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For the gallbladder and surrounding hepatobiliary tissues, these mechanisms translate into better local microcirculation, reduced oxidative and inflammatory stress, and enhanced cellular energy metabolism, all of which support intrinsic physiological processes governing bile concentration, smooth muscle contractility, and tissue resilience

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However, in resistant patients, oxidative stress causes a conformational change in Keap1, leading to the release of NRF2, which translocates to the nucleus and binds to antioxidant response element (ARE), activating the expression of downstream antioxidant genes, including GPX4, NQO1, HO-1 and SOD1 [33], and promoting the synthesis of GSH, as illustrated in Fig