JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY
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2018
·Vol. 29
·期 10
·1436-1443
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IF 2.873
Yi-Lin Sun,Peng-Hui Li,Ling Shi,Wan-Zhen Su,De-Sheng Li,Gen-Long Xue,Yue Zhao,Chang-Zhu Li,Ying Li,Yang Zhou,Shang-Xuan Li,Yang Zhang,Yan-Jie Lu,Zhen-Wei Pan
Introduction: Deficiency of testosterone was associated with the susceptibility of atrial fibrillation (AF). Angiotensin-II (AngII) receptor antagonists were shown to reduce AF by improving atrial electrical remodeling. This study investigated the effects and mechanism of valsartan, an AngII receptor antagonist, on the susceptibility to AF with testosterone deficiency. Methods and Results: Five-week-old male ICR mice were castrated and valsartan was administered orally (50 mg/kg/d). High-frequency electrical stimulation method was used to induce atrial arrhythmia. Patch-clamp technique was used for recording action potential duration (APD), transient outward potassium current ( I to ), sustained outward potassium current ( I ksus ), and late sodium current ( I Na-L ). Optical mapping technique was used to examine atrial conduction velocity (CV). The expression of connexin40 (Cx40) and Cx43 were detected by Western blot analysis. The occurrence rate of AF was significantly increased in castrated mice and APDs measured at 50% and 90% repolarization were markedly prolonged in castrated mice than controls, which were alleviated by the administration of valsartan. Valsartan suppressed the increase of I Na-L and rescued the reduction of I to and I ksus in castrated mice. The left atrial CV in castrated mice was decreased and the expression of Cx43 reduced than controls, which were restored after valsartan treatment. Conclusions: Valsartan reduced the susceptibility of AF in castrated mice, which may be related to the inhibition of action potential prolongation and improvement of atrial conduction impairment. This study indicates that valsartan may represent a useful agent for the prevention of AF pathogenesis in elderly male patients.
研究领域:
心脏病学
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药理学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES
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2022
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IF 8.025
Yan Kong,Jiawei Xu,Qi Han,Tiantian Zheng,Linliang Wu,Guicai Li,Yumin Yang
The composition and spatial structure of bioscaffold materials are essential for constructing tissue regeneration microenvironments. In this study, by using an electrospinning technique without any other additives, we successfully developed pure porcine decellularized nerve matrix (xDNME) conduits. The developed xDNME was composed of an obvious decellularized matrix fiber structure and effectively retained the natural components in the decellularized matrix of the nerve tissue. The xDNME conduit exhibited superior biocompatibility and the ability to overcome inter-species barriers. In vivo, after 12 weeks of implantation, xDNME significantly promoted the regeneration of rat sciatic nerve. The regenerated nerve fibers completely connected the two ends of the nerve defect, which were about 8 mm apart. The xDNME and xDNME-OPC groups showed myelin structures in the regenerated nerve fibers. In the xDNME group, the average thickness of the regenerated myelin sheath was 0.640 ± 0.013 μm, which was almost comparable to that in the autologous nerve group (0.646 ± 0.017 μm). Electrophysiological experiments revealed that both of the regenerated nerve fibers in the xDNME and xDNME-OPC groups had excellent abilities to transmit electrical signals. Respectively, the average conduction velocities of xDNME and xDNME-OPC were 8.86 ± 3.57 m/s and 6.99 ± 3.43 m/s. In conclusion, the xDNME conduits have a great potential for clinical treatment of peripheral nerve injuries, which may clinically transform peripheral nerve related regenerative medicine.
研究领域:
组织工程
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再生医学
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神经科学
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生物材料
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产品关联
DOI
PubMed
高影响因子
BIOMATERIALS
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2024
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IF 12.8
Xiaolan Ou,Ze Wang,Daojiang Yu,Wenlai Guo,Andrei V. Zvyagin,Quan lin,Wenrui Qu
ABSTRACT Diabetic peripheral neuropathy (DPN) is a prevalent complication of diabetes mellitus (DM), significantly contributing to the risk of amputation and mortality. Reactive oxygen species (ROS) can induce both neurological and structural harm through direct impact and pyroptosis, underscoring the critical role of ROS regulation in mitigating DPN. In this research endeavor, we propose harnessing the inherent antioxidant properties of sulfhydryl groups by grafting them onto gold nanodots through an amidation reaction, resulting in the creation of ROS-responsive AuNDs. Additionally, we aim to synthesize AuNDs-VEGF, wherein VEGF is attached to AuNDs via electrostatic interactions, as a therapeutic strategy for addressing DPN in rat models. The results of in vivo experiments showed that AuNDs and AuNDs-VEGF nanoparticles could increase the nerve conduction velocity, shorten the latency of nerve conduction in the sciatic nerve, promote the regeneration of nerve trophectodermal vessels, improve the structure and function of the sciatic nerve, reduce the apoptosis of neural cells, and alleviate the atrophy of the gastrocnemius muscle. Thus, VEGF-loaded ROS-responsive nanodots present a promising avenue for ameliorating diabetic peripheral neuropathy. This innovative approach not only extends the application possibilities of nanodots but also introduces a novel avenue for the treatment of diabetic neuropathy.
研究领域:
纳米技术
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神经科学
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糖尿病研究
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药学
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生物医学工程
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产品关联
DOI
PubMed
高影响因子
PHYTOTHERAPY RESEARCH
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2023
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IF 7.2
Man Hu,Wen Jiang,Chen Ye,Ting Hu,Qingqing Yu,Moran Meng,Lijuan Sun,Jichao Liang,Yong Chen
Schwann cells injury induced by high glucose (HG) contributes to the development of diabetic peripheral neuropathy (DPN). Honokiol has been reported to regulate glucose metabolism, however, its effect on DPN and the precise molecular mechanisms remain unclear. This study aimed to investigate the role of AMPK/SIRT1/PGC-1α axis in the protective effects of honokiol on DPN. The biochemical assay and JC-1 staining results demonstrated that honokiol reduced HG-induced oxidative stress and ferroptosis as well as mitochondrial dysfunction in Schwann cells. RT-qPCR and western blotting were utilized to investigate the mechanism of action of honokiol, and the results showed that HG-induced inhibition of AMPK/SIRT1/PGC-1α axis and changes of downstream gene expression profile were restored by honokiol. Moreover, silencing of Sirt1 by siRNA delivery markedly diminished the changes of gene expression profile induced by honokiol in HG-induced Schwann cells. More importantly, we found that administration of honokiol remarkably attenuated DPN via improving sciatic nerve conduction velocity and increasing thermal and mechanical sensitivity in streptozotocin-induced diabetic rats. Collectively, these results demonstrate that honokiol can attenuate HG-induced Schwann cells injury and peripheral nerve dysfunction, suggesting a novel potential strategy for treatment of DPN.
研究领域:
神经科学
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药理学
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糖尿病
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细胞生物学
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分子生物学
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产品关联
DOI
PubMed
高影响因子
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