Comfortable lifestyle-induced imbalance of neuro-endocrine-immunity network: a possible mechanism of vascular endothelial dysfunction.
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.
The Laboratory of Collateral Diseases, Pharmaceutical Research Academy, Hebei Medical University, Shijiazhuang 050035, China.
Guo-qiang
GQ
Yuan
Zhen-hua
ZH
Jia
Hai-tao
HT
Yang
Shi-zhen
SZ
Wu
Huai-lin
HL
Gao
Cong
C
Wei
Hui-ming
HM
Zhu
Yi-ling
YL
Wu
D000818:Animals; D001011:Aorta / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000648:ultrastructure; D015415:Biomarkers / Q000032:analysis / Q000378:metabolism; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D004195:Disease Models, Animal; D016232:Endothelins / Q000378:metabolism; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D007107:Immune System / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D008297:Male; D015213:Neuroimmunomodulation / Q000502:physiology*; D009490:Neurosecretory Systems / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D009569:Nitric Oxide / Q000378:metabolism; D019413:Qi; D051381:Rats; D017208:Rats, Wistar; D057185:Sedentary Behavior; D013577:Syndrome; D016710:Yin Deficiency / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology
D015415:Biomarkers; D016232:Endothelins; D009569:Nitric Oxide