| Purpose: This study aims to study cadmium poisoning in human umbilical vein endothelial cells from oxidative damage and apoptosis and sub-chronic cadmium poisoning of free radicals in vascular endothelial cells, and telomerase activity in the relevant indicators, And research supervisor Professor Zhang-jingsheng prescription Guanxinkang protective effects of cadmium poisoning on the vascular endothelial cell senescence and the role of anti-aging Guanxinkang, To further reveal the cause of environmental medicine due to vascular aging mechanism toxin and the role of anti-aging medicine, aging blood vessels so as to provide a theoretical basis for the prevention and control.Part?, cadmium intoxication on human umbilical vein endothelial cells from oxidative injury and the protective effect of Guanxinkangmethod: By human umbilical vein endothelial cells in vitro, divided into 6 groups, the establishment of the normal control group, 1,5,10,30,60?mol / L concentration of cadmium chloride model of group and Western medicine (zinc sulfate), Guanxinkang(traditional Chinese medicine low , Middle and high dose) group, continue to foster 24h, 48h, 72h, the observed telomerase activity, SOD and GSH-Px activity and MDA content.Results:1. telomerase activity: comparison with the control group, all groups were significantly decreased telomerase activity. (P <0.05)Western medicine, Guanxinkang group, compared with model group, 24h of the western group, Guanxinkang low dose 1-10?mol / L cadmium chloride, Guanxinkang, the high dose group 1-30?mol / L cadmium chloride increased telomerase activity. (P <0.05) 48h of the western group, Guanxinkang high dose group 1-30?mol / L chloride, medicine low dose group in the 1-10?mol / L cadmium chloride increased activity of telomerase. (P <0.05) 72h the 5?mol / L of cadmium chloride Western medicine, Guanxinkang group, telomerase activity increased. (P <0.05)2. superoxide dismutase (SOD) activity: comparison with the control group, SOD activity in each group were significantly decreased. (P <0.05) Western medicine, Guanxinkang group, compared with model group, 48h of the western group of 1-60?mol / L cadmium chloride, Guanxinkang in the dose group 1-30?mol / L cadmium chloride, Guanxinkang high-dose group 1-10?mol / L of cadmium chloride SOD activity were increased. (P <0.05) 72h dose of Guanxinkang in the 1,5?mol / L cadmium chloride, Guanxinkang high-dose group 1-10?mol / L of cadmium chloride were significantly higher SOD activity. (P <0.05)3. glutathione peroxidase (GSH-Px) activity: comparison with the control group, each group of GSH-Px activity were significantly reduced. (P <0.05) and Western medicines, Guanxinkang group and model group, 24h, 48h, 72h of 1-60?mol / L of cadmium chloride, GSH-Px activity were significantly increased.4. malondialdehyde (MDA) content: comparison with the control group, 24h, 48h in the model group and the 5-60?mol / L of cadmium chloride western medicine group, MDA content in Guanxinkang group were significantly increased. (P <0.05) 72h of Guanxinkang in addition to the high dose group, 1-5?mol / L cadmium chloride, other groups MDA levels were significantly increased. (P <0.05)Western medicine, Guanxinkang group, compared with model group, 24h and 48h of Western medicine, Guanxinkang group 1-60?mol / L cadmium chloride content of MDA decreased. (P <0.05) 72h of 1?mol / L cadmium chloride dose of Guanxinkang in the 1-10?mol / L cadmium in Guanxinkang in high dose group decreased MDA content, a significant difference. (P <0.05)Part?, cadmium intoxication on human umbilical vein endothelial cells apoptosis and the protective effect of Guanxinkang method: The main materials and experimental methods and the first part of the same, to continue to foster 24h, 48h, 72h, the observed content of Bcl-2, BAX protein, Bcl-2/BAX ratio and Caspase-3 enzyme.Results:1. Bcl-2 levels: compared with the control group, Bcl-2 in each group were significantly reduced. (P <0.05)Western medicine, Guanxinkang group, compared with model group, 24h of the West, Guanxinkang group of Bcl-2 levels were significantly increased. (P <0.05) 48h of the western group, Guanxinkang, the high dose group 1-60?mol / L cadmium chloride, low dose of Guanxinkang 1?mol / L of cadmium chloride Bcl-2 levels increased. (P <0.05) 72h of Western medicine, Guanxinkang dose 5-60?mol / L, Guanxinkang high-dose group 1-60?mol / L of cadmium chloride Bcl-2 levels increased. (P <0.05)2. BAX protein content: comparison with the control group, each group of BAX protein content increased. (P <0.05)Western medicine, Guanxinkang group and model group,1-60?mol / L of cadmium chloride decreased BAX protein content. (P <0.05)3. Bcl-2/BAX ratio: with the normal control group, each group Bcl-2/BAX ratio decreased. (P <0.05)Western medicine, Guanxinkang group, compared with model group, 24h, 72h of Western medicine, Guanxinkang group Bcl-2/BAX ratios were significantly increased. (P <0.05) 48h of the western group, Guanxinkang, the high dose group 1-60?mol / L cadmium and low dose of Guanxinkang 1?mol / L of cadmium chloride Bcl-2/BAX ratio increased. (P <0.05)4. Caspase-3 activity: comparison with the control group, in addition to Western medicine group 24h 1?mol / L cadmium than the groups of Caspase-3 activity increased, 48h, 72h of each group were Caspase-3 activity Increased. (P <0.05)Western medicine, Guanxinkang group, compared with model group, 24h of the western group, Guanxinkang, the high dose group of Caspase-3 activity was significantly reduced. (P <0.05) 48h, 72h western medicine and Guanxinkangs Section of the Caspase-3 activity were reduced. (P <0.05)Part?, sub-chronic cadmium poisoning in vascular endothelial cells from oxidative damage and protective effect of Guanxinkangmethod: 72 healthy male Wistar rats were randomly divided into 6 groups, namely control group, model group, western medicine group, Guanxinkang low, medium and high dose group, 12 in each group, each weighing 250±50g. In addition to other control group were given 0.05mg/kg cadmium solution, for 2 weeks after stopping cadmium, while western medicine to the 2ml solution of zinc sulfate, Guanxinkang low, medium and high dose groups, respectively, to 1.5g / (kg·d), 3g / (kg·d), 6g / (kg·d) of the Guanxinkang particles to 60 consecutive days, the modeling results of the all group after the death of five rats. For sample preparation, animal drawn out immediately after urethane anesthesia rats serum, abdominal aortic endothelium was observed telomerase activity, SOD activity and MDA content and histopathological changes.Results: compared with the control group, each group of telomerase activity and decreased SOD activity, MDA content was significantly increased. (P <0.05) and Western medicines, Guanxinkang group and model group, telomerase activity and increased SOD activity, MDA content was decreased. (P <0.05)Histopathological changes Result: The obvious intimal thickening, uplift and diffuse wall edema can be seen, some fall off, the gap has widened under the endothelium, smooth muscle cells showed morphological changes, disorganized, visible foam cells, wear Been moved to the internal elastic membrane lining; western group intimal morphology similar to the normal group, slightly more smooth muscle cells, arranged in neat, no foam cell infiltration, no edema and uplift, no loss; medicine low dose group Intimal morphology was similar with the western medicine; Guanxinkang dose group endometrium morphology of vascular Guanxinkang low dose group performed better than a good small subendothelial space, the cell continuously, no foam cell infiltration, no uplift, edema and Off, no cells migrated through the internal elastic membrane to the intima; Guanxinkang high-dose group and intimal changes in structure and morphology similar to Guanxinkang in the dose group, and no other abnormal morphological changes.Conclusion:1. cadmium poisoning induced by vascular endothelial cells in lipid peroxidation, the formation of a large number of reactive oxygen species, diminished capacity to make antioxidant enzymes, which may lead to vascular endothelial cell senescence.2. cadmium toxicity to vascular endothelial cells produce large amounts of peroxide, reduced ability of antioxidant enzymes, which promote apoptosis, leading to endothelial cell senescence.3. This study proved that aging Guanxinkang of cadmium in vascular endothelial cells with anti-oxidation and inhibit cell apoptosis, which could delay vascular aging.4. environmental toxin onto the body, the body's yin and yang, qi and blood disorders, gas-poor, or damage internal organs, leading to internal organs and metabolic disorders, it will produce phlegm, blood stasis and other pathological product, accelerated aging body. This is the Chinese environmental toxin causes aging blood vessels due to the possible mechanism of vascular aging so as to provide a theoretical basis for the prevention and control. |
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