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These findings suggest that manoeuvres designed to increase mucosal GSH content may be useful to withstand the lethal consequences of oxidative stress that may contribute to attenuate the activation and recruitment of related factors that participate in the development of IBD, including VCAM-1 and ICAM-1 (Sans et al, 1999)

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[87] found that artemisinin could activate the ATF4/CHOP/CHAC1 pathway in ERS to block GSH synthesis, ultimately inducing ferroptosis in Burkitts lymphoma

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