IndraLab

Statements


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"Baicalin inhibits NA (Ding et al., 2014; Jin et al., 2018) and TLR7/MYD88 signaling pathway activation to suppress inflammation in mice infected with influenza A virus (Wan et al., 2014)."

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"These observed changes suggest that the primary mechanism of baicalin (1) in antiviral in inhibiting immunologic injury involves inhibiting NF-κB and TLR7/MyD88 pathway, followed by reducing the inflammatory cytokine expression."

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"Baicalin down-regulated the TLR2/4, MyD88, and NF-kappaB signaling, and inhibited subsequent proinflammatory responses."

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"In RAW264.7 cells with CD14 knockdown, baicalin pretreatment did not prevent inflammatory responses and activation of MyD88 and NF-kappaB p65 pathway induced by high concentrations (1000mug/mL) of LPS."

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"Wan and colleagues [XREF_BIBR] demonstrated that baicalin inhibits TLR7 and MYD88 signaling pathway activation to suppress lung inflammation in mice infected with influenza A virus."

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"In conclusion, baicalin effectively reduced the pathological damage and inflammation of the lungs by downregulating the TLR7 and MYD88 mediated signaling pathway."

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"Baicalin inhibits TLR7 and MYD88 signaling pathway activation to suppress lung inflammation in mice infected with influenza A virus."

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"These observed changes suggest that the primary mechanism of baicalin (1) in antiviral in inhibiting immunologic injury involves inhibiting NF-κB and TLR7/MyD88 pathway, followed by reducing the inflammatory cytokine expression.HNFs plays a vital role in the proliferation of hepatitis B virus (HBV) and the underlying mechanism involved in up-regulating HNF1α expression, increasing HNF4α expression, and promoting pgRNA biosynthesis and transcription (Huang."

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"Baicalin inhibits NA (Ding et al., 2014; Jin et al., 2018) and TLR7/MYD88 signaling pathway activation to suppress inflammation in mice infected with influenza A virus ."