黄芪—丹参配伍对腺嘌呤诱导慢性肾功能衰竭大鼠心血管钙化的影响
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摘要
【目的】观察黄芪—丹参配伍应用对慢性肾功能衰竭(肾衰)大鼠心血管钙化的影响。【方法】将25只大鼠随机分为空白组,模型组,培哚普利组,黄芪—丹参低、高剂量组,每组5只。除空白组外,其余各组均采用腺嘌呤喂饲法建立肾衰大鼠模型。各给药组在造模同时开始给药干预。培哚普利组给予培哚普利叔丁胺片(剂量为0.42 mg·kg-1·d-1)灌胃,黄芪—丹参低、高剂量组给予黄芪—丹参水煎提取液(剂量分别为1.0、4.0 g·kg-1·d-1)灌胃。共给药4周。给药结束后分别测定大鼠体质量,左心室指数,血清丙氨酸氨基转移酶(ALT)、天门冬氨酸氨基转移酶(AST)及血肌酐(SCr)、血尿酸(SUA)水平,主动脉组织钙离子(Ca2+)、碱性磷酸酶(ALP)含量及血清成纤维细胞生长因子23(FGF-23)水平。【结果】与空白组比较,模型组大鼠体质量降低,左心室指数升高,SCr水平升高,主动脉组织Ca2+含量显著降低、ALP含量升高,血清FGF-23水平升高(P <0.05),但SUA水平无明显变化(P> 0.05);与模型组比较,黄芪—丹参低、高剂量组大鼠SCr水平、主动脉ALP含量、血清FGF-23水平降低(P <0.05),但体质量、左心室指数、主动脉组织Ca2+含量均无明显差异(P> 0.05)。【结论】黄芪—丹参配伍通过降低ALP、FGF-23水平可能控制肾衰大鼠心血管钙化。
Objective To observe the effect of compatibility of Radix Astragali and Radix Salviae Miltiorrhizae(Huangqi-Danshen)on cardiovascular calcification of the adenine-induced chronic renal failure rats. Methods Twenty-five rats were randomly divided into 5 groups,namely blank group,model group,Perindopril group,low-and high-dose Huangqi-Danshen groups. A rat model of renal failure was established by adenine feeding methodin the rats except for the blank group. The 3 medicaiton groups were given the medicine at the same time for modeling.Perindopril group was given intragastric administration of Perindopril(at the dosage of 0.42 mg·kg-1·d-1),thelow-and high-dose Huangqi-Danshen groups were given Huangqi-Danshen Decoction(at the dosage of 1.0,4.0 g·kg-1·d-1),the treatment covering 4 weeks. After medication,we observed the body mass,left ventricleindex, the levels of serum alanine aminotransferase(ALT) and aspartate amino transferase(AST), serumcreatinine(SCr),serum uric acid(SUA),the contents of calcium ions(Ca2+)and alkaline phosphatase(ALP)inaorta tissues,and serum level of fibroblast growth factor 23(FGF-23). Results Compared with the blank group,the body mass was decreased,the left ventricle index was increased,SCr level was enhanced,the Ca2 +contentwas reduced and ALP content was increased in aortic tissues,and the serum FGF-23 level was increased in themodel group(P < 0.05),but SUA level had no obvious changes(P > 0.05). Compared with the model group,SCrlevel,ALP content,and FGF-23 level in aortic tissues was decreased(P < 0.05),while the body mass,the leftventricle index,Ca2+content in aortic tissues had no obvious changes(P > 0.05). Conclusion The compatibility of Huangqi-Danshen has probable effects on reliving the cardiovascular calcification of the renal failure rats throughdecreasing ALP and FGF-23 levels.
Objective To observe the effect of compatibility of Radix Astragali and Radix Salviae Miltiorrhizae(Huangqi-Danshen)on cardiovascular calcification of the adenine-induced chronic renal failure rats. Methods Twenty-five rats were randomly divided into 5 groups,namely blank group,model group,Perindopril group,low-and high-dose Huangqi-Danshen groups. A rat model of renal failure was established by adenine feeding methodin the rats except for the blank group. The 3 medicaiton groups were given the medicine at the same time for modeling.Perindopril group was given intragastric administration of Perindopril(at the dosage of 0.42 mg·kg-1·d-1),thelow-and high-dose Huangqi-Danshen groups were given Huangqi-Danshen Decoction(at the dosage of 1.0,4.0 g·kg-1·d-1),the treatment covering 4 weeks. After medication,we observed the body mass,left ventricleindex, the levels of serum alanine aminotransferase(ALT) and aspartate amino transferase(AST), serumcreatinine(SCr),serum uric acid(SUA),the contents of calcium ions(Ca2+)and alkaline phosphatase(ALP)inaorta tissues,and serum level of fibroblast growth factor 23(FGF-23). Results Compared with the blank group,the body mass was decreased,the left ventricle index was increased,SCr level was enhanced,the Ca2 +contentwas reduced and ALP content was increased in aortic tissues,and the serum FGF-23 level was increased in themodel group(P < 0.05),but SUA level had no obvious changes(P > 0.05). Compared with the model group,SCrlevel,ALP content,and FGF-23 level in aortic tissues was decreased(P < 0.05),while the body mass,the leftventricle index,Ca2+content in aortic tissues had no obvious changes(P > 0.05). Conclusion The compatibility of Huangqi-Danshen has probable effects on reliving the cardiovascular calcification of the renal failure rats throughdecreasing ALP and FGF-23 levels.
引文
[1] London G M,Marchais S J,Guerin A P,et al. Arterial structure and function in end-stage renal disease[J]. Nephrol Dial Transplant,2002,17(10):1713.
[2] Goldsmith D,MacGinley R,Smith A,et al. How important and how treatable is vascular stiffness as a cardiovascular risk factor in renal failure[J]. Nephrol Dial Transplant,2002,17(6):965.
[3]陈艳,汪雄,彭吉霞,等.黄芪皂苷在大鼠血管钙化中的作用及可能机制[J].广东医学,2011,32(7):824.
[4]苏保林,陈刚毅,李敬.丹参酮胶囊对糖尿病肾病患者成纤维细胞生长因子23-Klotho轴及血管钙化的影响[J].云南中医学院学报,2016,39(2):11.
[5] Thakur R,Sharma A,Lingaraju M C,et al. Ameliorative effect of ursolic acid on renal fibrosis in adenine-induced chronic kidney disease in rats[J]. Biomed Pharmacother,2018,101:972.
[6]马子兴,俞腾飞.高血磷诱导慢性肾衰患者血管钙化机制的研究进展[J].北方药学,2017,14(9):151.
[7]孙娅楠,李思耐,马淑骅,等.黄芪、丹参注射液对乳鼠肥大心肌细胞钙瞬变的影响[J].中华中医药杂志,2013,28(5):1356.
[8]汪奕忱,庄燕,顾阳,等.黄芪注射液联合复方丹参注射液治疗心力衰竭临床疗效Meta分析[J].中医药导报,2016,22(24):62.
[9]唐妮,高静,吴晨曦,等.丹参黄芪鲫鱼药膳汤预防大鼠早期动脉粥样硬化实验研究[J].辽宁中医药大学学报,2016,18(5):45.
[10] Silver J, Levi R. Cellular and molecular mechanisms of secondary hyperparathyroidism[J]. Clin Nephrol, 2005, 63(2):119.
[11] Shobeiri N,Pang J,Adams M A,et al. Cardiovascular disease in an adenine-induced model of chronic kidney disease:the temporal link between vascular calcification and haemodynamic consequences[J]. J Hypertens,2013,31(1):160.
[12] Kircelli F, Peter M E, Ok E S, et al. Magnesium reduces calcification in bovine vascular smooth muscle cells in a dosedependent manner[J]. Nephrol Dial Transplant, 2012, 27(2):514.
[13] Ou Y, Liu Z, Li S, et al. Citrate attenuates vascular calcification in chronic renal failure rats[J]. APMIS,2017,125(5):452.
[14]马玲.慢性炎症对终末期肾病大鼠血管钙化的影响及机制研究[D].泸州:泸州医学院,2011.
[15] Cunningham J,Locatelli F,Rodriguez M. Secondary hyperparathyroidism:pathogenesis,disease progression,and therapeutic options[J]. Clin J Am Soc Nephrol,2011,6(4):913.
[16] Quinn S J,Thomsen A R,Pang J L,et al. Interactions between calcium and phosphorus in the regulation of the production of fibroblast growth factor 23 in vivo[J]. Am J Physiol Endocrinol Metab,2013,304(3):310.
[17] Isakova T,Wahl P,Vargas G S,et al. Fibroblast growth factor23 is elevated before parathyroid hormone and phosphate in chronic kidney disease[J]. Kidney Int,2011,79(12):1370.
[18] Isakova T,Xie H,Yang W,et al. Fibroblast growth factor 23and risks of mortality and end-stage renal disease in patients with chronic kidney disease[J]. JAMA,2011,305(23):2432.
[19] Imanishi Y,Inaba M,Nakatsuka K,et al. FGF-23 in patients with end-stage renal disease on hemodialysis[J]. Kidney Int,2004,65(5):1943.
[20] Mace M L,Gravesen E,Hofman-Bang J,et al. Key role of the kidney in the regulation of fibroblast growth factor 23[J]. Kidney Int,2015,88(6):1304.
[2] Goldsmith D,MacGinley R,Smith A,et al. How important and how treatable is vascular stiffness as a cardiovascular risk factor in renal failure[J]. Nephrol Dial Transplant,2002,17(6):965.
[3]陈艳,汪雄,彭吉霞,等.黄芪皂苷在大鼠血管钙化中的作用及可能机制[J].广东医学,2011,32(7):824.
[4]苏保林,陈刚毅,李敬.丹参酮胶囊对糖尿病肾病患者成纤维细胞生长因子23-Klotho轴及血管钙化的影响[J].云南中医学院学报,2016,39(2):11.
[5] Thakur R,Sharma A,Lingaraju M C,et al. Ameliorative effect of ursolic acid on renal fibrosis in adenine-induced chronic kidney disease in rats[J]. Biomed Pharmacother,2018,101:972.
[6]马子兴,俞腾飞.高血磷诱导慢性肾衰患者血管钙化机制的研究进展[J].北方药学,2017,14(9):151.
[7]孙娅楠,李思耐,马淑骅,等.黄芪、丹参注射液对乳鼠肥大心肌细胞钙瞬变的影响[J].中华中医药杂志,2013,28(5):1356.
[8]汪奕忱,庄燕,顾阳,等.黄芪注射液联合复方丹参注射液治疗心力衰竭临床疗效Meta分析[J].中医药导报,2016,22(24):62.
[9]唐妮,高静,吴晨曦,等.丹参黄芪鲫鱼药膳汤预防大鼠早期动脉粥样硬化实验研究[J].辽宁中医药大学学报,2016,18(5):45.
[10] Silver J, Levi R. Cellular and molecular mechanisms of secondary hyperparathyroidism[J]. Clin Nephrol, 2005, 63(2):119.
[11] Shobeiri N,Pang J,Adams M A,et al. Cardiovascular disease in an adenine-induced model of chronic kidney disease:the temporal link between vascular calcification and haemodynamic consequences[J]. J Hypertens,2013,31(1):160.
[12] Kircelli F, Peter M E, Ok E S, et al. Magnesium reduces calcification in bovine vascular smooth muscle cells in a dosedependent manner[J]. Nephrol Dial Transplant, 2012, 27(2):514.
[13] Ou Y, Liu Z, Li S, et al. Citrate attenuates vascular calcification in chronic renal failure rats[J]. APMIS,2017,125(5):452.
[14]马玲.慢性炎症对终末期肾病大鼠血管钙化的影响及机制研究[D].泸州:泸州医学院,2011.
[15] Cunningham J,Locatelli F,Rodriguez M. Secondary hyperparathyroidism:pathogenesis,disease progression,and therapeutic options[J]. Clin J Am Soc Nephrol,2011,6(4):913.
[16] Quinn S J,Thomsen A R,Pang J L,et al. Interactions between calcium and phosphorus in the regulation of the production of fibroblast growth factor 23 in vivo[J]. Am J Physiol Endocrinol Metab,2013,304(3):310.
[17] Isakova T,Wahl P,Vargas G S,et al. Fibroblast growth factor23 is elevated before parathyroid hormone and phosphate in chronic kidney disease[J]. Kidney Int,2011,79(12):1370.
[18] Isakova T,Xie H,Yang W,et al. Fibroblast growth factor 23and risks of mortality and end-stage renal disease in patients with chronic kidney disease[J]. JAMA,2011,305(23):2432.
[19] Imanishi Y,Inaba M,Nakatsuka K,et al. FGF-23 in patients with end-stage renal disease on hemodialysis[J]. Kidney Int,2004,65(5):1943.
[20] Mace M L,Gravesen E,Hofman-Bang J,et al. Key role of the kidney in the regulation of fibroblast growth factor 23[J]. Kidney Int,2015,88(6):1304.