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硫化氢在缺血再灌注损伤中的治疗潜力。

Therapeutic Potential of Hydrogen Sulfide in Ischemia and Reperfusion Injury.

机构信息

Department of Typhoid, School of Basic Medical Sciences, Heilongjiang University of Chinese Medicine, Harbin 150040, China.

Department of Pharmacology, School of Basic Medical Sciences, Heilongjiang University of Chinese Medicine, Harbin 150040, China.

出版信息

Biomolecules. 2024 Jun 22;14(7):740. doi: 10.3390/biom14070740.

DOI:10.3390/biom14070740
PMID:39062455
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11274451/
Abstract

Ischemia-reperfusion (I/R) injury, a prevalent pathological condition in medical practice, presents significant treatment challenges. Hydrogen sulfide (HS), acknowledged as the third gas signaling molecule, profoundly impacts various physiological and pathophysiological processes. Extensive research has demonstrated that HS can mitigate I/R damage across multiple organs and tissues. This review investigates the protective effects of HS in preventing I/R damage in the heart, brain, liver, kidney, intestines, lungs, stomach, spinal cord, testes, eyes, and other tissues. HS provides protection against I/R damage by alleviating inflammation and endoplasmic reticulum stress; inhibiting apoptosis, oxidative stress, and mitochondrial autophagy and dysfunction; and regulating microRNAs. Significant advancements in understanding the mechanisms by which HS reduces I/R damage have led to the development and synthesis of HS-releasing agents such as diallyl trisulfide-loaded mesoporous silica nanoparticles (DATS-MSN), AP39, zofenopril, and ATB-344, offering a new therapeutic avenue for I/R injury.

摘要

缺血再灌注(I/R)损伤是医学实践中常见的病理状况,治疗存在巨大挑战。硫化氢(HS)作为第三气体信号分子,深刻影响多种生理和病理生理过程。大量研究表明,HS 可减轻多个器官和组织的 I/R 损伤。本综述探讨了 HS 在预防心脏、脑、肝、肾、肠、肺、胃、脊髓、睾丸、眼等组织的 I/R 损伤中的保护作用。HS 通过减轻炎症和内质网应激、抑制细胞凋亡、氧化应激和线粒体自噬及功能障碍,以及调节 microRNAs,发挥对 I/R 损伤的保护作用。对 HS 减轻 I/R 损伤机制的深入理解,促使开发和合成了 HS 释放剂,如二烯丙基三硫负载介孔硅纳米粒子(DATS-MSN)、AP39、佐芬普利和 ATB-344,为 I/R 损伤提供了新的治疗途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebe6/11274451/f57224224a02/biomolecules-14-00740-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebe6/11274451/4bd36242bbeb/biomolecules-14-00740-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebe6/11274451/b6f9a07a240e/biomolecules-14-00740-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebe6/11274451/9bd4e755ae85/biomolecules-14-00740-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebe6/11274451/c20cf33be539/biomolecules-14-00740-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebe6/11274451/d9b81788394a/biomolecules-14-00740-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebe6/11274451/f57224224a02/biomolecules-14-00740-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebe6/11274451/4bd36242bbeb/biomolecules-14-00740-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebe6/11274451/b6f9a07a240e/biomolecules-14-00740-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebe6/11274451/9bd4e755ae85/biomolecules-14-00740-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebe6/11274451/c20cf33be539/biomolecules-14-00740-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebe6/11274451/d9b81788394a/biomolecules-14-00740-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ebe6/11274451/f57224224a02/biomolecules-14-00740-g006.jpg

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