AI Article Synopsis
- The study examined how LF affects inflammation by targeting specific microRNAs, HMGB1 expression, and the TLR4-MyD88-NF-кB signaling pathway in activated mouse macrophage cells.
- The researchers utilized various methods, including MTT assays for cell metabolism and ELISA for cytokine levels, to assess the effects of LF on inflammation markers and pathways.
- Results showed that LF reduces pro-inflammatory cytokines, downregulates key inflammatory proteins and microRNAs, and demonstrates potential as an effective anti-inflammatory treatment.
Article Abstract
Objective: This current study evaluated the underlying mechanisms of LF against the inflammatory microRNAs (miRNAs), HMGB1 expression, and TLR4-MyD88-NF-кB pathway in LPS-activated murine RAW264.7 cells.
Methods: MTT assay was used to assess cell metabolism and the cell culture levels of the cytokines (TNF-α, IL-6) were evaluated by Enzyme-linked immunosorbent assay (ELISA). The expression of miRNAs was quantified by using qPCR and the expression of HMGB1, TLR4, MyD88, and phosphorylated NF-κB (P-p65) were determined with Western blot and qPCR, respectively.
Results: The results indicated that LF downregulates IL-6 and TNF-α expression. LF exhibited the degradation of P-p65 and reduced the production of HMGB1, TLR4, and MyD88 in LPS-induced inflammatory response. Importantly, in parallel with the suppression of cytokines and HMGB1-TLR4-MyD88-NF-кB pathway, LF could induce a decrease in inflammatory selected miRNAs, -155, and -146a expression.
Conclusions: Altogether, these findings provide LF as a prominent anti-inflammatory agent that could modulate HMGB1, -155, -146a, and TLR4/MyD88/NF-кB pathway.
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| http://dx.doi.org/10.1080/08923973.2021.1872616 | DOI Listing |
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