https://www.selleckchem.com/products/2-d08.html
Dimethyl itaconate activated Nrf2 and promoted the expression of Nrf2 and its downstream factor HO-1 and NQO-1. The regulatory activities of dimethyl itaconate on inflammatory cytokine production, mouse survival rate were abolished in septic Nrf2-/- mice. Dimethyl itaconate suppressed the inflammatory responses of macrophages in sepsis. Endometriosis (EM) is a common gynecological disease affecting 10-15% of women of reproductive age. However, molecular mechanisms and pathogenesis are still not completely understood. Furthermore, due to t
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