Introduction 3. Methods 3.1 Animal model preparation 3.2 Experiments 3.3 Data analysis 4. Results 4.1 Noninvasive blood pressure, weight loss, and cardiac weight index of rats 4.2 Von Kossa staining in the aorta 4.3 The calcium content and the activity of ALP in the aorta tissue 4.4 Masson's trichrome staining 4.5 The content of the C-reactive protein, IL-6, TNF-α and MCP-1 in serum 4.6 The content of Urotensin II and aldosterone in the aorta tissue 4.7 The change of the immunoreactivity 5. Discussion 6. Conclusions 7. Author contributions 8. Ethics approval and consent to participate 9. Acknowledgment 10. Funding 11. Conflict of interest 12. Availability of data and materials 13. References
Objectives Aim: To observe aortic and cardiac aldosterone expression and its receptor changes in rats with vascular calcification, and exogenous aldosterone effects on vascular calcification, so as to explore the significance of aldosterone in vascular calcification. Methods Male SD rats were randomly divided into five groups. (1) Normal control group; (2) Aldosterone group: rats were received aldosterone subcutaneously for 6 weeks (20 mgin 0.1 ml ethanol, 1/ d); (3) Calcification group: rats were received intramuscular injection with vitamin D3 (300 000 IU/kg) and anintragastric dose of nicotine (25 mg/kg, in peanut oil) at 8:00 on the first day; nicotine was gavaged again at 18:00 on the same day. (4) Calcification +aldosterone group: Rats were treated as the calcification group, and also received aldosterone subcutaneously for 6 weeks (20 mg in 0.1 mlethanol, 1/days). (5) Calcification+spironolactone group: Rats were treated as the calcification group, with the exception of oral gavage of spironolactone (40 mg/kg/d)] for 6 weeks. The control group received normal saline injection, oral gavage of peanut oil, and ethanol treatment. At the end of the experiment, the extent of aortic calcification was confirmed by Von Kossa staining and measurement of calcium content. Alkaline phosphatases activity was also evaluated. The deposition of collagen in cardiovascular tissues was measured by masson staining. The content of aldosterone and urotensin II in plasma and aorta were determined by radioimmunoassay. The immunoactivity of mineralocorticoid receptor and urotensin II receptor were evaluated by immunohistochemistry. The content of C-reactive peptide, interleukin-6, tumour necrosis factor-α and monocyte chemoattractant protein-1 in the serum were determined by radioimmunoassay. Results Von Kossa staining showed significant aortic calcium deposition in calcified rats. Aortic calcification was further aggravated when aldosterone was added. It was decreased in calcification +spirolactone group as compared with the calcification group, and the calcification+aldosterone group. In addition, aortic calcium content in aldosterone group increased, but not statistically significant ( p>0.05), compared with the control group. In calcification group, the aortic calcium content increased by63.45% p<0.01), and 27.55% p<0.05), respectively, compared with the controls and the aldosterone group. In calcification+aldosterone group, it was elevated by 121.72% p<0.01), 73.02% p<0.01), and 35.65% p<0.01), respectively, compared with the controls, the aldosterone group, and the calcification group. However, in calcification+spironolac-tone group, it decreased by 41.31% p<0.01), and 56.73% p<0.01), than the calcification group and calcification+aldosterone group respectively. Alkaline phosphatase activity showed a similar trend. Vascular and myocardial collagen staining showed that the most obvious staining is seen in the calcification +aldosterone group. It was slightly reduced in the calcification +spironolactone group than the calcifie...
The present study aimed to assess the role of urocortin II (UII) in the process of vascular calcification in vitro by using a calcification model, and to detect the changes in the mRNA and protein levels of associated markers in rat adventitial fibroblasts (AFs) during their phenotypic transformation to osteoblast cells,and clarify the main signal transduction pathway of UII responsible for regulating vascular calcification and AF phenotypic transformation of osteoblast cells and prove that UII was an endogenous factor promoting vascular calcification, so as to provide an effective experimental basis for the clinical regulation of related diseases caused by vascular calcification. Finally we successfully constructed the calcified cell model, found that UII was an endogenous substance regulating vascular calcification, regulated the vascular calcification by promoting apoptosis and inhibiting autophagy through up- and down-regulated Bax and Bcl-2/Beclin-1 level, and the Wnt/β-catenin signaling pathway was involved.
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