This study examined the expressions of miR-22 and miR-135a in rats with acute edematous pancreatitis （AEP） and their target genes in order to shed light on the involvement of miR-22 and miR-135a in the pathogenesis of acute pancreatitis （AP）. The in vivo model of AEP was established by introperitoneal injection of L-arginine （150 mg/kg） in rats. The miRNA microarray analysis was used to detect the differential expression of miRNAs in pancreatic tissue in AEP and normal rats. The in vitro AEP model was established by inducing the rat pancreatic acinar cell line （AR42J） with 50 ng/mL re- combinant rat TNF-ct. Real-time quantitative RT-PCR was employed to detect the expression of miR-22 and miR-135a in AR42J cells. Lentiviruses carrying the miRNA mimic and anti-miRNA oligonucleotide （AMO） of miR-22 and miR-135a were transfected into the AR42J cells. The AR42J cells transfected with vehicle served as control. Western blotting was used to measure the expression of activated cas- pase3 and flow cytometry analysis to detect the apoptosis of AR42J cells. Targets of miR-22 and miR-135a were predicted by using TargetScan, miRanda, and TarBase. Luciferase reporter assay and quantitative real-time RT-PCR were performed to confirm whether ErbB3 and Ptk2 were the target gene of miR-22 and miR-135a, respectively. The results showed that the expression levels of miR-22 and miR-135a were obviously increased in AEP group compared with the control group in in-vivo and in-vitro models. The expression levels of miR-22 and miR-135a were elevated conspicuously and the expression levels of their target genes were reduced significantly in AR42J cells transfected with Ienti- viruses carrying the miRNA mimic. The apoptosis rate was much higher in the TNF-ct-induced cells than in non-treated cells. The AR42J cells transfected with miRNA AMOs expressed lower level of miR-22 and miR-135a and had lower apoptosis rate, but the expression levels of ErbB3 and Ptk2 were increased obviously. It was concluded that the expression
目的探讨高脂血症性急性重症胰腺炎(hyperlipidemia-induced severe acute pancreatitis,HLSAP)患者行早期肠内营养治疗的安全性及疗效。方法 HLSAP患者68例,入院确诊72h后行肠内营养治疗者36例为延迟营养组,入院确诊72h内行肠内营养治疗者32例为早期营养组,比较2组患者腹痛缓解时间、血及尿淀粉酶恢复时间,治疗2周后血清总蛋白、白蛋白和血清C反应蛋白水平变化、急性生理性及慢性健康状况评分Ⅱ(Acute Physiology And Chronic Health Evaluation ScoreⅡ,APACHEⅡ)评分、住院时间、并发症发生率等。结果早期营养组腹痛缓解时间[(3.6±1.2)d]、血淀粉酶恢复时间[(6.0±1.0)d]、尿淀粉酶恢复时间[(17.1±2.2)d]和住院时间[(28.2±2.4)d)]短于延迟营养组[(5.9±1.4)d、(9.5±1.4)d、(19.7±1.8)d、(33.3±3.9)d)](P<0.05),治疗2周后血清总蛋白[(57.7±3.4)g/L]、白蛋白[(25.9±2.4)g/L]高于延迟营养组[(51.9±2.6)g/L、(21.1±2.9)g/L](P<0.05),治疗后APACHEⅡ评分(7.1±2.5)和血清C反应蛋白水平[(40.1±20.7)mg/L]低于延迟营养组[(8.7±3.1)分,(104.3±21.9)mg/L](P<0.05);延迟营养组并发症发生率(66.7%)、病死率(19.4%)与早期营养组(43.8%,15.6%)比较差异均无统计学意义(P>0.05)。结论 HLSAP患者入院确诊72h内进行肠内营养治疗安全、有效,可加速患者康复,缩短住院时间。
