ArticleExperimental and therapeutic medicine2014
Effect of salidroside on lung injury by upregulating peroxisome proliferator-activated receptor γ expression in septic rats.
Article in Experimental and therapeutic medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Ferroptosis and hyperoxic lung injury: insights into pathophysiology and treatment approaches.Frontiers in pharmacology · 2025Review
- Salidroside attenuates sepsis-induced acute lung injury by inhibiting ferroptosis-dependent pathway.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2024Article
- Salidroside protects against intestinal barrier dysfunction in septic mice by regulating IL‑17 to block the NF‑κB and p38 MAPK signaling pathways.Experimental and therapeutic medicine · 2023Article
- Salidroside protects against ventilation-induced lung injury by inhibiting the expression of matrix metalloproteinase-9.Pharmaceutical biology · 2021Article
- Salidroside ameliorates sepsis-induced acute lung injury and mortality via downregulating NF-κB and HMGB1 pathways through the upregulation of SIRT1.Scientific reports · 2017Article
- The protective mechanism of salidroside modulating miR-199a-5p/TNFAIP8L2 on lipopolysaccharide-induced MLE-12 cells.International journal of immunopathology and pharmacologyArticle
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Successful drug treatment for sepsis-related acute lung injury (ALI) remains a major clinical problem. Thus, the aim of the present study was to investigate the beneficial effects of salidroside on ameliorating cecal ligation and puncture (CLP)-induced lung inflammation. Rats underwent CLP surgery to induce ALI and 800 mg/kg salidroside (i.v.) was administered 24 h after the CLP challenge. Subsequently, biochemical changes in the blood and lung tissues, as well as morphological and histological alterations in the lungs, that were associated with inflammation and injury were analysed. CLP was shown to significantly increase the serum levels of plasma tumour necrosis factor-α and interleukin-6, -1β and-10. In addition, CLP increased pulmonary oedema, thickened the alveolar septa and caused inflammation in the lung cells. These changes were ameliorated by the administration of 800 mg/kg salidroside (i.v.) 24 h after the CLP challenge. This post-treatment drug administration also significantly attenuated the lipopolysaccharide-induced activation of nuclear factor-κβ and increased the release of peroxisome proliferator-activated receptor γ in the lung tissue. Therefore, salidroside administered following the induction of ALI by CLP significantly prevented and reversed lung tissue injuries. The positive post-treatment effects of salidroside administration indicated that salidroside may be a potential candidate for the management of lung inflammation in CLP-induced endotoxemia and septic shock.
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