ReferenceID 2591
Parthenolide, bioactive compound of Chrysanthemum parthenium L., ameliorates fibrogenesis and inflammation in hepatic fibrosis via regulating the crosstalk of TLR4 and STAT3 signaling pathway
Phytother Res
The current study focused on the regulatory effects of parthenolide (PNL), a bioactive component derived from Chrysanthemum parthenium L., against hepatic fibrosis via regulating the crosstalk of toll-like receptor 4 (TL
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Record Fields
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- Reference Id
- 2591
- Evidence Id
- 19181
- Core Evidence Id
- 19181
- Source Reference Id
- 5174
- Herb2 Reference Id
- HBREF005971
- Subject Paper Key
- HBIN038876_34250656
- Pubmed Id
- 34250656
- Doi
- 10.1002/ptr.7214
- Paper Title
- Parthenolide, bioactive compound of Chrysanthemum parthenium L., ameliorates fibrogenesis and inflammation in hepatic fibrosis via regulating the crosstalk of TLR4 and STAT3 signaling pathway
- Paper Abstract
- The current study focused on the regulatory effects of parthenolide (PNL), a bioactive component derived from Chrysanthemum parthenium L., against hepatic fibrosis via regulating the crosstalk of toll-like receptor 4 (TLR4) and signal transducer and activator of transcription 3 (STAT3) in activated hepatic stellate cells (HSCs). HSCs or Raw 264.7 macrophages were activated by TGF-beta or LPS for 1 hr, respectively, and then treated with PNL, CLI-095 (TLR4 inhibitor), or Niclosamide (STAT3 inhibitor) for the indicated time to detect the crosstalk of TLR4 and STAT3. PNL significantly decreased the expressions of alpha-SMA, collagen I, and the ratio of TIMP1 and MMP13 in TGF-beta-activated HSCs. PNL significantly reduced the releases of pro-inflammatory cytokines, including IL-6, IL-1beta, IL-1alpha, IL-18, and regulated signaling P2X7r/NLRP3 axis activation. PNL obviously induced the apoptosis of activated HSCs by regulating bcl-2 and caspases family. PNL significantly inhibited the expressions of TLR4 and STAT3, including their downstream signaling. PNL could regulate the crosstalk of TLR4 and STAT3, which were verified by their inhibitors in activated HSCs or Raw 264.7 cell macrophages. Thus, PNL could decrease the expressions of fibrosis markers, reduce the releases of inflammatory cytokines, and also induce the apoptosis of activated HSCs. In conclusion, PNL could bi-directionally inhibit TLR4 and STAT3 signaling pathway, suggesting that blocking the crosstalk of TLR4 and STAT3 might be the potential mechanism of PNL against hepatic fibrosis.
- Journal
- Phytother Res
- Publish Year
- 2021
- Experiment Subject
- raw 264.7 cell macrophages; raw 264.7 macrophages; tgf-beta-activated hscs
- Experiment Type
- Cell Experiment
- Phenotype Related
- Fibrosis; Hepatic Fibrosis
- Paper Title Cn
- Paper Title En
- Parthenolide, bioactive compound of Chrysanthemum parthenium L., ameliorates fibrogenesis and inflammation in hepatic fibrosis via regulating the crosstalk of TLR4 and STAT3 signaling pathway
- Bilingual Status
- semi_complete