Abstract Title:

Berberine modulates ASK1 signaling mediated through TLR4/TRAF2 via upregulation of miR-23a.

Abstract Source:

Toxicol Appl Pharmacol. 2018 Sep 18. Epub 2018 Sep 18. PMID: 30240693

Abstract Author(s):

Sali Sujitha, Palani Dinesh, Mahaboobkhan Rasool

Article Affiliation:

Sali Sujitha


The current study was designed to explore the underlying therapeutic effect of berberine (BBR), an alkaloid compound against LPS (1 μg/ml)/TNFα (10 ng/ml) mediated ASK1 signaling in RAW 264.7 and adjuvant-induced arthritic synovial macrophages (AA-SM) with relation to miR-23a levels. LPS and TNFα stimulation abrogated the expression of miR-23a resulting in TLR4/TRAF2 mediated ASK1 activation and downstream phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK). BBR (25-75 μM) treatment ameliorated the gene expression levels of TLR4, TRAF2, TNFα, IL-6, and IL-23 through the upregulation of miR-23a. Subsequently, BBR suppressed the levels of TLR4/TRAF2 mediated phosphorylation of ASK1/p38 and attenuated the expression of various pro-inflammatory cytokines (TNFα, IL-6&IL-23) in RAW 264.7 and AA-SM cells. BBR was able to counteract these factors through activation of miR-23a levels in LPS/TNFα stimulated RAW 264.7 macrophages and AA-SM cells. NQDI1 (30 μM) treatment inhibited ASK1 activation resulting in basal levels of miR-23a, owing to the conclusion that ASK1 activation downregulates miR-23a levels inside the cells. Overall, our current findings predict that BBR is a potential candidate for therapeutic targeting of TLR4/TRAF2 mediated ASK1 activation in inflammatory and in RA pathogenesis possibly through post-transcriptional gene silencing via miR-23a.

Study Type : In Vitro Study

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