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Abstract：
UNASSIGNED: To investigate mechanisms underlying the effects of Da-Cheng-Qi decoction (DCQD) on severe acute pancreatitis (SAP) capillary leakage syndrome.
UNASSIGNED: In this study, a SAP rat model was established using retrograde perfusion of 5% sodium taurocholate into the biliopancreatic duct. The study included three randomized groups: control, SAP (modeling), and DCQD (via gavage at 2 h pre-modeling and 2 and 4 h post-modeling). HPLC was used to analyzed major components of DCQD. Pathological changes and capillary permeability in the rat pancreatic tissues were examined. mRNA levels of claudin 5, occludin, zonula occludin-1 (ZO-1), and junctional adhesion molecules (JAM-C) were assessed using qRT-PCR. Tight junction-associated protein expression was evaluated using immunofluorescence and Western blot analyses. Human umbilical vein endothelial cells (HUVECs) were used to investigate the mechanism m of DCQD.
UNASSIGNED: Serum levels of amylase, TNF-α, IL-1β, IL-2, and IL-6 were higher in the SAP group compared to the DCQD group (p < 0.05). DCQD treatment significantly attenuated rat pancreas damage (p < 0.05) and reduced tissue capillary permeability compared to the SAP group (p < 0.05). Claudin 5, occludin, and ZO-1 expression in the rat tissues was upregulated, but JAM-C was downregulated by DCQD treatment (p < 0.05). HUVEC permeability was improved by DCQD in a dose-time-dependent manner compared to the SAP group (p < 0.05). DCQD also upregulated claudin 5, occludin, and ZO-1 expression in vitro (p < 0.05).
UNASSIGNED: DCQD can improve capillary permeability in both in vivo and in vitro models of SAP by upregulating expression of claudin 5, occludin, and ZO-1, but not JAM-C.
UNASSIGNED: In this study, a SAP rat model was established using retrograde perfusion of 5% sodium taurocholate into the biliopancreatic duct. The study included three randomized groups: control, SAP (modeling), and DCQD (via gavage at 2 h pre-modeling and 2 and 4 h post-modeling). HPLC was used to analyzed major components of DCQD. Pathological changes and capillary permeability in the rat pancreatic tissues were examined. mRNA levels of claudin 5, occludin, zonula occludin-1 (ZO-1), and junctional adhesion molecules (JAM-C) were assessed using qRT-PCR. Tight junction-associated protein expression was evaluated using immunofluorescence and Western blot analyses. Human umbilical vein endothelial cells (HUVECs) were used to investigate the mechanism m of DCQD.
UNASSIGNED: Serum levels of amylase, TNF-α, IL-1β, IL-2, and IL-6 were higher in the SAP group compared to the DCQD group (p < 0.05). DCQD treatment significantly attenuated rat pancreas damage (p < 0.05) and reduced tissue capillary permeability compared to the SAP group (p < 0.05). Claudin 5, occludin, and ZO-1 expression in the rat tissues was upregulated, but JAM-C was downregulated by DCQD treatment (p < 0.05). HUVEC permeability was improved by DCQD in a dose-time-dependent manner compared to the SAP group (p < 0.05). DCQD also upregulated claudin 5, occludin, and ZO-1 expression in vitro (p < 0.05).
UNASSIGNED: DCQD can improve capillary permeability in both in vivo and in vitro models of SAP by upregulating expression of claudin 5, occludin, and ZO-1, but not JAM-C.
摘要：
■探讨大承气汤(DCQD)治疗重症急性胰腺炎(SAP)毛细血管渗漏综合征的作用机制。
■在这项研究中，采用5%牛磺胆酸钠逆行灌注胆胰管建立SAP大鼠模型。该研究包括三个随机组：对照组，SAP（建模），和DCQD(在建模前2小时和建模后2小时和4小时通过管饲法)。HPLC用于分析DCQD的主要成分。检查大鼠胰腺组织的病理变化和毛细血管通透性。claudin5、occludin、小带闭合蛋白-1(ZO-1)，使用qRT-PCR评估和连接粘附分子（JAM-C）。使用免疫荧光和蛋白质印迹分析评估紧密连接相关蛋白的表达。采用人脐静脉内皮细胞(HUVECs)研究DCQD的发生机制。
■血清淀粉酶水平，TNF-α,IL-1β,IL-2和IL-6在SAP组高于DCQD组(p<0.05)。与SAP组相比，DCQD治疗可显着减轻大鼠胰腺损伤（p<0.05），并降低组织毛细血管通透性（p<0.05）。Claudin5,occludin,ZO-1在大鼠组织中的表达上调,但JAM-C被DCQD治疗下调(p<0.05)。与SAP组相比,DCQD以剂量-时间依赖性方式改善HUVEC通透性(p<0.05)。DCQD也上调claudin5，occludin，和ZO-1的体外表达(p<0.05)。
■DCQD可以通过上调claudin5，occludin的表达来改善SAP体内和体外模型中的毛细血管通透性，和ZO-1，但不是JAM-C。
■在这项研究中，采用5%牛磺胆酸钠逆行灌注胆胰管建立SAP大鼠模型。该研究包括三个随机组：对照组，SAP（建模），和DCQD(在建模前2小时和建模后2小时和4小时通过管饲法)。HPLC用于分析DCQD的主要成分。检查大鼠胰腺组织的病理变化和毛细血管通透性。claudin5、occludin、小带闭合蛋白-1(ZO-1)，使用qRT-PCR评估和连接粘附分子（JAM-C）。使用免疫荧光和蛋白质印迹分析评估紧密连接相关蛋白的表达。采用人脐静脉内皮细胞(HUVECs)研究DCQD的发生机制。
■血清淀粉酶水平，TNF-α,IL-1β,IL-2和IL-6在SAP组高于DCQD组(p<0.05)。与SAP组相比，DCQD治疗可显着减轻大鼠胰腺损伤（p<0.05），并降低组织毛细血管通透性（p<0.05）。Claudin5,occludin,ZO-1在大鼠组织中的表达上调,但JAM-C被DCQD治疗下调(p<0.05)。与SAP组相比,DCQD以剂量-时间依赖性方式改善HUVEC通透性(p<0.05)。DCQD也上调claudin5，occludin，和ZO-1的体外表达(p<0.05)。
■DCQD可以通过上调claudin5，occludin的表达来改善SAP体内和体外模型中的毛细血管通透性，和ZO-1，但不是JAM-C。
