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塞来昔布通过对肝内纤维化和血管生成的双重抑制作用改善肝硬化大鼠的门静脉高压。

Celecoxib ameliorates portal hypertension of the cirrhotic rats through the dual inhibitory effects on the intrahepatic fibrosis and angiogenesis.

机构信息

Division of Peptides Related with Human Diseases, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.

出版信息

PLoS One. 2013 Jul 26;8(7):e69309. doi: 10.1371/journal.pone.0069309. Print 2013.

Abstract

BACKGROUND

Increased intra-hepatic resistance to portal blood flow is the primary factor leading to portal hypertension in cirrhosis. Up-regulated expression of cyclooxygenase-2 (COX-2) in the cirrhotic liver might be a potential target to ameliorate portal hypertension.

OBJECTIVE

To verify the effect of celecoxib, a selective inhibitor of COX-2, on portal hypertension and the mechanisms behind it.

METHODS

Cirrhotic liver model of rat was established by peritoneal injection of thiacetamide (TAA). 36 rats were randomly assigned to control, TAA and TAA+celecoxib groups. Portal pressures were measured by introduction of catheters into portal vein. Hepatic fibrosis was assessed by the visible hepatic fibrotic areas and mRNAs for collagen III and α-SMA. The neovasculature was determined by hepatic vascular areas, vascular casts and CD31 expression. Expressions of COX-2, vascular endothelial growth factor (VEGF), VEGF receptor-2 (VEGFR-2) and related signal molecules were quantitated.

RESULTS

Compared with TAA group, the portal pressure in TAA+celecoxib group was significantly decreased by 17.8%, p<0.01. Celecoxib treatment greatly reduced the tortuous hepatic portal venules. The data of fibrotic areas, CD31expression, mRNA levels of α-SMA and collagen III in TAA+celecoxib group were much lower than those in TAA group, p<0.01. Furthermore, the up-regulation of hepatic mRNA and protein levels of VEGF, VEGFR-2 and COX-2 induced by TAA was significantly inhibited after celecoxib treatment. The expressions of prostaglandin E2 (PGE2), phosphorylated extracellular signal-regulated kinase (p-ERK), hypoxia-inducible factor-1α (HIF-1α), and c-fos were also down-regulated after celecoxib treatment.

CONCLUSIONS

Long term administration of celecoxib can efficiently ameliorate portal hypertension in TAA rat model by its dual inhibitory effects on the intrahepatic fibrosis and angiogenesis. The anti-angiogenesis effect afforded by celecoxib may attribute to its modulation on VEGF/VEGFR-2 through the down-regulation of integrated signal pathways involving PGE2- HIF-1α- VEGF and p-ERK- c-fos- VEGFR-2.

摘要

背景

肝内对门静脉血流阻力增加是肝硬化导致门静脉高压的主要因素。环氧化酶-2(COX-2)在肝硬化肝脏中的表达上调可能是改善门静脉高压的潜在靶点。

目的

验证 COX-2 选择性抑制剂塞来昔布对门静脉高压的影响及其机制。

方法

采用腹腔注射硫代乙酰胺(TAA)建立大鼠肝硬化模型。36 只大鼠随机分为对照组、TAA 组和 TAA+塞来昔布组。通过向门静脉内置入导管测量门静脉压力。通过肝纤维化的可见肝纤维化面积和胶原 III 和α-SMA 的 mRNA 评估肝纤维化。通过肝血管面积、血管铸型和 CD31 表达确定新生血管。定量检测 COX-2、血管内皮生长因子(VEGF)、VEGF 受体-2(VEGFR-2)和相关信号分子的表达。

结果

与 TAA 组相比,TAA+塞来昔布组的门静脉压力降低了 17.8%,p<0.01。塞来昔布治疗显著减少了扭曲的肝门静脉小静脉。TAA+塞来昔布组的纤维化面积、CD31 表达、α-SMA 和胶原 III 的 mRNA 水平均明显低于 TAA 组,p<0.01。此外,TAA 诱导的肝组织中 VEGF、VEGFR-2 和 COX-2 的 mRNA 和蛋白水平上调在塞来昔布治疗后明显受到抑制。塞来昔布治疗后,前列腺素 E2(PGE2)、磷酸化细胞外信号调节激酶(p-ERK)、缺氧诱导因子-1α(HIF-1α)和 c-fos 的表达也下调。

结论

长期给予塞来昔布可通过双重抑制肝内纤维化和血管生成作用有效改善 TAA 大鼠模型的门静脉高压。塞来昔布的抗血管生成作用可能归因于其通过下调涉及 PGE2-HIF-1α-VEGF 和 p-ERK-c-fos-VEGFR-2 的整合信号通路来调节 VEGF/VEGFR-2。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4049/3724827/f7e9013bfc5e/pone.0069309.g001.jpg

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