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硫化氢通过抑制炎症和氧化应激减轻双酚 A 引发的肺损伤。

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

机构信息

Biochemistry and Molecular Biology Department, Faculty of Vet. Med, Benha University, Benha, Egypt.

Health Radiation Research, National Center for Radiation Research and Technology, Egyptian Atomic Energy Authority, Cairo, Egypt.

出版信息

BMC Pharmacol Toxicol. 2022 Dec 30;23(1):98. doi: 10.1186/s40360-022-00636-9.

DOI:10.1186/s40360-022-00636-9
PMID:36585682
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9805095/
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 (HS) 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, HS 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, HS 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.

摘要

外源性雌激素双酚 A(BPA)是一种常用的工业化学物质,与内分泌干扰有关。本研究的目的是研究慢性 BPA 暴露对成年雌性大鼠呼吸系统的影响,以及硫化氢(HS)供体硫氢化钠(NaHS)的潜在缓解作用。检测支气管肺泡灌洗液(BALF)中的生物标志物,包括总蛋白含量、总细胞计数、中性粒细胞%、细胞间黏附分子-1(ICAM-1)和转化生长因子-β(TGF-β)。NaHS 显著降低了促炎细胞因子(IFN-β和MCAF),还降低了(即 VCAM-1、VEGF、VIM、MMP-2、MMP-9),并降低了丙二醛,增加了 SOD 和 GSH-PX 的活性。值得注意的是,HS 诱导 p-细胞外信号调节激酶(p-ERK)、p-Jun N-末端激酶(p-JNK)和 p-p38 的表达水平显著降低,HS 抑制 BPA 诱导的肺泡上皮细胞炎症和损伤。这些结果表明,NaHS 可能通过抑制 ERK/JNK/p-p38MAPK 信号通路来预防炎症,随后抑制炎症、上皮细胞损伤和细胞凋亡可能为肺损伤的治疗提供新的思路。

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本文引用的文献

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