Abstract
There is no specific drug to treat severe acute pancreatitis (SAP), which induces substantial medical and social burden. Many studies have reported the beneficial effects of emodin against SAP in vivo and in vitro. However, the underlying mechanism has been unclear. This paper described the design and implementation of anti-inflammatory and antioxidant activity of emodin. Emodin restored the pathological damage of SAP and simultaneously decreased the high levels of serum amylase, lipase, TNF-α, and IL-18 in the peripheral blood of SAP rat. Emodin reversed reactive oxygen species (ROS) in neutrophils derived from SAP rat. The levels of voltage-dependent anion channel 1 (VDAC1), NOD-like receptor protein 3 (NLRP3), caspase-1, and IL-18 were examined to analyze the change of inflammasome-related mediators between SAP and emodin treatment. These findings suggest that emodin plays its protective role on SAP against oxidative stress and inflammasome signals.
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