Therapeutic Potential of Hydrogen Sulfide in Ischemia and Reperfusion Injury

被引:3
|
作者
Sun, Xutao [1 ]
Wu, Siyu [2 ]
Mao, Caiyun [2 ]
Qu, Ying [2 ]
Xu, Zihang [2 ]
Xie, Ying [3 ]
Jiang, Deyou [3 ]
Song, Yunjia [2 ]
机构
[1] Heilongjiang Univ Chinese Med, Sch Basic Med Sci, Dept Typhoid, Harbin 150040, Peoples R China
[2] Heilongjiang Univ Chinese Med, Sch Basic Med Sci, Dept Pharmacol, Harbin 150040, Peoples R China
[3] Heilongjiang Univ Chinese Med, Sch Basic Med Sci, Dept Synopsis Golden Chamber, Harbin 150040, Peoples R China
关键词
H2S donor; ischemia-reperfusion; mechanisms; inflammation; apoptosis; CEREBRAL ISCHEMIA/REPERFUSION INJURY; ISOLATED RAT HEARTS; MYOCARDIAL-ISCHEMIA; NITRIC-OXIDE; SPINAL-CORD; ALCOHOL-CONSUMPTION; DOWN-REGULATION; PROTECTS CARDIOMYOCYTES; INHIBITING AUTOPHAGY; LIVER-REGENERATION;
D O I
10.3390/biom14070740
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Ischemia-reperfusion (I/R) injury, a prevalent pathological condition in medical practice, presents significant treatment challenges. Hydrogen sulfide (H2S), acknowledged as the third gas signaling molecule, profoundly impacts various physiological and pathophysiological processes. Extensive research has demonstrated that H2S can mitigate I/R damage across multiple organs and tissues. This review investigates the protective effects of H2S in preventing I/R damage in the heart, brain, liver, kidney, intestines, lungs, stomach, spinal cord, testes, eyes, and other tissues. H2S 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 H2S reduces I/R damage have led to the development and synthesis of H2S-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.
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页数:31
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