硫氧还蛋白-1在重症急性胰腺炎中的作用

Role of Thioredoxin-1 in Severe Acute Pancreatitis

在重症急性胰腺炎(severe acute pancreatitis, SAP)中,肠道黏膜屏障的破坏可引起肠道细菌移位,诱发或加重全身性感染。硫氧还蛋白(thioredoxin, Trx)系统在机体氧化还原平衡和细胞增殖中发挥重要的调节作用,其中Trx-1除具有氧化还原和抗氧化活性外,还有细胞生长调节作用、调控转录因子及基因表达作用、抗凋亡作用等多种生物活性。本研究旨在探讨Trx-1在SAP大鼠肠道屏障损伤中的作用。健康成年雄性Sprague-Dawley大鼠随机分为假手术组、SAP组、SAP 重组人硫氧还蛋白(Trx-1)组。采用5%牛磺胆酸钠逆行注射胆管建立大鼠SAP模型。SAP前24 h腹腔注射重组人硫氧还蛋白,24 h后采集各组血清和肠道组织标本进行分析。Trx预处理通过增加Trx-1的量显著降低SAP的全身炎症反应和减轻肠道上皮损伤。我们的研究表明,Trx-1表达上调可以减轻SAP中肠黏膜屏障的损伤。

In severe acute pancreatitis (SAP), disruption of the intestinal mucosal barrier can cause intestinal bacterial translocation and induce or exacerbate systemic infections. The thioredoxin (Trx) system plays an important regulatory role in redox homeostasis and cell proliferation in the organism, in which Trx-1, in addition to its redox and antioxidant activities, also has a variety of biological activities, such as cell growth regulation, modulation of transcription factors and gene expression, and anti-apoptotic effects. The aim of this study was to investigate the role of Trx-1 in intestinal barrier injury in SAP rats. Healthy adult male Sprague-Dawley rats were randomly divided into sham-operated group, SAP group, and SAP recombinant human thioredoxin (Trx) group. The rat SAP model was established by retrograde injection of 5% sodium taurocholate into the bile ducts. Recombinant human thioredoxin was injected intraperitoneally 24 h before SAP, and serum and intestinal tissue specimens were collected from each group 24 h later for analysis. Trx pretreatment significantly reduced the systemic inflammatory response and attenuated intestinal epithelial injury in SAP by increasing the amount of TRX-1. Our study suggests that upregulation of Trx-1 expression attenuates intestinal mucosal barrier damage in SAP.