Table 1.
Primer of rat gene used for quantitative realtime PCR analysis.
Table 2.
Hemodynamics in BDL rats with thalidomide treatment.
Table 3.
Plasma, Hepatic and Mesenteric Levels of Various Pathogenic Factors.
Fig 1.
Dose-response curves and area under curves (AUC) of in situ perfusion of cirrhotic microvessels.
Chronic thalidomide treatment improves vasoconstrictive hypo-responsiveness to arginine vasopressin (AVP) (A,B) and attenuates vasodilatory hyper-responsiveness to acetycholine (ACh) (C,D) in superior mesenteric arteries (SMA) and portosystemic collateral vessels (PS collaterals); #: P < 0.05 vs. C-V group.
Fig 2.
In vivo and in vitro effects of thalidomide treatment on mesenteric and human umbilical vein endothelial cells (HUVECs)-induced angiogenesis.
Representative CD31 immunofluoresence (IF) staining angiogenesis images (A) and bar graphs of vascular length (B) and area (C) in mesenteric window. Representative images and bar graph of HUVECs tube formation (D,E) and migration (F,G) assays after 36hr of treatment; †: P<0.05 vs. S-V; δ: p< 0.05 vs. C-T rats;#: p < 0.01 vs. VEGF+TNFα; *: p < 0.05 vs. buffer group.
Fig 3.
Effects of thalidomide treatment on various cirrhotic vascular/mesenteric/intestinal inflammatory, angiogenic and vasodilatory markers.
Protein and mRNA expressions in splenorenal shunts (BDL) and left renal vein (sham). (A,B), and mesenteric tissues (C,D); (E).H-E staining for severity of mucosal injury (suzuki score) of small intestine; (F). IHC staining for inflammasome expression (NLRP3/caspase-1/IL-1β) of ileum. †p<0.05 vs. S-V rats; δ p< 0.05 vs. C-T rats. Genes were normalized to 18S RNA as an internal control.
Fig 4.
Acute effects of thalidomide on various cirrhotic vascular/mesenteric/intestinal inflammatory and angiogenic markers in human umbilical vein endothelial cells (HUVECs) system.
Various protein (A-B), mRNA (C) and cytokines (D) levels in supernatant of HUVECs with different treatments. #: p < 0.01 vs. VEGF+TNFα; *: p < 0.05 vs. buffer group.
Fig 5.
Schematic representative hypothesis of chronic thalidomide treatment effects on cirrhotic rats of our study.
TNFα: tumor necrosis factor-α; IVC: inferior vena cava; SMV: superior mesenteric vein; eNOS: endothelial nitric oxide synthase; NO: nitric oxide.