IndraLab

Statements


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"Western blotting results suggested that dioscin inhibited the activation of NLRP3 through down-regulating the protein expressions of NLRP3, apoptosis associated speck like protein containing a caspase recruitment domain (ASC), cleaved-caspase-1, as well as IL-1beta."

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"In vitro experiments, the results showed that dioscin inhibited the inflammatory response and the activation of NLRP3 inflammasome, but the survival rate of mouse mammary epithelial cells (mMECs) induced by LPS+ATP is increased."

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"Meanwhile, dioscin dramatically suppressed NLRP3 inflammasome activation."

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"Moreover, dioscin also can reduce the production of proinflammatory factors such as interleukin-1 beta (IL-1beta) and inhibit the activation of NLRP3 inflammasome in LPS induced mice mastitis."

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"Dioscin Reduces LPS+ATP-Induced Activation of NF-kappaB Signaling Pathway and NLRP3 Inflammasome in mMECs."