Search

Atrial fibrillation (AF) is a common arrhythmia. Angiotensin‐receptor blocker (ARB) is related to AF treatment. This study explored the mechanism of ARB in AF. AF rat models were established by Ach‐CaCl2 mixed solution injection. Rats were treated with ARB by gavage and injected with pcDNA3.1‐based frizzled homolog 8 (FZD8) overexpression plasmids (oe‐FZD8) through the tail vein. The 12‐lead electrocardiogram was recorded by biological signal acquisition and processing system and AF duration was recorded, and atrial effective refractory period (AERP) was monitored by electrophysiology. Atrial fibrosis degree, FZD8 messenger RNA and protein levels, collagen I, collagen III, transforming growth factor β1 (TGF‐β1), fibronectin, α smooth muscle actin (α‐SMA), WBT‐5B, and p‐JNK1/2 levels, interleukin 1 β (IL‐1β) and interleukin 6 (IL‐6) levels were detected by Masson staining, reverse transcription quantitative polymerase chain reaction, western blot assay, immunohistochemistry, and enzyme‐linked immunosorbent assay. ACh‐CaCl2‐induced AF rats showed a large area of fused necrosis, abnormal collagen fibre proliferation, high atrial fibrosis degree, and increased atrial fibrosis area in atrial interstitium, elevated collagen I, collagen III, TGF‐β1, fibronectin, α‐SMA, IL‐1β, and IL‐6 levels, whereas these trends were averted by ARB treatment. FZD8 was highly expressed in AF rat myocardium. ARB repressed FZD8 expression, prolonged AERP and reduced AF incidence. FZD8 overexpression annulled the effects of ARB on improving AF rat myocardial fibrosis. ARB inactivated the WNT‐5A pathway by suppressing FZD8. ARB inactivated the WNT‐5A pathway by silencing FZD8, therefore, alleviating AF rat atrial fibrosis. [ABSTRACT FROM AUTHOR]

Herein biodegradable poly(ε-caprolactone) was electrospun into tubular microfibrous scaffolds and modified by the surface heparinization and wrapping of Type I collagen suture for enhancing anticoagulation activity and mechanical properties. The resulting scaffolds were featured by a double distribution of microfiber diameters ranged in 2.74 ± 0.44 and 5.15 ± 0.63 µm on the outer surface with tensile strength of 1.36 ± 0.37 MPa and Young's modulus of 8.31 ± 1.87 MPa. The burst pressure after embedded with collagen suture was increased to 2419 ± 121 mmHg, remarkably higher than that of the poly(ε-caprolactone)-only scaffolds (1500 ± 136 mmHg) and native vessels. The scaffolds were evaluated in six rabbits for 20 weeks via a carotid artery interpositional model demonstrating a good patency. The effective cell infiltration, and rapid endothelialization and smooth muscle cell maturation were observed. There was no calcification in 20 weeks, and only one developed the aneurysm dilation after 16 weeks. It suggested that the surface heparinization is beneficial to improve the hydrophilicity and anticoagulation property of scaffolds, and embedment of collagen suture is useful to reinforce the mechanical properties and burst pressure. [ABSTRACT FROM AUTHOR]

Decellularized arteries have been considered as promising scaffolds for small-diameter vascular substitutes. However, weakened mechanical properties, immunological rejection and rapid degradation after transplantation still exist after decellularization. Previous studies indicated that genipin cross-linking can solve these problems. Therefore, genipin was selected as the cross-linking agent for the pre-treatment of decellularized arteries in our study. Histological analysis, scanning electron microscopy, mechanical properties analysis and subcutaneous embedding experiment were adopted to investigate the efficiency of decellularization and the effect of genipin cross-linking on improving mechanical, structural and biological properties of decellularized arteries. Decellularization protocols based on three trypsin concentrations were used to prepare decellularized arteries, after decellularization, arteries were cross-linked with genipin. Results showed that 0.5% trypsin was the most efficient concentration to remove cellular components and preserve ECM. However, mechanical properties of 0.5% trypsin decellularized arteries weakened significantly, while genipin cross-linking improved mechanical properties of decellularized arteries to the same level as fresh arteries. After 4 weeks subcutaneous embedding, cross-linked arteries caused the mildest inflammatory response. In conclusion, genipin could be employed as an ideal cross-linking agent to strengthen mechanical properties, enhance the resistance to degradation and reduce the antigenicity of decellularized arteries for small-diameter blood vessel tissue engineering applications. [ABSTRACT FROM AUTHOR]