ArticlePloS one2015
Salidroside Protects against Cadmium-Induced Hepatotoxicity in Rats via GJIC and MAPK Pathways.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 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
- Salidroside ameliorates acute liver transplantation rejection in rats by inhibiting neutrophil extracellular trap formation.Acta biochimica et biophysica Sinica · 2024Article
- Article
- Salidroside alleviates hepatic ischemia-reperfusion injury during liver transplant in rat through regulating TLR-4/NF-κB/NLRP3 inflammatory pathway.Scientific reports · 2022Article
- Applicability of Scrape Loading-Dye Transfer Assay for Non-Genotoxic Carcinogen Testing.International journal of molecular sciences · 2021Review
- Senna alexandrina extract supplementation reverses hepatic oxidative, inflammatory, and apoptotic effects of cadmium chloride administration in rats.Environmental science and pollution research international · 2020Article
- Gap Junction Intercellular Communication Negatively Regulates Cadmium-Induced Autophagy and Inhibition of Autophagic Flux in Buffalo Rat Liver 3A Cells.Frontiers in pharmacology · 2020Article
- Cadmium Induces Acute Liver Injury by Inhibiting Nrf2 and the Role of NF-κB, NLRP3, and MAPKs Signaling Pathway.International journal of environmental research and public health · 2019Article
- Salidroside attenuates oxidized low‑density lipoprotein‑induced endothelial cell injury via promotion of the AMPK/SIRT1 pathway.International journal of molecular medicine · 2019Article
- Modelling cadmium-induced cardiotoxicity using human pluripotent stem cell-derived cardiomyocytes.Journal of cellular and molecular medicine · 2018Article
- Salidroside mediates apoptosis and autophagy inhibition in concanavalin A-induced liver injury.Experimental and therapeutic medicine · 2018Article
- Mixing ratio optimization for functional complex extracts ofJournal of functional foods · 2018Article
- Modeling cadmium-induced endothelial toxicity using human pluripotent stem cell-derived endothelial cells.Scientific reports · 2017Article
- Salidroside inhibits high-glucose induced proliferation of vascular smooth muscle cells via inhibiting mitochondrial fission and oxidative stress.Experimental and therapeutic medicine · 2017Article
- Salidroside pretreatment attenuates apoptosis and autophagy during hepatic ischemia-reperfusion injury by inhibiting the mitogen-activated protein kinase pathway in mice.Drug design, development and therapy · 2017Article
- Salidroside Modulates Insulin Signaling in a Rat Model of Nonalcoholic Steatohepatitis.Evidence-based complementary and alternative medicine : eCAM · 2017Article
- Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway.Molecules (Basel, Switzerland) · 2016Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is known that cadmium (Cd) induces cytotoxicity in hepatocytes; however, the underlying mechanism is unclear. Here, we studied the molecular mechanisms of Cd-induced hepatotoxicity in rat liver cells (BRL 3A) and in vivo. We observed that Cd treatment was associated with a time- and concentration-dependent decrease in the cell index (CI) of BRL 3A cells and cellular organelle ultrastructure injury in the rat liver. Meanwhile, Cd treatment resulted in the inhibition of gap junction intercellular communication (GJIC) and activation of mitogen-activated protein kinase (MAPK) pathways. Gap junction blocker 18-β-glycyrrhetinic acid (GA), administered in combination with Cd, exacerbated cytotoxic injury in BRL 3A cells; however, GA had a protective effect on healthy cells co-cultured with Cd-exposed cells in a co-culture system. Cd-induced cytotoxic injury could be attenuated by co-treatment with an extracellular signal-regulated kinase (ERK) inhibitor (U0126) and a p38 inhibitor (SB202190) but was not affected by co-treatment with a c-Jun N-terminal kinase (JNK) inhibitor (SP600125). These results indicate that ERK and p38 play critical roles in Cd-induced hepatotoxicity and mediate the function of gap junctions. Moreover, MAPKs induce changes in GJIC by controlling connexin gene expression, while GJIC has little effect on the Cd-induced activation of MAPK pathways. Collectively, our study has identified a possible mechanistic pathway of Cd-induced hepatotoxicity in vitro and in vivo, and identified the participation of GJIC and MAPK-mediated pathways in Cd-induced hepatotoxicity. Furthermore, we have shown that salidroside may be a functional chemopreventative agent that ameliorates the negative effects of Cd via GJIC and MAPK pathways.
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