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柠檬酸盐可减轻慢性肾衰竭大鼠的血管钙化。

Citrate attenuates vascular calcification in chronic renal failure rats.

作者信息

Ou Yan, Liu Zengying, Li Shuiqin, Zhu Xiaojing, Lin Yan, Han Jin, Duan Zhaoyang, Jia Lining, Gui Baosong

机构信息

Department of Nephrology, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.

Department of Rehabilitation Medicine of Yan An University Affiliated Hospital, Yan'an, Shaanxi, China.

出版信息

APMIS. 2017 May;125(5):452-458. doi: 10.1111/apm.12667. Epub 2017 Mar 23.

DOI:10.1111/apm.12667
PMID:28332248
Abstract

Vascular calcification (VC) is a major contributor of cardiovascular dysfunction in chronic renal failure (CRF). Citrate binds calcium and inhibits the growth of calcium crystals. This present study intends to evaluate the effect of citrate on VC in adenine-induced CRF rats. The rats were randomly divided into five groups: the control group, the citrate control group, model group, model rats with low-dose treatment of citrate (216 mg/kg) and model rats with high-dose treatment of citrate (746 mg/kg). The rats were euthanized at 5 weeks with their blood and aorta in detection. The results showed that serum level of blood urea nitrogen, serum creatinine, phosphorus, calcium, and related renal failure function marker were elevated in the model group. Furthermore, the aortic calcium accumulation and alkaline phosphatase activity were significantly increased in the model group compared with control groups. Additionally, hematoxylin-eosin staining results demonstrated that the vascular calcification in aorta is significantly increased in the model group. Finally, the expression of VC-related proteins including bone morphogenetic protein and osteocalcin were increased in the model group, whereas alpha-smooth muscle actin was decreased in the model group compared with the control group. However, treatment with citrate caused a reversal effect of all the above events in a dose-dependent manner. In conclusion, citrate may attenuate vascular calcification in adenine-induced CRF rats.

摘要

血管钙化(VC)是慢性肾衰竭(CRF)中心血管功能障碍的主要促成因素。柠檬酸盐能结合钙并抑制钙晶体的生长。本研究旨在评估柠檬酸盐对腺嘌呤诱导的CRF大鼠血管钙化的影响。将大鼠随机分为五组:对照组、柠檬酸盐对照组、模型组、低剂量柠檬酸盐治疗的模型大鼠(216 mg/kg)和高剂量柠檬酸盐治疗的模型大鼠(746 mg/kg)。在第5周对大鼠实施安乐死,并检测其血液和主动脉。结果显示,模型组的血清尿素氮、血清肌酐、磷、钙水平以及相关肾衰竭功能标志物均升高。此外,与对照组相比,模型组的主动脉钙沉积和碱性磷酸酶活性显著增加。另外,苏木精-伊红染色结果表明,模型组主动脉的血管钙化显著增加。最后,与对照组相比,模型组中包括骨形态发生蛋白和骨钙素在内的VC相关蛋白表达增加,而α-平滑肌肌动蛋白减少。然而,柠檬酸盐治疗以剂量依赖的方式使上述所有情况发生逆转。总之,柠檬酸盐可能减轻腺嘌呤诱导的CRF大鼠的血管钙化。

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