Authors
Xiansu Chi, Shuang Zheng, Chunyan Guo, Jiawei Wang, Ze Chang, Xiaoxuan Cao, Libin Jiang, Yunling Zhang, Wei Shen
Published in
Drug design, development and therapy. Volume 20. Pages 608894. Epub Jun 12, 2026.
Abstract
Ischemia-percussion (I/R) injury describes a paradoxical phenomenon in which blood flow restoration following ischemia not only fails to salvage the tissue but also exacerbates tissue injury. Due to the unique physiological functions, cell types, and metabolic requirements of different tissues, their responses and vulnerability to ischemia/reperfusion injuries vary significantly. The limited understanding of complex mechanisms underlying I/R injury in different organs further thwarts the advancement of effective therapeutic interventions, the translational application of promising interventional strategies still faces many obstacles. Salidroside, a natural bioactive constituent of traditional medicinal plants, demonstrates great potential in combating I/R injuries in various organs. Salidroside exerts organ-specific regulatory effects based on the unique characteristics of damage in different organs, simultaneously alleviates I/R injuries by common mechanism include inhibiting oxidative stress, reducing inflammatory responses, regulating cell apoptosis, and inhibiting ferroptosis. To summarize the evidence, we searched the PubMed and Web of Science databases from inception to February 28, 2026, using "salidroside" (and its synonym "rhodioloside") and "ischemia-reperfusion injury" (and its MeSH term "reperfusion injury") as core keywords. This narrative review summarizes the common and organ-specific protective mechanisms of salidroside against I/R injury across different organs and points out the limitations of existing studies in terms of evidence quality, dose standardization, thereby providing research directions for further development of related pharmaceutical formulations and their clinical translation.
PMID:
42311463
Bibliographic data and abstract were imported from PubMed on 15 Sep 2026.
Read full publication at:
Please sign in
to see all details.
Advertisement
Stats
- Recommendations n/a n/a positive of 0 vote(s)
- Views 11
- Comments 0