Acute pancreatitis (AP) is one of the most frequent gastrointestinal diseases and has no specific treatment. It has been shown that dysfunction of pancreatic acinar cells can lead to AP progression. Emodin is a natural product, which can alleviate the symptoms of AP. However, the mechanism by which emodin regulates the function of pancreatic acinar cells remains unclear. Thus, the present study aimed to investigate the mechanism by which emodin modulates the function of pancreatic acinar cells. To mimic AP in vitro, pancreatic acinar cells were cotreated with caerulein and lipopolysaccharide (LPS). Exosomes were isolated using the ExoQuick precipitation kit. Western blot analysis, Nanosight Tracking analysis and transmission electron microscopy were performed to detect the efficiency of exosome separation. Gene expression was detected by reverse transcription‑quantitative PCR. The levels of IL‑1β and TNF‑α were detected by ELISA. The data indicated that emodin significantly decreased the levels of IL‑1β and TNF‑α in the supernatant samples derived from AR42J cells cotreated with caerulein and LPS. In addition, emodin significantly promoted the proliferation of AR42J cells cotreated with caerulein and LPS, and inhibited apoptosis, while the effect of emodin was reversed by long non‑coding (lnc)RNA taurine upregulated 1 (TUG1) overexpression. The expression level of TUG1 in AR42J cells or exosomes derived from AR42J cells was significantly increased following treatment of the cells with LPS and caerulein, while this effect was notably reversed by emodin treatment. In addition, exosomes derived from caerulein and LPS cotreated AR42J cells inhibited the differentiation and anti‑inflammatory function of regulatory T cells, while treatment of the cells with emodin significantly decreased this effect. In conclusion, the data indicated that emodin inhibited the induction of inflammation in AR42J cells by regulating the expression of cellular and exosomal lncRNA. Therefore, emodin may be used as a potential agent for the treatment of AP.

中文翻译：

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大黄素通过调节 lncRNA TUG1 和外泌体 lncRNA TUG1 抑制急性胰腺炎的进展。

急性胰腺炎（AP）是最常见的胃肠道疾病之一，目前尚无特效治疗方法。已经表明，胰腺腺泡细胞功能障碍可导致 AP 进展。大黄素是一种天然产物，可以缓解AP的症状。然而，大黄素调节胰腺腺泡细胞功能的机制仍不清楚。因此，本研究旨在探讨大黄素调节胰腺腺泡细胞功能的机制。在体外模拟 AP，胰腺腺泡细胞与caerulein和脂多糖（LPS）共同处理。使用 ExoQuick 沉淀试剂盒分离外泌体。进行蛋白质印迹分析、Nanosight Tracking 分析和透射电子显微镜以检测外泌体分离的效率。通过逆转录定量PCR检测基因表达。ELISA法检测IL-1β和TNF-α水平。数据表明，大黄素显着降低了来自与雨蛙素和 LPS 共同处理的 AR42J 细胞的上清液样品中 IL-1β 和 TNF-α 的水平。此外，大黄素显着促进与雨蛙素和 LPS 共同处理的 AR42J 细胞的增殖，并抑制细胞凋亡，而大黄素的作用被长链非编码 (lnc)RNA 牛磺酸上调 1 (TUG1) 过表达所逆转。在用 LPS 和 caerulein 处理细胞后，AR42J 细胞或源自 AR42J 细胞的外泌体中 TUG1 的表达水平显着增加，而大黄素处理显着逆转了这种作用。此外，来自caerulein和LPS共同处理的AR42J细胞的外泌体抑制了调节性T细胞的分化和抗炎功能，而用大黄素处理细胞则显着降低了这种作用。总之，数据表明大黄素通过调节细胞和外泌体 lncRNA 的表达来抑制 AR42J 细胞炎症的诱导。因此，大黄素可作为治疗AP的潜在药物。而大黄素处理显着逆转了这种效果。此外，来自caerulein和LPS共同处理的AR42J细胞的外泌体抑制了调节性T细胞的分化和抗炎功能，而用大黄素处理细胞则显着降低了这种作用。总之，数据表明大黄素通过调节细胞和外泌体 lncRNA 的表达来抑制 AR42J 细胞炎症的诱导。因此，大黄素可作为治疗AP的潜在药物。而大黄素处理显着逆转了这种效果。此外，来自caerulein和LPS共同处理的AR42J细胞的外泌体抑制了调节性T细胞的分化和抗炎功能，而用大黄素处理细胞则显着降低了这种作用。总之，数据表明大黄素通过调节细胞和外泌体 lncRNA 的表达来抑制 AR42J 细胞炎症的诱导。因此，大黄素可作为治疗AP的潜在药物。数据表明，大黄素通过调节细胞和外泌体 lncRNA 的表达来抑制 AR42J 细胞炎症的诱导。因此，大黄素可作为治疗AP的潜在药物。数据表明，大黄素通过调节细胞和外泌体 lncRNA 的表达来抑制 AR42J 细胞炎症的诱导。因此，大黄素可作为治疗AP的潜在药物。