Sinomenine activation of Nrf2 signaling prevents hyperactive inflammation and kidney injury in a mouse model of obstructive nephropathy
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SIN reduces inflammation, oxidative stress, and renal damage in UUO mice.

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SIN is an Nrf2 activator and it activates Nrf2 signaling through Keap1 degradation.

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SIN inhibits the M1 and promotes the M2 polarization in macrophages.

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SIN Nrf2-dependently relieves renal inflammation and NF-kB signaling.

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Nrf2 is essential for SIN functions in inflammation inhibition and renoprotection.

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