Combinatorial chemistry & high throughput screening · 2026
Mume Fructus Total Flavonoids Modulate miR-145-3p Expression to Inhibit Lipopolysaccharide-induced Inflammatory Cytokine Production in BV2 Cells.
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Wang Chunling, Gu Lian, Yang Zhengwei, Su Jinli, Wen Xiaodong
Аннотация
INTRODUCTION: The inhibition of microglia-mediated inflammatory responses is of great importance for the treatment of neurodegenerative diseases. Mume Fructus total flavonoids (MFTF) are one of the major bioactive components of Mume Fructus, a traditional food and medicinal herb in China. This study aimed to clarify the anti-inflammatory effect of MFTF on lipopolysaccharide (LPS)-induced microglial inflammation and to elucidate its underlying mechanism.
METHODS: Ultra-high-performance liquid chromatography coupled with Quadrupole Time-offlight mass spectrometry was used to analyze the chemical composition of MFTF. BV2 cells were stimulated with LPS (100 ng/mL) for 24 h to establish an in vitro inflammatory model. Cell viability was tested by the Cell Counting Kit-8 assay. Cell proliferation was assessed by the 5- Ethynyl-2'-deoxyuridine assay. Cell polarization and miR-145-3p expression were analysed by real-time quantitative PCR. The expression of apoptosis- and inflammation-related proteins was analyzed by Western Blotting. RNA sequencing was used to explore the potential mechanisms by which MFTF regulates the inflammation of BV2.
RESULTS: A total of 379 compounds have been identified in MFTF. MFTF promoted the proliferation, downregulated the expression of pro-inflammatory markers (iNOS, IL-1β, and CD86), and upregulated the expression of anti-inflammatory markers (Arg-1, IL-10, and CD206) of BV2 cells following LPS stimulation. In addition, MFTF inhibited the expression of pro-apoptotic protein Bad and inflammatory mediators COX-2 and iNOS, while promoting the anti-apoptotic protein Bcl-2. Further, MFTF unregulated miR-145-3p expression in LPS-stimulated BV2 cells, and inhibition of miR-145-3p partially abolished the anti-inflammatory, anti-apoptotic, and proproliferative effects of MFTF. RNA sequencing results showed MFTF may inhibit the inflammation in BV2 cells by regulating the Toll-like receptor signalling pathway, NOD-like receptor signalling pathway, and NF-κB signalling pathway.
DISCUSSION: Our findings demonstrated that MFTF inhibited pro-inflammatory polarization (M1) while promoting proliferation and anti-inflammatory polarization (M2) of microglia, potentially through the upregulation of miR-145-3p. These results indicated that MFTF could attenuate microglial inflammation, thereby supporting our hypothesis that MFTF may have therapeutic potential in alleviating neurodegenerative diseases.
CONCLUSION: These results uncovered a potential mechanism underlying the antineuroinflammatory effects of MFTF and provide a theoretical basis for its therapeutic application in neuroinflammatory disorders.
METHODS: Ultra-high-performance liquid chromatography coupled with Quadrupole Time-offlight mass spectrometry was used to analyze the chemical composition of MFTF. BV2 cells were stimulated with LPS (100 ng/mL) for 24 h to establish an in vitro inflammatory model. Cell viability was tested by the Cell Counting Kit-8 assay. Cell proliferation was assessed by the 5- Ethynyl-2'-deoxyuridine assay. Cell polarization and miR-145-3p expression were analysed by real-time quantitative PCR. The expression of apoptosis- and inflammation-related proteins was analyzed by Western Blotting. RNA sequencing was used to explore the potential mechanisms by which MFTF regulates the inflammation of BV2.
RESULTS: A total of 379 compounds have been identified in MFTF. MFTF promoted the proliferation, downregulated the expression of pro-inflammatory markers (iNOS, IL-1β, and CD86), and upregulated the expression of anti-inflammatory markers (Arg-1, IL-10, and CD206) of BV2 cells following LPS stimulation. In addition, MFTF inhibited the expression of pro-apoptotic protein Bad and inflammatory mediators COX-2 and iNOS, while promoting the anti-apoptotic protein Bcl-2. Further, MFTF unregulated miR-145-3p expression in LPS-stimulated BV2 cells, and inhibition of miR-145-3p partially abolished the anti-inflammatory, anti-apoptotic, and proproliferative effects of MFTF. RNA sequencing results showed MFTF may inhibit the inflammation in BV2 cells by regulating the Toll-like receptor signalling pathway, NOD-like receptor signalling pathway, and NF-κB signalling pathway.
DISCUSSION: Our findings demonstrated that MFTF inhibited pro-inflammatory polarization (M1) while promoting proliferation and anti-inflammatory polarization (M2) of microglia, potentially through the upregulation of miR-145-3p. These results indicated that MFTF could attenuate microglial inflammation, thereby supporting our hypothesis that MFTF may have therapeutic potential in alleviating neurodegenerative diseases.
CONCLUSION: These results uncovered a potential mechanism underlying the antineuroinflammatory effects of MFTF and provide a theoretical basis for its therapeutic application in neuroinflammatory disorders.