Acute Pancreatitis (AP) is a multifactorial disease. It was characterized by severe inflammation and acinar cell destruction. Thus, the present study was initiated to evaluate the role the of Cinnamic acid nanoparticles (CA-NPs) as a modulator for the redox signaling pathway involved in the development of pancreatitis. AP in rats was induced by L-arginine and exposure to gamma radiation. The pancreatic injury was evaluated using biochemical and histological parameters. Upon the oral administration of CA-NPs, both the severity of acute pancreatitis and the serum levels of amylase and lipase were decreased. Furthermore, the malondialdehyde (MDA) levels of the pancreatic tissue were significantly reduced and the depletion of glutathione was considerably restored. The injury and apoptosis of pancreatic tissues were markedly improved by the reduction of the caspase-3 levels. Additionally, the alleviation of pancreatic oxidative damage by CA-NPs was accompanied by a down-regulation of the NLRP3, NF-κB, and ASK1/MAPK signaling pathways. Collectively, the current findings showed that CA-NPs could protect the pancreatic acinar cell from injury not only by its antioxidant, anti-inflammatory effect but also by modulation of the redox-sensitive signal transduction pathways contributed to acute pancreatitis severity. Accordingly, cinnamic acid nanoparticles have therapeutic potential for the management of acute pancreatitis.

急性胰腺炎（AP）是一种多因素疾病。它的特征是严重的炎症和腺泡细胞破坏。因此，启动本研究以评估肉桂酸纳米颗粒（CA-NPs）作为参与胰腺炎发展的氧化还原信号通路调节剂的作用。L-精氨酸诱导大鼠AP并暴露于γ射线。使用生化和组织学参数评估胰腺损伤。口服CA-NP后，急性胰腺炎的严重程度以及淀粉酶和脂肪酶的血清水平均降低。此外，胰腺组织的丙二醛（MDA）水平显着降低，并且谷胱甘肽的消耗得以显着恢复。降低caspase-3水平可显着改善胰腺组织的损伤和凋亡。此外，CA-NP减轻胰腺氧化损伤的同时，NLRP3，NF-κB和ASK1 / MAPK信号通路也被下调。总的来说，当前的发现表明，CA-NPs不仅可以通过其抗氧化，抗炎作用，而且可以通过调节氧化还原敏感信号转导通路来保护胰腺腺泡细胞免受损伤，从而导致急性胰腺炎的严重程度。因此，肉桂酸纳米颗粒具有治疗急性胰腺炎的治疗潜力。总的来说，当前的发现表明，CA-NPs不仅可以通过其抗氧化，抗炎作用，而且可以通过调节氧化还原敏感信号转导通路来保护胰腺腺泡细胞免受损伤，从而导致急性胰腺炎的严重程度。因此，肉桂酸纳米颗粒具有治疗急性胰腺炎的治疗潜力。总的来说，当前的发现表明，CA-NPs不仅可以通过其抗氧化，抗炎作用，而且可以通过调节氧化还原敏感信号转导通路来保护胰腺腺泡细胞免受损伤，从而导致急性胰腺炎的严重程度。因此，肉桂酸纳米颗粒具有治疗急性胰腺炎的治疗潜力。