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As the levels of pro-inflammatory prostaglandins increase, the capability of clearance must also be improved to maintain low level prostaglandin and prevent additional inflammation

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In the acute GA model, luteolin inhibited the expressions of TLR2 and TLR4 mRNAs, reduced their protein expression levels, and ameliorated acute inflammation in GA by downregulating the TLR/MyD88/NF-B signaling pathway, which in turn inhibited the expression of the downstream inflammatory factors IL-1, IL-6, and TNF- (175)