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Downstream signaling through IRAK and TRAF6 via the MyD88 adaptor protein activates the IKK/NFB pathway, promoting the release of pro-inflammatory cytokines such as TNF, IL1, and IL6 and increasing reactive oxygen species (ROS), thereby generating a localized inflammatory storm. [81] In vivo studies have shown that MPs exposure upregulates TLR4, MyD88, and phosphorylated NFB, while inhibitors of TLR2/4 markedly reduce inflammatory damage, highlighting the importance of this pathway in MPs-induced immune toxicity [82]

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Triptolide and its analogs have been shown to inhibit NF-B signaling, which in pancreatic cancer cells results in elevated oxidative stress, reduced Bcl-2 expression, and activation of mitochondrial apoptosis pathways (100)

Endocrinology 2015, 156, 25412551