ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2022
Salidroside alleviates cadmium-induced toxicity in mice by restoring the notch/HES-1 and RIP1-driven inflammatory signaling axis.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed, 10 citations in OpenAlex.
- Salidroside in heavy metal toxicity: a mechanistic review of antioxidant, anti-inflammatory, and anti-apoptotic pathways.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Ameliorative Effects of Urolithin A Against Cadmium-Induced NLRP3-Mediated Pyroptosis and Cognitive Deficits Via Regulating Aryl Hydrocarbon Receptor Signaling.Biological trace element research · 2026Article
- Cadmium exposure at low environmental levels induces cognitive decline in aged male mice.Neurotoxicology · 2026Article
- Salidroside Attenuates Epilepsy and Cognitive Dysfunction in Rats by Downregulating Complement C3-C3aR Pathway-Mediated Activation of Microglia and Astrocytes.Neurochemical research · 2025Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectiveSalidroside (SAL) is a marker glycoside of Rhodiola rosea with significant antioxidant, anti-inflammatory, and other health benefits. In this study, we determined its neuroprotective effects against Cd-induced toxicity in cultured cells and mice. MATERIALS AND
methodsGL261 cell and Cd-intoxicated mouse model were used. ICP-MS and MWM were performed to measure Cd content and Cd-induced cognitive impairment in mice, respectively.
resultsSAL attenuated Cd toxicity in GL261 cells as well as protected mice from substantial organic damage and cognitive deficits. SAL treatment alleviated Cd-induced oxidative stress, glial cell activation, and elevation of pro-inflammatory factors including TNF-α, IL-1β, and IL-6. Cd-induced cognitive deficits observed in the Morris water maze in mice were rescued by SAL. At the mechanistic level, SAL maintained the activity of antioxidant enzymes such as SOD and GSH-Px in the serum and brain, and scavenged the peroxidation product MDA, thereby restoring redox homeostasis in vivo, attenuating neuronal damage, and ultimately antagonized Cd-induced toxicity. Furthermore, Cd activated the RIP1-driven inflammatory signaling pathway and Notch/HES-1 signaling axis in the brain, leading to inflammation and neuronal loss, which could be attenuated by SAL.
conclusionSAL is a natural product with good anti-Cd effects, indicating that Rhodiola rosea is promising plant that is worthy of cultivation for health and economic benefits.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.