ArticleFood science & nutrition2021
Shikonin protects against lipopolysaccharide-induced inflammation and apoptosis in human nucleus pulposus cells through the nuclear factor-kappa B pathway.
Article in Food science & nutrition, 2021. 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, 9 citations in OpenAlex.
- A Narrative Review of Protective Effects of Natural Compounds Against Lipopolysaccharide-Induced Injuries.Food science & nutrition · 2025Review
- Bioactive metabolites of botanical drugs in the treatment of intervertebral disc degeneration-a review of promising therapeutic candidate.Frontiers in pharmacology · 2025Review
- Ginsenoside Rg1 relieves rat intervertebral disc degeneration and inhibits IL-1β-induced nucleus pulposus cell apoptosis and inflammation via NF-κB signaling pathway.In vitro cellular & developmental biology. Animal · 2024Article
- Shikonin alleviates asthma phenotypes in mice via an airway epithelial STAT3-dependent mechanism.Open medicine (Warsaw, Poland) · 2024Article
- Kukoamine A attenuates lipopolysaccharide-induced apoptosis, extracellular matrix degradation, and inflammation in nucleus pulposus cells by activating the P13K/Akt pathway.Bioengineered · 2022Article
- Shikonin protects against lipopolysaccharide-induced inflammation and apoptosis in human nucleus pulposus cells through the nuclear factor-kappa B pathway.Food science & nutrition · 2021Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo investigate the protective effect and mechanism of shikonin on human intervertebral disk degeneration.
methodsHuman primary nucleus pulposus (NP) cells cultured in vitro were used for the experiments. The effects of different concentrations of shikonin (1, 2, 4, 8, and 16 µM) on the activity of lipopolysaccharide (LPS)-induced NP cells were determined using the CCK-8 assay, and the appropriate drug concentration was determined. The experiment was divided into the control, LPS, and LPS + shikonin groups. ELISA and Western blot were used to detect the expression of the inflammatory factors tumor necrosis factor (TNF)-α and interleukin (IL)-1β. NP cell apoptosis was measured using Western blot and caspase 3 activity. Western blot and immunofluorescence assays were used to detect the protein expression of p-P65 and P65 and the nuclear translocation of P65.
resultsThe CCK-8 assay showed that shikonin had no cytotoxic effect on NP cells and increased the activity of LPS-induced NP cells, especially at a concentration of 4 μM. Shikonin reversed the expression of the inflammatory cytokines TNF-α and IL-1β and apoptosis-related molecules Bax, Bcl-2, and cleaved caspase 3 in LPS-induced NP cells. In addition, shikonin significantly decreased apoptosis and caspase-3 activity in LPS-induced NP cells. Furthermore, shikonin treatment significantly inhibited the expression of p-P65 and nuclear translocation of P65, and nuclear factor-kappa B (NF-κB) pathway inhibitor Pyrrolidinedithiocarbamate ammonium (PDTC) significantly enhanced the anti-inflammatory and antiapoptotic effects of shikonin in LPS-induced NP cells.
conclusionShikonin significantly inhibited the inflammatory response and apoptosis of human primary NP cells, possibly through the NF-κB pathway.
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