Comfortable lifestyle-induced imbalance of neuro-endocrine-immunity network: a possible mechanism of vascular endothelial dysfunction / 中国结合医学杂志

<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSIONS</b>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.</p>

Changes in common chemical signal molecules of neuroendocrine-immune network and intervention of Tongxinluo in rats under hypoxia qi-asthenia condition / 第二军医大学学报

Objective: To investigate the changes in common chemical signal molecules of neuroendocrine-immune (NEI) network and intervention of Tongxinluo (TXL, ultramicro-pulverization) of rats under hypoxia qi-asthenia condition. Methods: Forty-five male Wistar rats were randomly assigned to the following groups: control group, qi-asthenia model group and TXL group (n=15). The rats in the former 2 groups were gavaged with CMC-Na (10 ml/ kg) once daily; those in the TXL group were gavaged with TXL (ultramicrot-pulverization) suspended in CMC-Na (10 ml/kg) once daily; After gavage, animals in the qi-asthenia model group and TXL group were placed in a cabin with normal pressure hypoxia (7 h daily, 6 d weekly for 5 weeks). At the end of the experiment, the biological characters of rats were observed and arterial blood gas was analyzed. The serum contents of serotonin (5-HT), norepinephrine (NE), epinephrine (E), dopamine (DA) and IFN-γ and TRH level in the hypothalamus were examined by enzyme linked immunosorbent assay (ELISA); the serum contents of corticosterone (Cort), T3,T4,IL-1β,TNF-α, and corticotropin release hormone(CRH) in the hypothalamus, and adrenocorticotropic hormone/thyroid stimulating hormone(ACTH/TSH) in the hypophysis cerebri were examined using radio-immunity method. Results: Compared with control group, the biological character scores of rats in the qi-asthenia model group were significantly bigher(P

The effects of Tongxinluo Supermicro Powder on nuclear factor-kappaB, intercellular adhesion molecule-1 and vascular cell adhesion molecule-1 expression in aorta of rabbits fed with high-lipid diet / 中华心血管病杂志

<p><b>OBJECTIVE</b>To observe the effects of Tongxinluo Supermicro Powder on the nuclear factor-kappaB (NF-kappaB), inter-cell adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression in aorta of rabbits fed with high-lipid diet.</p><p><b>METHODS</b>Healthy male New Zealand rabbits were randomly divided into 4 groups (n = 8 each): control group, model group, atorvastatin group (3 mg x kg(-1) x d(-1) per gavage), and Tongxinluo group (0.31 g x kg(-1) x d(-1) per gavage). At the end of 6 weeks, the expression of NF-kappaB, ICAM-1 and VCAM-1 were observed by immunochemistry methods, Western blotting and reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULT</b>The nuclear translocation of NF-kappaB in aortic endothelial cells and the gene expressions of NF-kappaB, ICAM-1 and VCAM-1 at protein and mRNA levels of the model group was significantly increased compared that in the control group (all P < 0.05), these effects could be significantly attenuated by atorvastatin and Tongxinluo Supermicro Powder (P < 0.01 vs. model group).</p><p><b>CONCLUSIONS</b>Similar as atorvastatin, Tongxinluo Supermicro Powder could relieve the process of atherosclerosis by decreasing the nuclear translocation of NF-kappaB and reducing the expression of ICAM-1, VCAM-1 in this model.</p>

Experimental study on effect of Tongxinluo on nerve cell apoptosis after cerebral ischemia in middle cerebral arterial obstructive model rats / 中国中西医结合杂志

<p><b>OBJECTIVE</b>To explore the action mechanism of Tongxinluo Capsule (TXL) in protecting brain from ischemic damage.</p><p><b>METHODS</b>SD rats were divided into five groups randomly, the sham operation group, the model group, the MK-801 group, the large and low dosage TXL groups (TXLL and TXLS). After the middle cerebral arterial obstructive (MCAO) model was established, peritoneal injection of MK-801 0.5 mg/kg per day was given to the MK-801 group, and 1.0 g/(kg x d) and 0.5 g/(kg x d) of TXL powder was administered in twice via gastrogavage to the two TXL groups respectively. The nerve cell apoptosis rate, protein and mRNA expressions of Caspase-3, p53 and heat shock protein (HSP70) were observed using flow cytometry, Western blot and RT-PCR technique.</p><p><b>RESULTS</b>Both TXL and MK-801 could obviously lower the apoptosis rate in model rat (P < 0.05, P < 0.01), TXLL showed the optimal effect. Caspase-3, p53 protein and mRNA expression in the model group were obviously higher than those in the sham operated group. As compared with the model group, the expressions of Caspase-3 and p53 were lower and those of HSP70 and mRNA were higher in the two TXL and MK-801 groups (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>TXL displays it brain protective effect through reducing nerve cell apoptosis rate in MCAO model rats, the mechanism may be related to its actions in inhibiting apoptosis related factors Caspase-3 and p53, and promoting stress protecting factor HSP70.</p>