Hydrogen Gas Inhalation (4%) could Reduce Lung Inflammation and Blood Pressure in Rats with Monocrotaline-Induced Pulmonary Hypertension | Chapter 9 | Medicine and Medical Research: New Perspectives Vol. 2

 

The aim of this study was to investigate the effects of inhaling atmospheric air containing 4% hydrogen on the symptoms and progression of PH in male Wistar rats using the MCT-induced model. Interstitial lung diseases (IPD), associated with inflammatory processes and the appearance of fibrosis, lead to impaired ventilation-perfusion ratio and hypoxia. Recently, strategies and drug approaches for the treatment of IPD-associated pulmonary hypertension have been widely discussed. Hydrogen has been shown to exhibit selective antioxidant properties against hydroxyl radicals and exert antioxidant and anti-inflammatory effects. Because monocrotaline causes oxidative stress, the monocrotaline-induced model of pulmonary hypertension is appropriate for researching compounds having antioxidant properties. On day 1, male Wistar rats were subcutaneously injected with either a water-alcohol solution of monocrotaline or control solution consisting solely of water and alcohol. One group of monocrotaline-injected animals was placed in a plastic box continuously ventilated with atmospheric air containing 4% molecular hydrogen, while the two other groups (one injected with monocrotaline and the other with vehicle) were placed in boxes ventilated with atmospheric air. After 21 days, hemodynamic parameters were measured under urethane narcosis. The results showed that, although hydrogen inhalation had no effect on the main markers of pulmonary hypertension induced by monocrotaline injection, there was a reduction in systemic blood pressure due to its systolic component, and a decrease in TGF- β expression, as well as a reduction in tryptase-containing mast cells. The results in combination with previous published results indicate that molecular hydrogen may be a useful therapeutic agent to combat pulmonary hypertension. Further research with larger sample sizes and exploring different routes of administration, concentrations and durations is needed to determine the optimal therapeutic approach. Overall, these findings suggest that molecular hydrogen may hold promise as a therapeutic agent in the treatment of pulmonary hypertension, in patients but further investigation is warranted.

 

Author(s) Details

Tatyana Kuropatkina
Faculty of Medicine, Lomonosov Moscow State University, Lomonosovsky Prospect 27-1, 119991 Moscow, Russia.

 

Dmitrii Atiakshin
Research Institute of Experimental Biology and Medicine, N.N. Burdenko Voronezh State Medical University, Moskovsky Prispect, 185, 394066, Voronezh, Russia and RUDN University, Miklukho-Maklaya St 6, 117198, Moscow, Russia.

 

 

Fedor Sychev
Faculty of Biology, Lomonosov Moscow State University, Leninskie Gory 1-12, 119234 Moscow, Russia.

 

Marina Artemieva
Faculty of Medicine, Lomonosov Moscow State University, Lomonosovsky Prospect 27-1, 119991 Moscow, Russia and Faculty of Biology, Lomonosov Moscow State University, Leninskie Gory 1-12, 119234 Moscow, Russia.

 

Tatyana Samoilenko
Research Institute of Experimental Biology and Medicine, N.N. Burdenko Voronezh State Medical University, Moskovsky Prispect, 185, 394066, Voronezh, Russia.

 

Olga Gerasimova
Research Institute of Experimental Biology and Medicine, N.N. Burdenko Voronezh State Medical University, Moskovsky Prispect, 185, 394066, Voronezh, Russia.

 

Viktoria Shishkina
Research Institute of Experimental Biology and Medicine, N.N. Burdenko Voronezh State Medical University, Moskovsky Prispect, 185, 394066, Voronezh, Russia.

 

Khaydar Gufranov
Faculty of Medicine, Lomonosov Moscow State University, Lomonosovsky Prospect 27-1, 119991 Moscow, Russia.

 

Natalia Medvedeva
Faculty of Biology, Lomonosov Moscow State University, Leninskie Gory 1-12, 119234 Moscow, Russia.

 

Tyler W. Le Baron
Department of Kinesiology and Outdoor Recreation, Southern Utah University, Cedar City, 84720, Utah, USA and Molecular Hydrogen Institute, Cedar City, Utah, 84720, USA.

 

Oleg Medvedev
Faculty of Medicine, Lomonosov Moscow State University, Lomonosovsky Prospect 27-1, 119991 Moscow, Russia and Laboratory of Experimental Pharmacology, National Medical Research Center of Cardiology, Ulitsa Akademika Chazova 15a, 121552 Moscow, Russia.

 

 

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Cross-linking Mast Cell Specific Gangliosides Stimulates the Release of Newly Formed Lipid Mediators and Newly Synthesized Cytokines: An Advanced Study | Chapter 4 | Technological Innovation in Pharmaceutical Research Vol. 4

 Mast cells are immune-regulatory cells that play a role in the inflammatory response. Mast cells are partially activated without the release of preformed mediators when GD1b generated gangliosides are cross-linked by mAbAA4. Following ganglioside cross-linking, the release of newly formed and newly synthesised mediators is investigated. The newly synthesised lipid mediators, prostaglandins D2 and E2, were produced when the gangliosides were crosslinked with mAbAA4, however leukotrienes B4 and C4 were not released. The impact of cross-linking these gangliosides on the activation of arachidonate cascade enzymes was then examined. The phosphorylation of cytosolic phospholipase A2 and enhanced production of cyclooxygenase-2 were both caused by ganglioside cross-linking. Ganglioside cross-linking did not cause 5-lypoxygenase to translocate from the cytosol to the nucleus. The newly produced mediators interleukin-4, interleukin-6, and TNF- were also released after cross-linking of GD1b generated gangliosides. After that, the impact of cross-linking the gangliosides on the MAP kinase pathway was examined. The phosphorylation of ERK1/2, JNK1/2, and p38, as well as the activation of both NFB and NFAT, was activated by cross-linking the gangliosides in a Syk-dependent way. As a result of cross-linking the mast cell-specific GD1b derived gangliosides, signalling pathways are activated, culminating in the release of newly generated and synthesised mediators. The current study contributes to a better understanding of the wide range of potential methods by which mast cells repress, enhance, and modulate non-FcRI driven immune responses.

Author (s) Details

Edismauro Garcia Freitas Filho
Department of Cell and Molecular Biology and Pathogenic Bioagents, Bandeirantes 3900, 14049-900, Ribeirão Preto, SP, Brazil.

Elaine Zayas Marcelino da Silva
Department of Cell and Molecular Biology and Pathogenic Bioagents, Bandeirantes 3900, 14049-900, Ribeirão Preto, SP, Brazil.

Camila Ziliotto Zanotto
Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Av. Bandeirantes 3900, 14049-900, Ribeirão Preto, SP, Brazil.

Constance Oliver
Department of Cell and Molecular Biology and Pathogenic Bioagents, Bandeirantes 3900, 14049-900, Ribeirão Preto, SP, Brazil.

Maria Célia Jamur
Department of Cell and Molecular Biology and Pathogenic Bioagents, Bandeirantes 3900, 14049-900, Ribeirão Preto, SP, Brazil.

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