually or even disappeared. H2 inhalation was first discovered in the clinic that can be used to control tumor progression and alleviate the adverse events of medications for patients with advanced non-small cell lung cancer. This study was approved by the Ethics Committee of Fuda Cancer Hospital of Jinan University on December 7, 2018 (approval No. Fuda20181207), and was registered at ClinicalTrials.gov (Identifier: NCT03818347) on January 28, 2019.

RESOURCES

Discussion

Molecular H2 has been used to treat pulmonary symptoms in animal models of acute lung injury,,,, asthma and chronic obstructive pulmonary disease.,, The principle of H2 therapy includes inhibition of secretion of cytokines such as interleukin-4, interleukin-13, interleukin-6 and tumor necrosis factor-α. H2 therapy can alleviate pulmonary inflammation without impairing anti-tumor effects., Therefore, H2 gas can be adopted as adjuvant therapy to suppress these symptoms.

Chemotherapy, targeted therapy, and immunotherapy are first-line treatments against advanced NSCLC.,, The vastly increased generation of reactive oxygen species during treatment is believed to contribute to adverse events, resulting in oxidative stress, inflammation and apoptosis., In the present study, H2 therapy was shown to alleviate drug-related adverse events, most of which have been reported in animal models, including lung injury caused by various factors,,,, hepatobiliary diseases,,, maculopapular rash, diarrhea and constipation,,, nausea and vomiting,, oral mucositis,, anemia, thrombocytopenia, and anorexia. We found that the prevalence of insomnia, dizziness and headache could be reduced significantly after H2 inhalation, which could be related to relief of diseases of the central nervous system, such as cerebral hemorrhage,,, Parkinson's disease, and Alzheimer's disease,, observed in animal experiments. The mechanism of action observed in animal experiments could be used as a reference for clinical research. Surprisingly, H2 therapy, which is non-toxic and can alleviate adverse events in multiple organs simultaneously, has been used rarely.

We found that H2 monotherapy could prolong the PFS of patients with advanced NSCLC from 4.4 ± 1.2 months to 7.9 ± 2.2 months, suggesting that H2 could inhibit the growth of lung cancer cells independently. This hypothesis has been bolstered by data from an in vitro and in vivo study, which confirmed that H2 can inhibit the proliferation, migration, and invasion of the lung-cancer cell lines and tumor growth in mouse model. These data suggested that H2 could serve as new therapy against lung cancer. However, for patients eligible for first-line treatment, drugs will produce more pronounced effects upon tumor control. Whether a combination of drug therapy and H2 therapy can elicit better tumor control must be studied further, but gradual reduction of most drug-associated adverse events after H2 inhalation is clear.

Several delivery methods of molecular H2 are available and convenient: inhalation, drinking H2-dissolved water, injection with H2-saturated saline, and taking a “H2 bath.” H2 is non-toxic, inexpensive, can be administered readily, can diffuse into tissues and cells and cross the blood–brain barrier. Hence, H2 could be used to treat tumors of the head, neck and chest. Because of the risk of explosion of H2 and oxygen mixed in air, often such gas mixtures are inhaled using catheters and masks whereas, in animal experiments, drinking or injection of H2-dissolved water is employed. Use of a machine with a sufficiently high flow rate (3 L/min) and inhalation duration every day (4–6 hours) of H2 in this trial may enable control of tumor growth and reduce the prevalence of adverse events of drugs.

In general, H2 inhalation was first discovered in the clinic that can be used to control tumor progression and alleviate the adverse events of medications in patients with advanced NSCLC. The main limitation of this study is that the number of patients enrolled is relatively small, and more accurate patient benefits are still awaiting the results of large samples. Whether this therapeutic effect can be improved further, as well as determination of the synergistic effect of drugs and H2 therapy, must be explored further.

Footnotes

Conflicts of interest

None declared.

Financial support

None.

Institutional review board statement

This study protocol received ethical approval from the Ethics Committee of Fuda Cancer Hospital of Jinan University on December 7, 2018 (approval No. Fuda20181207) and conformed to the specifications of the World Medical Association's Declaration of Helsinki.

Informed consent statement

The authors certify that they have obtained all appropriate patient consent forms. In the form the patients have given their consent for the images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity.

Reporting statement

This study followed the Transparent Reporting of Evaluations with Nonrandomized Designs (TREND) Statement.

Copyright transfer agreement

The Copyright License Agreement has been signed by all authors before publication.

Data sharing statement

Individual participant data that underlie the results reported in this article, after deidentification (text, tables, figures, and appendices). Study protocol and informed consent form will be available immediately following publication, without end date. Results will be disseminated through presentations at scientific meetings and/or by publication in a peer-reviewed journal. Anonymized trial data will be available indefinitely at www.figshare.com.

Plagiarism check

Checked twice by iThenticate.

Peer review

Externally peer reviewed.

References

1. Siegel RL, Miller KD, Jemal A. Cancer statistics, 2019. CA Cancer J Clin. 2019;69:7–34. [PubMed[]
2. Reinke LF, Feemster LC, Backhus LM, Gylys-Colwell I, Au DH. Assessment and management of symptoms for outpatients newly diagnosed with lung cancer. Am J Hosp Palliat Care. 2016;33:178–183. [PMC free article] [PubMed[]
3. de Groot PM, Chung JH, Ackman JB, et al. ACR Appropriateness Criteria® noninvasive clinical staging of primary lung cancer. J Am Coll Radiol. 2019;16:S184–S195. [PubMed[]
4. Rossi A, Di Maio M. Platinum-based chemotherapy in advanced non-small-cell lung cancer: optimal number of treatment cycles. Expert Rev Anticancer Ther. 2016;16:653–660. [PubMed[]
5. Kumarakulasinghe NB, van Zanwijk N, Soo RA. Molecular targeted therapy in the treatment of advanced stage non-small cell lung cancer (NSCLC) Respirology. 2015;20:370–378. [PubMed[]
6. Perrotta F, Rocco D, Vitiello F, et al. Immune checkpoint blockade for advanced NSCLC: a new landscape for elderly patients. Int J Mol Sci. 2019;20:2258. [PMC free article] [PubMed[]
7. Zhou JG, Tian X, Cheng L, et al. The risk of neutropenia and leukopenia in advanced non-small cell lung cancer patients treated with Erlotinib: a prisma-compliant systematic review and meta-analysis. Medicine. 2015;94:e1719. [PMC free article] [PubMed[]
8. Wang Z, Cai XJ, Chen LY, et al. Factors potentially associated with gemcitabine-based chemotherapy-induced thrombocytopenia in Chinese patients with nonsmall cell lung cancer. J Cancer Res Ther. 2018;14:S656–S660. [PubMed[]
9. Li J, Yuan Z, Wang Q, Fan W, Zhang G. Meta-analysis of overall incidence and risk of ALK inhibitors-induced liver toxicities in advanced non-small-cell lung cancer. Medicine (Baltimore) 2019;98:e13726. [PMC free article] [PubMed[]
10. Kelso GF, Porteous CM, Coulter CV, et al. Selective targeting of a redox-active ubiquinone to mitochondria within cells: antioxidant and antiapoptotic properties. J Biol Chem. 2001;276:4588–4596. [PubMed[]
11. Ferrer MD, Sureda A, Tauler P, Palacín C, Tur JA, Pons A. Impaired lymphocyte mitochondrial antioxidant defences in variegate porphyria are accompanied by more inducible reactive oxygen species production and DNA damage. Br J Haematol. 2010;149:759–767. [PubMed[]
12. Ohta S. Molecular hydrogen as a novel antioxidant: overview of the advantages of hydrogen for medical applications. Methods Enzymol. 2015;555:289–317. [PubMed[]
13. Matsushita T, Kusakabe Y, Kitamura A, Okada S, Murase K. Investigation of protective effect of hydrogen-rich water against cisplatin-induced nephrotoxicity in rats using blood oxygenation level-dependent magnetic resonance imaging. Jpn J Radiol. 2011;29:503–512. [PubMed[]
14. Meng X, Chen H, Wang G, Yu Y, Xie K. Hydrogen-rich saline attenuates chemotherapy-induced ovarian injury via regulation of oxidative stress. Exp Ther Med. 2015;10:2277–2282. [PMC free article] [PubMed[]
15. Terasaki Y, Suzuki T, Tonaki K, et al. Molecular hydrogen attenuates gefitinib-induced exacerbation of naphthalene-evoked acute lung injury through a reduction in oxidative stress and inflammation. Lab Invest. 2019;99:793–806. [PubMed[]
16. Ono H, Nishijima Y, Ohta S, et al. Hydrogen gas inhalation treatment in acute cerebral infarction: a randomized controlled clinical study on safety and neuroprotection. J Stroke Cerebrovasc Dis. 2017;26:2587–2594. [PubMed[]
17. Asanuma H, Kitakaze M. Translational study of hydrogen gas inhalation as adjuncts to reperfusion therapy for acute myocardial infarction. Circ J. 2017;81:936–937. [PubMed[]
18. Zhai Y, Zhou X, Dai Q, Fan Y, Huang X. Hydrogen-rich saline ameliorates lung injury associated with cecal ligation and puncture-induced sepsis in rats. Exp Mol Pathol. 2015;98:268–276. [PubMed[]
19. Sun Q, Cai J, Liu S, et al. Hydrogen-rich saline provides protection against hyperoxic lung injury. J Surg Res. 2011;165:e43–49. [PubMed[]
20. Liu S, Liu K, Sun Q, et al. Consumption of hydrogen water reduces paraquat-induced acute lung injury in rats. J Biomed Biotechnol. 2011;2011:305086. [PMC free article] [PubMed[]
21. Fang Y, Fu XJ, Gu C, et al. Hydrogen-rich saline protects against acute lung injury induced by extensive burn in rat model. J Burn Care Res. 2011;32:e82–e91. [PubMed[]
22. Xiao M, Zhu T, Wang T, Wen FQ. Hydrogen-rich saline reduces airway remodeling via inactivation of NF-κB in a murine model of asthma. Eur Rev Med Pharmacol Sci. 2013;17:1033–1043. [PubMed[]
23. Liu Z, Geng W, Jiang C, et al. Hydrogen-rich saline inhibits tobacco smoke-induced chronic obstructive pulmonary disease by alleviating airway inflammation and mucus hypersecretion in rats. Exp Biol Med (Maywood) 2017;242:1534–1541. [PMC free article] [PubMed[]
24. Liu X, Ma C, Wang X, et al. Hydrogen coadministration slows the development of COPD-like lung disease in a cigarette smoke-induced rat model. Int J Chron Obstruct Pulmon Dis. 2017;12:1309–1324. [PMC free article] [PubMed[]
25. Suzuki Y, Sato T, Sugimoto M, et al. Hydrogen-rich pure water prevents cigarette smoke-induced pulmonary emphysema in SMP30 knockout mice. Biochem Biophys Res Commun. 2017;492:74–81. [PubMed[]
26. Gao Y, Yang H, Fan Y, Li L, Fang J, Yang W. Hydrogen-rich saline attenuates cardiac and hepatic injury in doxorubicin rat model by inhibiting inflammation and apoptosis. Mediators Inflamm. 2016;2016:1320365. [PMC free article] [PubMed[]
27. Lu S, Chen Z, Hu C, et al. Nedaplatin plus Docetaxel versus Cisplatin plus Docetaxel as first-line chemotherapy for advanced squamous cell carcinoma of the lung - a multicenter, open-label, randomized, phase III trial. J Thorac Oncol. 2018;13:1743–1749. [PubMed[]
28. Choi YW, Jeon SY, Jeong GS, et al. EGFR exon 19 deletion is associated with favorable overall survival after first-line gefitinib therapy in advanced non-small cell lung cancer patients. Am J Clin Oncol. 2018;41:385–390. [PubMed[]
29. Reck M. Pembrolizumab as first-line therapy for metastatic non-small-cell lung cancer. Immunotherapy. 2018;10:93–105. [PubMed[]
30. Liou GY, Storz P. Reactive oxygen species in cancer. Free Radical Res. 2010;44:479–496. [PMC free article] [PubMed[]
31. Cui Q, Wang JQ, Assaraf YG, et al. Modulating ROS to overcome multidrug resistance in cancer. Drug Resist Updat. 2018;41:1–25. [PubMed[]
32. Fukuda KI, Asoh S, Ishikawa M, Yamamoto Y, Ohsawa I, Ohta S. Inhalation of hydrogen gas suppresses hepatic injury caused by ischemia/reperfusion through reducing oxidative stress. Biochem Biophys Res Commun. 2007;361:670–674. [PubMed[]
33. Tan YC, Xie F, Zhang HL, et al. Hydrogen-rich saline attenuates postoperative liver failure after major hepatectomy in rats. Clin Res Hepatol Gastroenterol. 2014;38:337–345. [PubMed[]
34. Liu Y, Yang L, Tao K, et al. Protective effects of hydrogen enriched saline on liver ischemia reperfusion injury by reducing oxidative stress and HMGB1 release. BMC Gastroenterol. 2014;14:12. [PMC free article] [PubMed[]
35. Zhou P, Lin B, Wang P, et al. The healing effect of hydrogen-rich water on acute radiation-induced skin injury in rats. J Radiat Res. 2019;60:17–22. [PMC free article] [PubMed[]
36. Zheng X, Mao Y, Cai J, et al. Hydrogen-rich saline protects against intestinal ischemia/reperfusion injury in rats. Free Radic Res. 2009;43:478–484. [PubMed[]
37. Chen H, Sun YP, Hu PF, et al. The effects of hydrogen-rich saline on the contractile and structural changes of intestine induced by ischemia-reperfusion in rats. J Surg Res. 2011;167:316–322. [PubMed[]
38. Shigeta T, Sakamoto S, Li XK, et al. Luminal injection of hydrogen-rich solution attenuates intestinal ischemia-reperfusion injury in rats. Transplantation. 2015;99:500–507. [PubMed[]
39. Liu X, Chen Z, Mao N, Xie Y. The protective of hydrogen on stress-induced gastric ulceration. Int Immunopharmacol. 2012;13:197–203. [PubMed[]
40. Zhang JY, Wu QF, Wan Y, et al. Protective role of hydrogen-rich water on aspirin-induced gastric mucosal damage in rats. World J Gastroenterol. 2014;20:1614–1622. [PMC free article] [PubMed[]
41. Kasuyama K, Tomofuji T, Ekuni D, et al. Hydrogen-rich water attenuates experimental periodontitis in a rat model. J Clin Periodontol. 2011;38:1085–1090. [PubMed[]
42. Yoneda T, Tomofuji T, Kunitomo M, et al. Preventive effects of drinking hydrogen-rich water on gingival oxidative stress and alveolar bone resorption in rats fed a high-fat diet. Nutrients. 2017;9:64. [PMC free article] [PubMed[]
43. Zhao S, Mei K, Qian L, et al. Therapeutic effects of hydrogen-rich solution on aplastic anemia in vivo. Cell Physiol Biochem. 2013;32:549–560. [PubMed[]
44. Takeuchi S, Wada K, Nagatani K, Osada H, Otani N, Nawashiro H. Hydrogen may inhibit collagen-induced platelet aggregation: an ex vivo and in vivo study. Intern Med. 2012;51:1309–1313. [PubMed[]
45. McCarty MF. Potential ghrelin-mediated benefits and risks of hydrogen water. Med Hypotheses. 2015;84:350–355. [PubMed[]
46. Manaenko A, Lekic T, Ma Q, Zhang JH, Tang J. Hydrogen inhalation ameliorated mast cell-mediated brain injury after intracerebral hemorrhage in mice. Crit Care Med. 2013;41:1266–1275. [PMC free article] [PubMed[]
47. Shao A, Wu H, Hong Y, et al. Hydrogen-rich saline attenuated subarachnoid hemorrhage-induced early brain injury in rats by suppressing inflammatory response: possible involvement of NF-kappaB pathway and NLRP3 inflammasome. Mol Neurobiol. 2016;53:3462–3476. [PubMed[]
48. Zhuang Z, Sun XJ, Zhang X, et al. Nuclear factor-κB/Bcl-XL pathway is involved in the protective effect of hydrogen-rich saline on the brain following experimental subarachnoid hemorrhage in rabbits. J Neurosci Res. 2013;91:1599–1608. [PubMed[]
49. Fu Y, Ito M, Fujita Y, et al. Molecular hydrogen is protective against 6-hydroxydopamine-induced nigrostriatal degeneration in a rat model of Parkinson's disease. Neurosci Lett. 2009;453:81–85. [PubMed[]
50. Fujita K, Seike T, Yutsudo N, et al. Hydrogen in drinking water reduces dopaminergic neuronal loss in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease. PLoS One. 2009;4:e7247. [PMC free article] [PubMed[]
51. Li J, Wang C, Zhang JH, Cai JM, Cao YP, Sun XJ. Hydrogen-rich saline improves memory function in a rat model of amyloid-beta-induced Alzheimer's disease by reduction of oxidative stress. Brain Res. 2010;1328:152–161. [PubMed[]
52. Wang C, Li J, Liu Q, et al. Hydrogen-rich saline reduces oxidative stress and inflammation by inhibit of JNK and NF-kappaB activation in a rat model of amyloid-beta-induced Alzheimer's disease. Neurosci Lett. 2011;491:127–132. [PubMed[]
53. Wang D, Wang L, Zhang Y, Zhao Y, Chen G. Hydrogen gas inhibits lung cancer progression through targeting SMC3. Biomed Pharmacother. 2018;104:788–797. [PubMed[]
54. Zhang JY, Liu C, Zhou L, et al. A review of hydrogen as a new medical therapy. Hepatogastroenterology. 2012;59:1026–1032. [PubMed[]
55. Ohta S. Recent progress toward hydrogen medicine: potential of molecular hydrogen for preventive and therapeutic applications. Curr Pharm Des. 2011;17:2241–2252. [PMC free article] [PubMed[]
56. Dixon BJ, Tang J, Zhang JH. The evolution of molecular hydrogen: a noteworthy potential therapy with clinical significance. Med Gas Res. 2013;3:10. [PMC free article] [PubMed[]

Articles from Medical Gas Research are provided here courtesy of Wolters Kluwer -- Medknow Publications

Plaats een reactie ...

Reageer op "Waterstoftherapie zorgt voor veel minder bijwerkingen en betere ziekteprogressie vrije overleving bij patienten met niet-kleincellige longkanker die werden behandeld met of chemo of immuuntherapie"


Gerelateerde artikelen
 

Gerelateerde artikelen

Studiepublicaties van niet-toxische >> Waterstoftherapie zorgt voor >> Groene thee extract - epigallocatechin-3-gallate >> Hyperthermie plus hoge dosis >> Hyperthermie plus voedingsprogramma >> Hyperthermie aanvullend op >> Paliatieve zorg naast standaard >> TCM - traditionele Chinese >> Voeding en voedingsupplementen >> Complementair - niet-toxisch >>