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Hydrogen sulfide attenuates lung injury instigated by Bisphenol-A via suppressing inflammation and oxidative stress.

ABSTRACT: The xenoestrogen bisphenol A (BPA), a commonly used industrial chemical, has been linked to endocrine disruption. The point of the study was to consider the effects of chronic BPA exposure on the respiratory system of adult female rats, and the potential mitigating benefits of Sodium hydrosulfide (NaHS), a donor of hydrogen sulfide (H₂S) administration. Detect biomarkers in Bronchoalveolar lavage fluid (BALF), including total protein content, Total cell counts, Neutrophils %, ICAM (intercellular adhesion molecule)-1 and TGF-β (Transforming growth factor beta). NaHS significantly reduced pro-inflammatory cytokines (IFN-β and MCAF,) also reduce (i.e. VCAM-1, VEGF, VIM, MMP-2, MMP-9), and reduced malondialdehyde and augmented activities of SOD and GSH-PX. Notably, H₂S induced a marked decrease in the expression levels of p-extracellular signal-regulated protein kinase (p-ERK), p-c-Jun N-terminal kinase (p-JNK), and p-p38, H₂S inhibits BPA-induced inflammation and injury in alveolar epithelial cells. These results suggest NaHS may prevent inflammation via the suppression of the ERK/JNK/ p-p38MAPK signaling pathway, Subsequent inhibition of inflammation, epithelial cell injury, and apoptosis may be providing insight into potential avenues for the treatment of lung injury.

SUBMITTER: Abo-Zaid OAR

PROVIDER: S-EPMC9805095 | biostudies-literature | 2022 Dec

REPOSITORIES: biostudies-literature

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Hydrogen sulfide attenuates lung injury instigated by Bisphenol-A via suppressing inflammation and oxidative stress.

Abo-Zaid Omayma A R OAR Moawed Fatma S M FSM Hassan Hend A HA Moustafa Enas M EM

BMC pharmacology & toxicology 20221230 1

The xenoestrogen bisphenol A (BPA), a commonly used industrial chemical, has been linked to endocrine disruption. The point of the study was to consider the effects of chronic BPA exposure on the respiratory system of adult female rats, and the potential mitigating benefits of Sodium hydrosulfide (NaHS), a donor of hydrogen sulfide (H<sub>2</sub>S) administration. Detect biomarkers in Bronchoalveolar lavage fluid (BALF), including total protein content, Total cell counts, Neutrophils %, ICAM (in ...[more]

PMID: 36585682

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Project description:In addition to the lung, the liver is considered another major target for paraquat (PQ) poisoning. Hydrogen sulfide (H2S) has been demonstrated to be effective in the inhibition of oxidative stress and inflammation. The aim of this study was to investigate the protective effect of exogenous H2S against PQ-induced acute liver injury. The acute liver injury model was established by a single intraperitoneal injection of PQ, evidenced by histological alteration and elevated serum aminotransferase levels. Different doses of NaHS were administered intraperitoneally one hour before exposure to PQ. Analysis of the data shows that exogenous H2S attenuated the PQ-induced liver injury and oxidative stress in a dose-dependent manner. H2S significantly suppressed reactive oxygen species (ROS) generation and the elevation of malondialdehyde content while it increased the ratio of GSH/GSSG and levels of antioxidant enzymes including SOD, GSH-Px, HO-1, and NQO-1. When hepatocytes were subjected to PQ-induced oxidative stress, H2S markedly enhanced nuclear translocation of Nrf2 via S-sulfhydration of Keap1 and resulted in the increase in IDH2 activity by regulating S-sulfhydration of SIRT3. In addition, H2S significantly suppressed NLRP3 inflammasome activation and subsequent IL-1β excretion in PQ-induced acute liver injury. Moreover, H2S cannot reverse the decrease in SIRT3 and activation of the NLRP3 inflammasome caused by PQ in Nrf2-knockdown hepatocytes. In summary, H2S attenuated the PQ-induced acute liver injury by enhancing antioxidative capability, regulating mitochondrial function, and suppressing ROS-induced NLRP3 inflammasome activation. The antioxidative effect of H2S in PQ-induced liver injury can at least partly be attributed to the promotion of Nrf2-driven antioxidant enzymes via Keap1 S-sulfhydration and regulation of SIRT3/IDH2 signaling via Nrf2-dependent SIRT3 gene transcription as well as SIRT3 S-sulfhydration. Thus, H2S supplementation can form the basis for a promising novel therapeutic strategy for PQ-induced acute liver injury.

Dataset Information

Hydrogen sulfide attenuates lung injury instigated by Bisphenol-A via suppressing inflammation and oxidative stress.

Publications

Hydrogen sulfide attenuates lung injury instigated by Bisphenol-A via suppressing inflammation and oxidative stress.

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