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Protective effect of hydrogen sulfide against stress-induced lung injury: involvement of Nrf2, NFκB/iNOS, and HIF-1α signaling pathways
Author(s) -
Fatma Ali,
Hanaa Hassanein Mohammed,
Doaa M. Ali
Publication year - 2022
Publication title -
cell stress and chaperones
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.994
H-Index - 87
eISSN - 1466-1268
pISSN - 1355-8145
DOI - 10.1007/s12192-021-01248-8
Subject(s) - sodium hydrosulfide , nitric oxide synthase , chemistry , malondialdehyde , oxidative stress , nitric oxide , western blot , tumor necrosis factor alpha , nf κb , pharmacology , endocrinology , medicine , apoptosis , biochemistry , hydrogen sulfide , sulfur , organic chemistry , gene
Stress is a common phenomenon that is attracting increasing attention. Hydrogen sulfide (H 2 S) is a gasotransmitter that plays an important role in many physiological and pathological events. Our study aimed to estimate the effect and the underlying mechanisms of the H 2 S donor, sodium hydrosulfide (NaHS), against immobilization stress (IS)-induced lung injury. Forty adult male rats were classified into control group, NaHS group, and IS groups with and without NaHS treatment. Serum was obtained to determine corticosterone (CORT), total antioxidant capacity (TAC), tumor necrosis factor-α (TNF-α), and interleukin-10 (IL-10) levels. Lung H 2 S, nitric oxide (NO), inducible nitric oxide synthase (iNOS), and malondialdehyde (MDA) levels were measured. Lung expressions of H 2 S synthesizing enzymes and Western blot analysis of nuclear factor erythroid 2-related factor 2 (Nrf2) and hypoxia-inducible factor 1 alpha (HIF 1α) were estimated. Histopathological changes and immunohistochemical assessment of nuclear factor kappa B (NF-κB) and caspase-3 were also done. Pretreatment with NaHS led to marked histological protection from lung damage seen in IS rats. Furthermore, pretreatment with NaHS before IS protected lung H 2 S levels and expressions of H 2 S-synthesizing enzymes. Similarly, the levels of CORT, TNF-α, IL-10, MDA, TAC, NO, iNOS, HIF-1 α, and nuclear Nrf2 and expressions of NF-kB and caspase 3 were all maintained at near control levels in contrast to that in the IS rats. In conclusion, NaHS is protective against stress-induced lung injury due to its antioxidant, anti-inflammatory, anti-fibrotic, and antiapoptotic effects. Thus, NaHS can be used to minimize stress complications on lung.

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