ReferenceID 4648
Baicalin prevents fibrosis of human trabecular meshwork cells via inhibiting the MyD88/NF-κB pathway
Eur J Pharmacol
Trabecular meshwork fibrosis contributes to increased aqueous humor outflow resistance, leading to elevated intraocular pressure in primary open-angle glaucoma. Baicalin, an extract from Scutellaria baicalensis Georgi, h
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- Reference Id
- 4648
- Evidence Id
- 21238
- Core Evidence Id
- 21238
- Source Reference Id
- 2566
- Herb2 Reference Id
- HBREF003363
- Subject Paper Key
- HBIN017516_36442621
- Pubmed Id
- 36442621
- Doi
- 10.1016/j.ejphar.2022.175425
- Paper Title
- Baicalin prevents fibrosis of human trabecular meshwork cells via inhibiting the MyD88/NF-κB pathway
- Paper Abstract
- Trabecular meshwork fibrosis contributes to increased aqueous humor outflow resistance, leading to elevated intraocular pressure in primary open-angle glaucoma. Baicalin, an extract from Scutellaria baicalensis Georgi, has shown anti-fibrotic effects in liver, lung, and kidney diseases. However, its anti-fibrotic effect on human trabecular meshwork (HTM) cells has not yet been clarified. In this study, we investigated its effects on TGF-β2-induced HTM fibrosis as well as the underlying regulatory mechanisms. HTM cells were pretreated with baicalin, TAK-242, and baicalin + TAK-242 for 2 h followed by treatment with or without 5 ng/mL TGF-β2 for 48 h. Cell viability was assayed using cell counting Kit-8 and fibronectin (FN), laminin (LN), and α-smooth muscle actin (α-SMA) were assessed by western blotting, reverse transcription-polymerase chain reaction (RT-PCR), and immunocytochemistry. Further, the protein and gene expression levels of the TLR4/MyD88/NF-κB pathway (TLR4, MyD88, and NF-κB p65) were also examined by western blotting and RT-PCR, respectively. Thus, we observed that high doses of baicalin (40 μM) decreased (p < 0.1) HTM cell viability and 20 μM baicalin pretreatment was identified as the optimum pretreatment concentration. TGF-β2 upregulated (p < 0.5) the expression of FN, LN, α-SMA, MyD88, NF-κB p65 proteins and mRNA in HTM cells, and these effects were inhibited by baicalin and TAK-242 (p < 0.5). However, western blot analysis showed that baicalin did not repress TLR4 expression in HTM cells. Therefore, our findings suggested that baicalin could prevent TGF-β2-induced extracellular matrix (FN, LN) deposition and α-SMA expression in HTM cells by inhibiting the MyD88/NF-κB pathway.
- Journal
- Eur J Pharmacol
- Publish Year
- 2022
- Experiment Subject
- human; htm cells; human trabecular meshwork (htm) cells
- Experiment Type
- Cell Experiment
- Phenotype Related
- Open-angle Glaucoma; Trabecular Meshwork Fibrosis; Htm Fibrosis; Liver, Lung, And Kidney Diseases
- Paper Title Cn
- Paper Title En
- Baicalin prevents fibrosis of human trabecular meshwork cells via inhibiting the MyD88/NF-κB pathway
- Bilingual Status
- semi_complete