气体信号分子对特发性肺纤维化的作用机制研究进展

doi:10.20047/j.issn1673-7210.2022.28.08

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Abstract The gaseous signaling molecules nitric oxide, carbon monoxide, and hydrogen sulfide have anti-inflammatory, antioxidant, and anti-apoptotic properties. In addition, by regulating TGF-β/Smads, PI3K/AKT, Nrf2/HO-1, and nuclear factor-κB signaling pathways, it can inhibit the proliferation and activation of fibroblasts, reduce collagen deposition and epithelial-mesenchymal transition, thereby reducing the proliferation and activation of fibroblasts, and improving idiopathic pulmonary fibrosis. This article reviews the anti-pulmonary fibrosis effects of three gas signal molecules and their molecular mechanisms, and opens up a new therapeutic approach for the use of gas signal molecules and their donors in the treatment of pulmonary fibrosis in the future.

Key words： Gas signal molecules Nitrogen monxide Carbon monoxide Hydrogen sulfide Idiopathic pulmonary fibrosis

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	LI Aohan BAI Yu WANG Qianqian CHEN Yingqing

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LI Aohan BAI Yu WANG Qianqian CHEN Yingqing. Research progress on the mechanism of action of gas signal molecules on idiopathic pulmonary fibrosis[J]. 中国医药导报, 2022, 19(28): 41-45.

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https://www.yiyaodaobao.com.cn/EN/10.20047/j.issn1673-7210.2022.28.08 OR https://www.yiyaodaobao.com.cn/EN/Y2022/V19/I28/41

[1] 张冬冬，李芮，刘晓明.黄芪干预肺纤维化的作用机制研究进展[J].中医药导报，2021，27（7）：143-147.
[2] Olson AL，Gifford AH，Inase N，et al. The epidemiology of idiopathic pulmonary fibrosis and interstitial lung diseases at risk of a progressive-fibrosing phenotype [J]. Eur Respir Rev，2018，27（150）：180077-180086.
[3] 邓龙，邹晓青，姜德建.治疗肺纤维化药物的评价与开发进展[J].中国新药杂志，2021，30（8）：712-717.
[4] Chen Y，Yuan S，Cao Y，et al. Gasotransmitters：Potential Therapeutic Molecules of Fibrotic Diseases [J]. Oxid Med Cell Longev，2021，2021：3206982.
[5] Cinelli MA，Do HT，Miley GP，et al. Inducible nitric oxide synthase：Regulation，structure，and inhibition [J]. Med Res Rev，2020，40（1）：158-189.
[6] Hendriks KD，Maassen H，Van Dijk PR，et al. Gasotransmitters in health and disease：a mitochondria-centered view [J]. Curr Opin Pharmacol，2019，45：87-93.
[7] Zaafan MA，Haridy AR，Abdelhamid AM. Amitriptyline attenuates bleomycin-induced pulmonary fibrosis：modulation of the expression of NF-κβ，iNOS，and Nrf2 [J]. Naunyn Schmiedebergs Arch Pharmacol，2019，392（3）：279-286.
[8] Hu S，Pi Q，Luo M，et al. Contribution of the NLRP3/IL-1β axis to impaired vasodilation in sepsis through facilitation of eNOS proteolysis and the protective role of melatonin [J]. Int Immunopharmacol，2021，93：107388.
[9] Peng L，Wen L，Shi QF，et al. Scutellarin ameliorates pulmonary fibrosis through inhibiting NF-κB/NLRP3-mediated epithelial-mesenchymal transition and inflammation [J]. Cell Death Dis，2020，11（11）：978.
[10] Caporarello N，Meridew JA，Aravamudhan A，et al. Vascular dysfunction in aged mice contributes to persistent lung fibrosis [J]. Aging Cell，2020，19（8）：e13196.
[11] Yao F，Abdel-Rahman AA. Tetrahydrobiopterin paradoxically mediates cardiac oxidative stress and mitigates ethanol-evoked cardiac dysfunction in conscious female rats [J]. Eur J Pharmacol，2021，909：174406.
[12] Saleh D，Barnes PJ，Giaid A. Increased production of the potent oxidant peroxynitrite in the lungs of patients with idiopathic pulmonary fibrosis [J]. Am J Respir Crit Care Med，1997，155（5）：1763-1769.
[13] Channon KM. Tetrahydrobiopterin and Nitric Oxide Synthase Recouplers [J]. Handb Exp Pharmacol，2021，264：339-352.
[14] Gielis JF，Lin JY，Wingler K，et al. Pathogenetic role of eNOS uncoupling in cardiopulmonary disorders [J]. Free Radic Biol Med，2011，50（7）：765-776.
[15] Korbut E，Brzozowski T，Magierowski M. Carbon Monoxide Being Hydrogen Sulfide and Nitric Oxide Molecular Sibling，as Endogenous and Exogenous Modulator of Oxidative Stress and Antioxidative Mechanisms in the Digestive System [J]. Oxid Med Cell Longev，2020，2020：5083876.
[16] Wang XP，Zheng WC，Bai Y，et al. Carbon Monoxide-Releasing Molecule-3 Alleviates Kupffer Cell Pyroptosis Induced by Hemorrhagic Shock and Resuscitation via sGC-cGMP Signal Pathway [J]. Inflammation，2021，44（4）：1330-1344.
[17] 房立平，唐朝枢，刘新民.内源性气体信号分子和调节肽在特发性肺纤维化发病中的作用[J].国际病理科学与临床杂志，2009，29（1）：10-14.
[18] Casanova N，Zhou T，Gonzalez-Garay ML，et al. Low Dose Carbon Monoxide Exposure in Idiopathic Pulmonary Fibrosis Produces a CO Signature Comprised of Oxidative Phosphorylation Genes [J]. Sci Rep，2019，9（1）：14802.
[19] Zhou Z，Song R，Fattman CL，et al. Carbon monoxide suppresses bleomycin-induced lung fibrosis [J]. Am J Pathol，2005，166（1）：27-37.
[20] Zaorska E，Tomasova L，Koszelewski D，et al. Hydrogen Sulfide in Pharmacotherapy，Beyond the Hydrogen Sulfide-Donors [J]. Biomolecules，2020，10（2）：323.
[21] Song K，Li Q，Yin XY，et al. Hydrogen Sulfide：A Therapeutic Candidate for Fibrotic Disease? [J]. Oxid Med Cell Longev，2015，2015：458720.
[22] Zou W，Zhang X，Zhao M，et al. Cellular proliferation and differentiation induced by single-layer molybdenum disulfide and mediation mechanisms of proteins via the Akt-mTOR-p70S6K signaling pathway [J]. Nanotoxicology，2017，11（6）：781-793.
[23] Ornatowski W，Lu Q，Yegambaram M，et al. Complex interplay between autophagy and oxidative stress in the development of pulmonary disease [J]. Redox Biol，2020， 36：101679.
[24] Chanda D，Otoupalova E，Smith SR，et al. Developmental pathways in the pathogenesis of lung fibrosis [J]. Mol Aspects Med，2019，65：56-69.
[25] 钟长军，李琳，李俊，等.氧化应激在特发性肺纤维化中的作用及其机制研究进展[J].中国药理学通报，2012， 28（2）：169-172.
[26] Zhou X，An G，Chen J. Inhibitory effects of hydrogen sulphide on pulmonary fibrosis in smoking rats via attenuation of oxidative stress and inflammation [J]. J Cell Mol Med，2014，18（6）：1098-1103.
[27] 冯欣丽，庄盼，刘军权.特发性肺纤维化的发病机制及药物治疗进展[J].中国医药导报，2021，18（29）：45-48.
[28] 刘玲.外源性H2S对肺纤维化大鼠肺组织p-AKT、HIF-1α表达的影响[D].衡阳：南华大学，2018.
[29] Tzavlaki K，Moustakas A. TGF-β Signaling [J]. Biomol-ecules，2020，10（3）：487.
[30] Wang L，Wang HL，Liu TT，et al. TGF-Beta as a Master Regulator of Diabetic Nephropathy [J]. Int J Mol Sci，2021， 22（15）：7881.
[31] Wang L，Meng J，Wang C，et al. Hydrogen sulfide alleviates cigarette smoke-induced COPD through inhibition of the TGF-β1/smad pathway [J]. Exp Biol Med （Maywood），2020，245（3）：190-200.
[32] Liang B，Xiao T，Long J，et al. Hydrogen sulfide alleviates myocardial fibrosis in mice with alcoholic cardiomyopathy by downregulating autophagy [J]. Int J Mol Med，2017，40（6）：1781-1791.
[33] 曹华，马红英，曹霞，等.外源性H2S对肺纤维化大鼠肺组织转化生长因子-β1及结缔组织生长因子的干预作用[J].中国老年学杂志，2014，34（1）：140-142.
[34] 辛灵恩，李龙.细胞衰老在特发性肺间质纤维化中作用的最新进展[J].河北医药，2021，43（10）：1567-1571.
[35] Fujita K. p53 Isoforms in Cellular Senescence- and Ageing-Associated Biological and Physiological Functions [J]. Int J Mol Sci，2019，20（23）：6023.
[36] Chao C. Mechanisms of p53 degradation [J]. Clinica chimica acta; international journal of clinical chemistry，2015， 438：139-147.
[37] Klein AM，De Queiroz RM，Venkatesh D，et al. The roles and regulation of MDM2 and MDMX：it is not just about p53 [J]. Genes Dev，2021，35（9/10）：575-601.
[38] 王秀丽.硫化氢在运动改善肺纤维化及肺泡上皮细胞衰老中的作用及机制[D].上海：上海体育学院，2019.
[39] 徐祎彤.硫化氢通过硫巯基化MDM2抑制肺上皮细胞的衰老从而改善博来霉素诱导的小鼠肺纤维化[D].上海：上海体育学院，2020.