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舒适生活方式引起的神经内分泌免疫网络失衡:血管内皮功能障碍的可能机制。

Comfortable lifestyle-induced imbalance of neuro-endocrine-immunity network: a possible mechanism of vascular endothelial dysfunction.

机构信息

The Laboratory of Collateral Diseases, Pharmaceutical Research Academy, Hebei Medical University, Shijiazhuang 050035, China.

出版信息

Chin J Integr Med. 2010 Feb;16(1):54-60. doi: 10.1007/s11655-010-0054-7. Epub 2010 Feb 4.

Abstract

OBJECTIVE

To observe the changes of vascular endothelial functions and general neuro-endocrine-immunity (NEI) network under the state of qi-deficiency syndrome induced by excessive idleness and to approach their internal relevance and illuminate initially the pathophysiological mechanism of vascular lesion induced by excessive idleness.

METHODS

A total of 100 male Wistar rats were randomly divided into the control group and the qi-deficiency syndrome model group, 50 rats in each group. The qi-deficiency syndrome model was established by feeding the animals with hyper-alimentation diet in combination with restricting movement for 10 weeks. Changes of common chemical signal molecules related to NEI and vascular endothelial functions were measured by the end of the experiment. Furthermore, their internal relevance was analyzed by the method of canonical correlation analysis.

RESULTS

The vascular endothelial structure and function were obviously injured in the model group. Compared with the control group, the chemical signal molecules, such as 5-hydroxytryptamine (5-HT), corticosterone (CORT), triiodothyronine (T3), tetraiodothyronine (T4), angiotensin II (Ang II), interleukin-1 (IL-1), and tumor necrosis factor-alpha (TNF-alpha) in peripheral blood of the model group (n=43) were changed significantly (P<0.05 or P<0.01). Canonical correlation analysis showed that vascular endothelial dysfunction was correlated to the changes of these signal molecules in the NEI network.

CONCLUSIONS

Comfort-based lifestyle induced not only vascular endothelial dysfunction but also an imbalance of the NEI network. Vascular endothelial dysfunction and the imbalanced NEI network interacted with each other, and an imbalance of the NEI network may be the pathophysiologic basis for the genesis and development of vascular endothelial dysfunction, even diseases of the blood vessel.

摘要

目的

观察过逸致虚证状态下血管内皮功能及一般神经内分泌免疫(NEI)网络的变化,初步探讨血管病变的病理生理学机制。

方法

将 100 只雄性 Wistar 大鼠随机分为对照组和虚证模型组,每组 50 只。采用高脂饮食喂养结合限制运动的方法建立虚证模型,实验结束时测量与 NEI 及血管内皮功能相关的常见化学信号分子的变化,并采用典型相关分析方法分析其内在相关性。

结果

模型组血管内皮结构和功能明显受损,与对照组比较,模型组外周血中 5-羟色胺(5-HT)、皮质酮(CORT)、三碘甲状腺原氨酸(T3)、甲状腺素(T4)、血管紧张素Ⅱ(Ang II)、白细胞介素-1(IL-1)和肿瘤坏死因子-α(TNF-α)等化学信号分子变化明显(P<0.05 或 P<0.01)。典型相关分析显示,血管内皮功能障碍与 NEI 网络中这些信号分子的变化相关。

结论

舒适的生活方式不仅导致血管内皮功能障碍,还导致 NEI 网络失衡。血管内皮功能障碍与 NEI 网络失衡相互作用,NEI 网络失衡可能是血管内皮功能障碍甚至血管疾病发生发展的病理基础。

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