Our previous studies have shown that abdominal paracentesis drainage (APD) is a safe and effective strategy for patients with severe acute pancreatitis (SAP). However, the underlying mechanisms behind APD treatment remain poorly understood. Given that apoptosis is a critical pathological response of SAP, we here aim to investigate the effect of APD on cell apoptosis in pancreatic tissues during SAP and to explore its potential molecular mechanism. SAP was induced by 5% sodium-taurocholate retrograde while APD group was inserted a drainage tube into the right lower abdomen of rats immediately after SAP induction. Histopathological staining, serum amylase, endotoxin and inflammatory mediators were measured. Cell apoptosis, apoptosis-related proteins and signaling pathway were also evaluated. Our results demonstrated that APD treatment significantly attenuated pancreatic damage and decreased the serum levels of amylase, endotoxin, TNF-α, IL-1 and IL-6 in rats with SAP. Notably, APD treatment enhanced cell apoptosis and reduced necrosis in pancreatic tissues, as evidenced by Tunnel staining, the increased pro-apoptosis proteins (Cleaved-caspase-3 and bax) and decreased anti-apoptosis protein (Bcl-2). Moreover, the effect of APD on cell apoptosis was further confirmed by the regulatory pathway of PI3K/AKT and NF-kB signaling pathway. These results suggest that APD attenuates the severity of SAP by enhancing cell apoptosis via suppressing PI3K/AKT signaling pathway. Our findings provide new insights for understanding the effectiveness of APD in patients with SAP.

中文翻译：

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腹腔穿刺引流可通过PI3K / AKT信号通路增强细胞凋亡，从而减轻严重的急性胰腺炎。

我们以前的研究表明，腹腔穿刺引流（APD）对于重症急性胰腺炎（SAP）患者是一种安全有效的策略。然而，APD治疗背后的潜在机制仍知之甚少。鉴于凋亡是SAP的关键病理反应，因此我们旨在研究APD对SAP胰腺组织细胞凋亡的影响，并探讨其潜在的分子机制。5％牛磺胆酸钠逆行诱导SAP，而APD组在SAP诱导后立即将引流管插入大鼠右下腹。测量组织病理学染色，血清淀粉酶，内毒素和炎性介质。还评估了细胞凋亡，凋亡相关蛋白和信号通路。我们的结果表明，APD处理可显着减轻SAP大鼠的胰腺损伤，并降低其淀粉酶，内毒素，TNF-α，IL-1和IL-6的血清水平。值得注意的是，APD处理可增强胰腺细胞的细胞凋亡并减少坏死，如隧道染色，促凋亡蛋白（Cleaved-caspase-3和bax）增加和抗凋亡蛋白（Bcl-2）减少所证明。此外，通过PI3K / AKT的调节途径和NF-kB信号传导途径进一步证实了APD对细胞凋亡的作用。这些结果表明，APD通过抑制PI3K / AKT信号通路来增强细胞凋亡，从而减轻了SAP的严重性。我们的发现为理解APD在SAP患者中的有效性提供了新的见解。SAP大鼠体内内毒素，TNF-α，IL-1和IL-6 值得注意的是，APD处理可增强胰腺细胞的细胞凋亡并减少坏死，如隧道染色，促凋亡蛋白（Cleaved-caspase-3和bax）增加和抗凋亡蛋白（Bcl-2）减少所证明。此外，通过PI3K / AKT的调节途径和NF-kB信号传导途径进一步证实了APD对细胞凋亡的作用。这些结果表明，APD通过抑制PI3K / AKT信号通路来增强细胞凋亡，从而减轻了SAP的严重性。我们的发现为理解APD在SAP患者中的有效性提供了新的见解。SAP大鼠体内内毒素，TNF-α，IL-1和IL-6 值得注意的是，APD处理可增强胰腺细胞的细胞凋亡并减少坏死，如隧道染色，促凋亡蛋白（Cleaved-caspase-3和bax）增加和抗凋亡蛋白（Bcl-2）减少所证明。此外，通过PI3K / AKT的调节途径和NF-kB信号传导途径进一步证实了APD对细胞凋亡的作用。这些结果表明，APD通过抑制PI3K / AKT信号通路来增强细胞凋亡，从而减轻了SAP的严重性。我们的发现为理解APD在SAP患者中的有效性提供了新的见解。促凋亡蛋白（Cleaved-caspase-3和bax）增加，抗凋亡蛋白（Bcl-2）降低。此外，通过PI3K / AKT的调节途径和NF-kB信号传导途径进一步证实了APD对细胞凋亡的作用。这些结果表明，APD通过抑制PI3K / AKT信号通路来增强细胞凋亡，从而减轻了SAP的严重性。我们的发现为理解APD在SAP患者中的有效性提供了新的见解。促凋亡蛋白（Cleaved-caspase-3和bax）增加，抗凋亡蛋白（Bcl-2）降低。此外，通过PI3K / AKT的调节途径和NF-kB信号传导途径进一步证实了APD对细胞凋亡的作用。这些结果表明，APD通过抑制PI3K / AKT信号通路来增强细胞凋亡，从而减轻了SAP的严重性。我们的发现为理解APD在SAP患者中的有效性提供了新的见解。