ArticleOxidative medicine and cellular longevity2022
Triptolide Induces Liver Injury by Regulating Macrophage Recruitment and Polarization via the Nrf2 Signaling Pathway.
Article in Oxidative medicine and cellular longevity, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 12 citations in OpenAlex.
- Liver-Directed Cyp2e1 RNA Interference Attenuates Hepatotoxicity Induced by Triptolide, a Bioactive Diterpenoid fromPharmaceuticals (Basel, Switzerland) · 2026Article
- Triptolide inhibits ovarian cancer growth and metastasis via reprogramming of tumor-associated macrophages.Cell stress · 2026Article
- Triptolide-mediated immunomodulation of macrophages: from pathophysiology to therapy.Annals of medicine · 2025Review
- Health position paper and redox perspectives - Bench to bedside transition for pharmacological regulation of NRF2 in noncommunicable diseases.Redox biology · 2025Review
- Flavonoids of Euphorbia hirta inhibit inflammatory mechanisms via Nrf2 and NF-κB pathways.Cell biochemistry and biophysics · 2025Article
- Antitumor mechanisms and future clinical applications of the natural product triptolide.Cancer cell international · 2024Review
- Mangiferin Ameliorates CClJournal of inflammation research · 2024Article
- The molecular pathogenesis of triptolide-induced hepatotoxicity.Frontiers in pharmacology · 2022Review
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Authors and funding
11 authors at 1 institution in 1 country.
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Abstract
Triptolide (TP) has limited usage in clinical practice due to its side effects and toxicity, especially liver injury. Hepatic macrophages, key player of liver innate immunity, were found to be recruited and activated by TP in our previous study. The nuclear factor-erythroid-2-related factor 2 (Nrf2) pathway exerts a protective role in TP-induced liver damage, but its effect on the functions of hepatic macrophage has not been elucidated. Here, we determined whether TP can regulate the recruitment and polarization of hepatic macrophages by inhibiting Nrf2 signaling cascade. Our results demonstrated that TP inhibited the Nrf2 signaling pathway in hepatic macrophages. The changes in hepatic macrophages were responsible for the increased susceptibility toward inflammatory stimuli, and hence, TP pretreatment could induce severe liver damage upon the stimulation of a nontoxic dose of lipopolysaccharides. In addition, the Nrf2 agonist protected macrophages from TP-induced toxicity and Nrf2 deficiency significantly aggravated liver injury by enhancing the recruitment and M1 polarization of hepatic macrophages. This study suggests that Nrf2 pathway-mediated hepatic macrophage polarization plays an essential role in TP-induced liver damage, which can serve as a potential therapeutic target for preventing hepatotoxicity induced by TP.
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