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It has been shown that Ginkgo biloba Extract (EGb 761) increases peripheral and cerebral blood flow and microcirculation and improves myocardial ischemia reperfusion injury. This study was designed to investigate the effect of EGb 761 on hepatic endothelial cells and hepatic microcirculation. Sixty male Wister rats were divided into normal, carbon tetrachloride (CCl₄) and EGb groups, and were given normal saline, CCl₄ and CCl₄ plus EGb 761, respectively, for 10 weeks. Samples were taken from the medial lobe of the rat livers ten weeks later. Hepatic sinusoidal endothelial cells and other parameters of hepatic microcirculation were observed under transmission electron microscopy (TEM). The amount of malondialdehyde (MDA), endothelin (ET-1), platelet-activating factor (PAF) and nitric oxide (NO) in liver tissue was determined by spectrophotometry and radioimmunoassay, respectively. Compared with the CCl₄ group, aggregation of blood cell or micro thrombosis in hepatic sinusoids, deposition of collagen in hepatic sinusoids and space of Disse, injury of endothelial cells and capillization of hepatic sinusoid was significantly reduced in the EGb group. The amount of MDA, ET-1 and PAF was markedly reduced in the EGb group than in the CCl₄ group, while no significant difference in the amount of NO was observed between the two groups. The results demonstrate that EGb 761 has protective effect on hepatic endothelial cells and hepatic microcirculation in rats with chronic liver injury induced by CCl₄. The mechanisms may involve its inhibition on ET-1, PAF and lipid peroxidation.

Angelica and ChuanXiong are used to cure ischemic heart disease in China. Previous studies found that these two herbs could increase myocardial blood flow, oxygen-supply and keep myocardial oxygen balance, etc. However, the mechanisms of angiogenic effects of these two herbs are not well-known. The purpose of this study was to assess the effects of Angelica and ChuanXiong on vascular endothelial growth factor (VEGF) expression in rat myocardial infarction, on endothelial cell proliferation and quantity of vessels on chick embryo chorioallantoic membrane (CAM). In this study, rats were divided randomly into either pre-treatment or acute-treatment group and sacrificed at the end of the treatments. VEGF expression using Western blot analysis was significantly increased in the groups pre-treated with ChuanXiong and Angelica when compared to the control group (p < 0.05). There was significant increase in VEGF expression in the rats treated acutely with Angelica (p < 0.05). In the contrary, the rats treated with ChuanXiong showed a decrease in VEGF expression when compared to the acute-treatment control group (p < 0.05). Similar results were observed in immunohistochemistry of VEGF expression in the myocardia. Our study also demonstrated that these two herbs significantly enhanced endothelial cell proliferation (p < 0.05) and revascularity in CAM (p < 0.05). The data showed that Angelica and ChuanXiong could affect VEGF expression in rat myocardial infarction, promote endothelial cell proliferation and stimulate quantity of vessels on CAM model. The results suggest that Angelica and ChuanXiong have angiogenic effects, and may provide some mechanisms for the treatment of myocardial infarction and peripheral ischemia.

The aim of this study was to evaluate, for the first time, the antagonistic effects of Gingko biloba leaf (GB) and Sophora japonica L. flower bud (SJ) extracts on cerebral vasoconstriction in response to KCl, extracellular Ca${}^{2+}$, histamine, 5-hydroxytryptamine (5-HT), 9,11-dideoxy-9$\alpha$,11$\alpha$-methanoepoxy prostaglandin (PG) F${}_{2\alpha }$(U46619) and bradykinin (BK), in order to explain their traditional application for diseases associated with cerebral vasospasm. Isolated porcine basilar arteries (PBA) and endothelial cells from them were used as the study materials. Neither SJ nor GB had any effect on the contractions induced by KCl and extracellular Ca${}^{2+}$. SJ significantly inhibited the contraction induced by histamine, 5-HT, U46619 and BK, whereas GB inhibited histamine-induced contraction, but had no effects on the contractions induced by 5-HT, U46619 and BK. In the presence of diphenhydramine (a H₁ receptor antagonist), ketanserin (a 5-HT₂ receptor antagonist) and ONO-3708 (a thromboxane (TX) A₂/PG receptor antagonist), the inhibitory effects of these extracts on the contractions induced by histamine, 5-HT and U46619 were abolished. SJ significantly inhibited the contractions induced by BK and PGF${}_{2\alpha }$, but in the presence of ONO-3708 (10${}^{-5}$ M) had no effect on them. BK enhanced the production of PGF${}_{2\alpha }$ from cultured PBA endothelium cells, and SJ significantly attenuated this enhancement. These results suggest that SJ and GB have a H₁-antagonistic effect, and that SJ also attenuates cerebral vasoconstriction mediated via 5-HT₂ and TXA₂/PG receptors. These findings appear to explain why SJ has been used traditionally as a therapeutic medication for cerebral vasospasm after cerebral hemorrhage.

In this paper, we develop a new discrete mathematical model for individual and collective cell motility. We introduce a mechanical model for the movement of a cell on a two-dimensional rigid surface to describe and investigate the cell–cell and cell–substrate interactions. The cell cytoskeleton is modeled as a series of springs and dashpots connected in parallel. The cell–substrate attachments and the cell protrusions are also included. In particular, this model is used to describe the directed movement of endothelial cells on a Matrigel plate. We compare the results from our model with experimental data. We show that cell density and substrate rigidity play an important role in network formation.

Vascular endothelial cells (ECs) are subjected to shear stress and cytokine stimulation. We studied the interplay between shear stress and cytokine in modulating the expression of adhesion molecule genes and the adhesive function of ECs. Shear stress (20 dynes/cm²) was applied to ECs prior to or following the addition of tumor necrosis factor (TNF)-α. Shear stress increased the TNF-α-induced expression of intercellular adhesion molecule-1 (ICAM-1) at both mRNA and surface protein levels, but decreased the TNF-α-induced expression of vascular adhesion molecule-1 (VCAM-1). The TNF-α-induced increase in EC adhesiveness for monocytic THP-1 cells was reduced by shear stress. After 24-h pre-shearing followed by 1 h of static incubation, the effect of pre-shearing on TNF-α-induced ICAM-1 mRNA expression vanished. The recovery of the TNF-α-induced VCAM-1 mRNA expression following pre-shearing, however, required a static incubation time of >6 h (completely recovery at 24 h). Pre- and post-shearing caused a reduction in the nuclear factor (NF)-κB-DNA binding activity induced by TNF-α in the EC nucleus. Our findings suggest that shear stress plays differential roles in modulating the TNF-α-induced EC expressions of ICAM-1 and VCAM-1 genes, which serve similar functions in vascular biology.

Gold nanoparticles (AuNPs) used for therapeutic applications preferentially accumulate in the liver following exposure. However, uptake and clearance by hepatic cells are not well understood. Time-dependent intracellular localization, uptake and clearance of 30 nm AuNPs were monitored in primary rat hepatocytes and liver sinusoidal endothelial cells (LSECs). Confocal Raman microscopy studies demonstrated the differences in the localization of AuNPs in hepatic cells over a 24 h period. The uptake of unmodified AuNPs over 24 h was 17% and 55% for hepatocytes and LSECs. The uptake of poly(ethylene glycol)-coated AuNPs was 3% and 1% over 24 h in hepatocytes and LSECs, respectively. Both cell types expelled approximately 60–70% of intracellular AuNPs within seven days. AuNP accumulation resulted in the disruption of the pericanalicular actin between adjoining hepatocytes. These trends suggest that AuNPs may affect actin organization, which could impair hepatic function long term.

We presented a new approach to produce Chitosan–Glutaraldehyde–Chitosan–Alginate (CGCA) hollow fiber with the capability of cell capture and adhesion for vascular tissue engineering. The CGCA hollow fiber was generated by sacrificing the inner part of alginate/chitosan (A/C) solid fiber using sodium citrate, followed by glutaraldehyde (GA) cross-linking chitosan to form stable imine bonds on the fiber surface. Furthermore, human umbilical vein endothelial cells (HUVEC) were captured by the CGCA hollow fiber surface and adhesive as layer pattern with good viability and normal morphology. This strategy facilitated the lumen structure formation with good biocompatibility by biomaterials modification, providing a promising and facile technique for blood vessel regeneration in vitro and in vivo.

Coronary atherosclerosis has long been recognized with high morbidity and mortality worldwide. The main cause of this group of diseases is thrombosis, resulting in insufficient oxygen perfusion by the blood to various organs in the body, thereby causing tissue necrosis. Dysfunction of vascular endothelial cell (ECs) is the major cause of atherosclerosis and thrombosis. Hemodynamic abnormalities are one of the many factors causing endothelial dysfunction. Shear stress and cyclic stretch are two major hemodynamic forces generated by pulsatile blood flow and pressure in the arterial vasculature. When hemodynamic abnormalities occur, endothelial dysfunction follows, this ultimately leads to atherosclerosis and thrombosis. Our objective, therefore, was to design and construct an unique hemodynamic equipment described herein. This hemodynamic device can concurrently produce shear stress and cyclic stretch to vascular ECs in vitro, and thus their morphological changes in response to simultaneous exposure to shear stress and cyclic stretch can be visualized in real-time via microscopy.

Intracellular tension transmission through basal actin stress fibers (SFs) running between separate focal adhesion sites has been proposed to play a role in sensing extracellular forces to adapt the adherent cell structure. However, quantitative descriptions of tension level in SFs are still poorly studied. Here, magnitude of preexisting tension in single SFs of endothelial cells was evaluated by in vitro tensile test. Single SFs were isolated from the cells with a combination of low ionic-strength solution and detergent extractions. A tensile test was conducted with a pair of micro-cantilevers driven by a piezo-electric actuator to measure the mechanical properties of the isolated single SF and the force required for stretching it up to its original length, yielding an estimate of the preexisting tension. The Young's modulus was estimated ~290 kPa assuming that the specimen was homogeneous. The magnitude of the preexisting tension, 4 nN on average, was comparable to previously reported data of the traction force generated by adherent cells at single adhesion sites to keep cell integrity. These data will contribute to quantitative understanding of intracellular stress transmission mechanism in adherent cells.