LncRNA-LUCAT1对雨蛙素诱导的急性胰腺炎细胞凋亡和周期的作用和机制研究  

The Effect and Mechanism of LncRNA-LUCAT1 on Cell Apoptosis and Cycle in Acute Pancreatitis Cells Induced by Caerulein

作　　者：孙旭日[1] 杨聪汉 吴金铠 SUN Xuri;YANG Conghan;WU Jinkai(The Second Affiliated Hospital of Fujian Medical University,Quanzhou 362000,China)

机构地区：[1]福建医科大学附属第二医院重症医学科,福建泉州362000

出　　处：《中华灾害救援医学》2024年第7期757-760,共4页Chinese Journal of Disaster Medicine

基　　金：福建省自然科学基金项目(2020J01237)。

摘　　要：目的探索LncRNA-LUCAT1对雨蛙素诱导的急性胰腺炎(Acute Pancreatitis,AP)腺泡细胞功能的影响。方法在大鼠胰腺腺泡细胞AR42J中敲低或过表达LUCAT1,利用CCK8检测细胞活性;Elisa检测IL-6、IL-1β、TNF-α、TAP和淀粉酶水平;流式细胞术检测细胞凋亡和周期;western blot检测凋亡和周期表达蛋白。结果CCK8检测结果显示,雨蛙素处理后AR42J细胞OD值显著下降,与对照组相比,LUCAT1过表达后OD值下降显著,而LUCAT1敲低后细胞OD值显著升高(P<0.05)。雨蛙素处理的AR42J细胞中淀粉酶和TAP含量升高,敲低LUCAT1可以使淀粉酶和TAP含量显著下降(P<0.05)。LUCAT1还能够上调炎症因子IL-6、IL-1β和TNF-α水平(P<0.05),加重雨蛙素诱导的腺泡细胞炎症反应。LUCAT1能够引起胰腺腺泡细胞过度凋亡和细胞周期阻滞,敲低LUCAT1则能够缓解雨蛙素诱导的细胞凋亡和细胞周期阻滞。LUCAT1促进了凋亡因子Bax、Cleaved-Caspase7和Cleaved-Caspase3水平,并下调了凋亡抑制因子Bcl-2表达,同时LUCAT1还抑制了周期蛋白Cyclin D1的表达。敲低LUCAT1则呈现相反的趋势。结论LUCAT1敲低能够有效抑制雨蛙素诱导的腺泡细胞凋亡和细胞周期阻滞,是AP治疗的潜在靶点。Objective To investigate the effects of LncRNA-LUCAT1 on the function of acinar cells in caerulein-induced acute pancreatitis(AP).Methods LUCAT1 was knocked down or overexpressed in rat pancreatic acinar cells(AR42J).Cell viability was assessed using the CCK-8 assay.The levels of IL-6,IL-1β,TNF-α,TAP,and amylase were measured using ELISA.Apoptosis and cell cycle were analyzed by flow cytometry.The expression of apoptosis and cell cycle proteins was detected by Western blot.Results The CCK-8 assay results showed a significant decrease in the OD value of AR42J cells after treating with caerulein.Compared to the control group,overexpression of LUCAT1 cause a further significant decrease in OD value,while knockdown of LUCAT1 significantly increased the OD value(P<0.05).In caerulein-treated AR42J cells,amylase and TAP levels were elevated;knockdown of LUCAT1 significantly reduced these levels(P<0.05).LUCAT1 also upregulated the levels of inflammatory cytokines IL-6,IL-1β,and TNF-α(P<0.05),exacerbating caerulein-induced inflammation in acinar cells.LUCAT1 induced excessive apoptosis and cell cycle arrest in pancreatic acinar cells,while knockdown of LUCAT1 alleviated caerulein-induced apoptosis and cell cycle arrest.LUCAT1 promoted the expression of pro-apoptotic factors Bax,Cleaved-Caspase7,and Cleaved-Caspase3 and downregulated the expression of the anti-apoptotic factor Bcl-2.Additionally,LUCAT1 inhibited the expression of the cell cycle protein Cyclin D1.Knockdown of LUCAT1 showed the opposite trends.Conclusion Knockdown of LUCAT1 effectively inhibits caerulein-induced apoptosis and cell cycle arrest in acinar cells,suggesting that LUCAT1 is a potential therapeutic target for AP.

关 键 词：胰腺炎 急性坏死性 雨蛙素 细胞凋亡 

分 类 号：R576[医药卫生—消化系统] R-332[医药卫生—内科学]