Department of Gastroenterology, The First Affiliated Hospital of Anhui Medical University, The Key Laboratory of Digestive Diseases of Anhui Province, 218 Jixi Road, Hefei, 230022, Anhui Province, China.
Dig Dis Sci. 2018 Dec;63(12):3359-3366. doi: 10.1007/s10620-018-5191-4. Epub 2018 Jul 5.
Acute pancreatitis (AP) is a common acute gastrointestinal disorders. Increasing evidence indicated that autophagy is involved in the development of AP. Resolvin D1 is an endogenous pro-resolving lipid mediator, which can protect mice from cerulein-induced acute pancreatitis and facilitate autophagy in macrophage, but its mechanism remians unclear.
To investigate the effect of resolvin D1 on autophagy in mouse models of cerulein-induced AP.
C57BL/6 mice were randomly divided into control group, AP group and resolvin D1 group. The models of cerulein-induced AP were constructed by intraperitoneally cerulein. Resolvin D1 group was established by intraperitoneally resolvin D1 based on AP models, simultaneously, control group received normal saline. The severity of AP, the level of inflammatory cytokines, the number of autophagic vacuoles, and the expression of autophagy-related markers were evaluated among three groups.
The AP models were established successfully. Compared to control group, the number of autophagic vacuoles and expressions of autophagy-related markers including Beclin-1, p62 and LC3-II were increased in AP models, In contrast, the degree of inflammation and levels of inflammatory cytokines in AP models were reduced after resolvin D1 treatment. Moreover, resolvin D1 attenuated the number of autophagic vacuoles and expressions of autophagy-related markers.
Autophagic flux is impaired in cerulein-induced AP. Resolvin D1 ameliorate the severity of mice with cerulein-induced acute pancreatitis, possible attributing to its reducing impaired autophagy and restoring autophagic flux.
急性胰腺炎（AP）是一种常见的急性胃肠道疾病。越来越多的证据表明自噬参与了 AP 的发展。解析素 D1 是一种内源性的促解决脂质介质，它可以保护小鼠免受鹅膏蕈碱诱导的急性胰腺炎，并促进巨噬细胞中的自噬，但它的机制尚不清楚。
研究解析素 D1 对鹅膏蕈碱诱导的 AP 小鼠模型中自噬的影响。
将 C57BL/6 小鼠随机分为对照组、AP 组和解析素 D1 组。通过腹腔内注射鹅膏蕈碱构建 AP 模型。解析素 D1 组在 AP 模型的基础上通过腹腔内注射解析素 D1 建立，同时对照组给予生理盐水。评估三组中 AP 的严重程度、炎症细胞因子水平、自噬空泡数量和自噬相关标志物的表达。
成功建立了 AP 模型。与对照组相比，AP 模型中自噬空泡的数量和自噬相关标志物如 Beclin-1、p62 和 LC3-II 的表达增加，而 AP 模型中炎症程度和炎症细胞因子水平在解析素 D1 处理后降低。此外，解析素 D1 减弱了自噬空泡的数量和自噬相关标志物的表达。
在鹅膏蕈碱诱导的 AP 中，自噬流受损。解析素 D1 改善了鹅膏蕈碱诱导的急性胰腺炎小鼠的严重程度，可能归因于其减少受损的自噬并恢复自噬流。
