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首页> 外文期刊>World journal of gastroenterology : >Cell-permeable Tat-NBD peptide attenuates rat pancreatitis and acinus cell inflammation response.
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Cell-permeable Tat-NBD peptide attenuates rat pancreatitis and acinus cell inflammation response.

机译：细胞可渗透的Tat-NBD肽可减轻大鼠胰腺炎和腺泡细胞炎症反应。

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AIM: To investigate the effects of Tat-NEMO-binding domain (NBD) peptide on taurocholate-induced pancreatitis and lipopolysaccharide (LPS)-stimulated AR42J acinus cells inflammatory response in rats. METHODS: Sodium taurocholate (5%) was used to induce the pancreatitis model. Forty-eight rats from the taurocholate group received an intravenous bolus of 13 mg/kg Tat-NBD (wild-type, WT) peptide, Tat-NBD (mutant-type, MT) peptide, NBD peptide or Tat peptide. The pancreatic histopathology was analyzed by hematoxylin staining. LPS was added to the culture medium to stimulate the AR42J cells. For pretreatment, cells were incubated with different peptides for 2 h before LPS stimulation. Expression of IL-1beta and TNF-alpha mRNA was analyzed using a semi-quantitative reverse-transcript polymerase chain reaction (RT-PCR) method. IL-1beta and TNF-alpha protein in culture medium were detected by enzyme linked immunosorbent assay (ELISA). NF-kappaB DNA-binding in pancreas was examined by electrophoretic mobility shift assays. P65 expression of AR42J was determined by Strept Actividin-Biotin Complex (SABC) method. RESULTS: Pretreatment with Tat-NBD (WT) peptide at a concentration of 13 mg/kg body wt showed beneficial effect in pancreaitis model. LPS (10 mg/L) resulted in an increase of IL-1beta mRNA, IL-1beta protein, TNF-alpha mRNA and TNF-alpha protein, whereas significantly inhibitory effects were observed when cells were incubated with Tat-NBD (WT). Consisting with p65 expression decrease analyzed by SABC method, NF-kappaB DNA-binding activity significantly decreased in Tat-NBD (WT) pretreatment group, especially at the largest dose. No significant changes were found in the control peptide group. CONCLUSION: Our result supports that active NF-kappaB participates in the pathogenesis of STC-induced acute pancreatitis in rats. Tat-NBD (WT) peptide has anti-inflammatory effects in this model and inhibits the inflammation of acinus simulated by LPS.
机译：目的：探讨Tat-NEMO结合域（NBD）肽对牛磺胆酸盐诱导的胰腺炎和脂多糖（LPS）刺激的AR42J腺泡细胞炎性反应的影响。方法：使用牛磺胆酸钠（5％）诱导胰腺炎模型。来自牛磺胆酸盐组的四十八只大鼠接受了13 mg / kg Tat-NBD（野生型，WT）肽，Tat-NBD（突变型，MT）肽，NBD肽或Tat肽的静脉推注。通过苏木精染色分析胰腺组织病理学。将LPS添加到培养基中以刺激AR42J细胞。为了进行预处理，在LPS刺激之前，将细胞与不同的肽孵育2小时。使用半定量逆转录聚合酶链反应（RT-PCR）方法分析IL-1beta和TNF-αmRNA的表达。通过酶联免疫吸附试验（ELISA）检测培养基中的IL-1β和TNF-α蛋白。通过电泳迁移率变动分析检查胰腺中的NF-κBDNA结合。通过链激活素-生物素复合物（SABC）方法测定AR42J的P65表达。结果：浓度为13 mg / kg体重的Tat-NBD（WT）肽预处理在胰腺炎模型中显示出有益的作用。 LPS（10 mg / L）导致IL-1beta mRNA，IL-1beta蛋白，TNF-alpha mRNA和TNF-alpha蛋白增加，而将细胞与Tat-NBD（WT）孵育时，观察到明显的抑制作用。与SABC方法分析的p65表达下降相一致，NF-κBDNA结合活性在Tat-NBD（WT）预处理组中显着下降，尤其是在最大剂量下。在对照肽组中未发现显着变化。结论：我们的结果支持活性NF-κB参与STC诱导的大鼠急性胰腺炎的发病机制。 Tat-NBD（WT）肽在该模型中具有抗炎作用，并抑制LPS模拟的腺泡炎症。

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