Objective To investigate the effects of LncRNA-LUCAT1 on the function of acinar cells in caer-ulein-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-1 β,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,over-expression 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;knock-down 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.LUCAT 1 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 LUCAT 1 effectively inhibits caerulein-induced apoptosis and cell cycle arrest in acinar cells,suggesting that LUCAT1 is a potential therapeutic target for AP.
维普
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