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大黄素通过上调肺组织中AQP1和AQP5的表达减轻重症急性胰腺炎诱导的急性肺损伤。

Emodin ameliorates acute lung injury induced by severe acute pancreatitis through the up-regulated expressions of AQP1 and AQP5 in lung.

作者信息

Xu Junfeng, Huang Bo, Wang Yu, Tong Caiyu, Xie Peng, Fan Rong, Gao Zhenming

机构信息

Department of General Surgery, the First People's Hospital of Xiaoshan District of Hangzhou City, Hangzhou, China.

Department of Hepatobiliary and Pancreatic Surgery, the Second Hospital of Dalian Medical University, Dalian, China.

出版信息

Clin Exp Pharmacol Physiol. 2016 Nov;43(11):1071-1079. doi: 10.1111/1440-1681.12627.

Abstract

The present study investigates the ameliorating effects of emodin on acute lung injury (ALI) induced by severe acute pancreatitis (SAP). An ALI rat model was constructed by sodium ursodeoxycholate and they were divided into four groups: SHAM, ALI, emodin and dexamethasone (DEX) (n=24 per group). Blood samples and lung tissues were collected 6, 12 and 24 hours after the induction of SAP-associated ALI. Lung wet/dry ratio, blood gases, serum amylase and tumor necrosis factor-α (TNF-α) were measured at each time point. The expressions of AQP1 and AQP5 in lung tissue were detected by immunohistochemical staining, western blotting and real-time PCR. As the results show, there were no statistical differences in the levels of serum amylase, lung wet/dry ratio, blood gases indexes, serum TNF-α and pathological changes between emodin and DEX groups. However, significant differences were observed when compared with the ALI group. AQP1 and AQP5 expressions were significantly increased and lung oedemas were alleviated with the treatment of emodin and DEX. The expressions of AQP1 and AQP5 were significantly decreased in SAP-associated ALI rats. Emodin up-regulated the expression of AQP1 and AQP5, it could reduce pulmonary oedema and ameliorate SAP-induced ALI. Regulations on AQP1 and AQP5 expression had a great value in clinical application.

摘要

本研究探讨大黄素对重症急性胰腺炎(SAP)诱导的急性肺损伤(ALI)的改善作用。采用熊去氧胆酸钠构建ALI大鼠模型,并将其分为四组:假手术组(SHAM)、ALI组、大黄素组和地塞米松(DEX)组(每组n = 24)。在诱导SAP相关ALI后6、12和24小时采集血样和肺组织。在每个时间点测量肺湿/干比、血气、血清淀粉酶和肿瘤坏死因子-α(TNF-α)。通过免疫组织化学染色、蛋白质印迹法和实时PCR检测肺组织中AQP1和AQP5的表达。结果显示,大黄素组和DEX组在血清淀粉酶水平、肺湿/干比、血气指标、血清TNF-α水平及病理变化方面无统计学差异。然而,与ALI组相比观察到显著差异。大黄素和DEX治疗后,AQP1和AQP5表达显著增加,肺水肿减轻。在SAP相关ALI大鼠中,AQP1和AQP5的表达显著降低。大黄素上调AQP1和AQP5的表达,可减轻肺水肿并改善SAP诱导的ALI。对AQP1和AQP5表达的调控在临床应用中具有重要价值。

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