以TRPV5介导的钙转运通路为靶点的补肾中药防治骨质疏松症作用机制研究
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摘要
目的:
本研究从钙转运通路入手,通过观察地塞米松诱导的肾虚骨质疏松症大鼠肾组织及骨组织钙转运通路相关蛋白TRPV5、CaBP-D28k、NCX1及PMCA1b基因和蛋白的表达,从分子水平揭示糖皮质激素诱导的肾虚骨质疏松症的病理机制,以及补肾中药的疗效机理。
材料与方法:
本实验采用地塞米松(2.5mg/kg,周两次)肌肉注射的方法复制肾虚骨质疏松症大鼠模型,同时以补肾中药对模型大鼠进行防治。正常大鼠作为标准对照组,模型大鼠作为空白对照组,以骨疏康颗粒作为阳性对照药,同时与健脾中药及活血中药作疗效比较。造模及给药时间为9周。9周后处死动物并取血清、股骨、肾组织等进行下列指标检测:应用双能X线吸收法检测大鼠离体股骨上1/3骨密度(BMD);用生化方法检测血清钙、磷、碱性磷酸酶(ALP)的含量;酶联免疫吸附法(ELISA)检测血清抗酒石酸酸性磷酸酶(TRAP)的含量;用实时定量PCR法(Real-Time Quantitative PCR)及蛋白免疫印迹法(Western Blotting)法检测各组大鼠肾、骨组织TRPV5、CaBP-D28k、NCX1、PMCA1b mRNA和蛋白的表达。
结果:
1.大鼠离体股骨上1/3骨密度(BMD)结果显示:与正常组比较,模空组大鼠BMD明显下降(P<0.01);与模空组比较,各用药组大鼠股骨上1/3 BMD均升高,其中以补肾中药组升高程度最显著,有统计学意义(P<0.01)。
2.大鼠骨代谢生化指标结果显示:与正常组比较,模空组大鼠血清抗酒石酸酸性磷酸酶(TRAP)含量明显升高(P<0.01);与模空组比较,各用药组大鼠血清TRAP含量均有不同程度的下降,以补肾组和骨疏康组降低作用最明显(P<0.01),接近正常组水平。与正常组比较,模空组大鼠血清ALP含量升高,但无统计学意义;与模空组比较,各用药组大鼠血清ALP含量均上升,以补肾中药组和活血中药组升高程度最为显著,但统计学差异不明显。与正常组比较,模空组大鼠血钙含量升高,但无统计学意义;与模空组比较,各治疗组大鼠血钙含量均升高,其中补肾中药组和骨疏康组血钙升高较其他组明显(P<0.01)。各组大鼠血磷变化不明显,仅骨疏康组血磷水平升高,与正常组比较(P<0.01)。
3.大鼠肾组织TRPV5 mRNA和蛋白表达结果显示:与正常组比较,模空组TRPV5 mRNA和蛋白表达水平均明显下降(P<0.01);与模空组比较,除活血组外,各治疗组TRPV5 mRNA和蛋白表达水平均有不同程度的上调,其中补肾组上调趋势最显著(P<0.01)。
4.大鼠肾组织CaBP-D28k蛋白表达结果显示:各组大鼠肾组织均可检测到CaBP-D28k蛋白的表达,与正常组比较,模空组CaBP-D28k蛋白表达量明显降低(P<0.01);与模空组比较,各治疗组CaBP-D28k蛋白表达显示出不同程度的升高,其中补肾组升高趋势最明显(P<0.01)。
5.大鼠肾组织NCX1、PMCA1b mRNA和蛋白表达结果显示:与正常组比较,模空组NCX1 mRNA和蛋白表达水平明显下降(P<0.01);与模空组比较,各治疗组均可不同程度的上调NCX1 mRNA和蛋白表达水平,其中以补肾组上调作用最为显著(P<0.01)。各组大鼠肾组织均可检测到PMCA1b蛋白的表达,与正常组比较,模空组PMCA1b蛋白表达量明显降低(P<0.01);与模空组比较,各治疗组PMCA1b蛋白表达显示出不同程度的升高,其中补肾组升高趋势最为显著(P<0.01)。
6.大鼠骨组织TRPV5 mRNA和蛋白表达结果显示:与正常组比较,模空组骨组织TRPV5 mRNA和蛋白表达水平均明显升高(P<0.01);与模空组比较,各治疗组均可不同程度的下调TRPV5 mRNA和蛋白表达水平,以补肾中药组下调作用最显著(P<0.01)。
7.大鼠骨组织CaBP-D28k蛋白表达结果显示:各组大鼠骨组织均可检测到CaBP-D28k蛋白的表达,与正常组比较,模空组CaBP-D28k蛋白表达量明显升高(P<0.01);与模空组比较,各治疗组CaBP-D28k蛋白表达量均明显降低,其中补肾中药组的下调作用最显著(P<0.01)。
8.大鼠骨组织NCX1 mRNA和蛋白表达结果显示:与正常组比较,模空组骨组织NCX1 mRNA和蛋白表达水平均明显升高(P<0.01);与模空组比较,各治疗组均可不同程度的下调NCX1 mRNA和蛋白表达水平,其中补肾组下调作用最为显著(P<0.01)。
结论:
1.采用地塞米松肌肉注射法(2.5mg/kg,周两次),连续9周,可以成功诱导肾虚骨质疏松症大鼠模型。
2.正常大鼠肾组织可以在基因、蛋白水平表达TRPV5和NCX1,蛋白水平表达CaBP-D28k和PMCA1b,表明正常大鼠肾组织存在TRPV5介导的钙转运通路,在维持机体钙代谢稳定方面起重要作用。
3.正常大鼠骨组织可以在基因、蛋白水平表达TRPV5和NCX1,蛋白水平表达CaBP-D28k,表明正常大鼠骨组织存在TRPV5介导的钙转运通路,在骨代谢及机体钙稳态的调节方面起重要作用。
4.模型大鼠肾组织TRPV5、CaBP-D28k、NCX1和PMCA1b基因和蛋白表达的下降,提示TRPV5介导的肾钙转运通路相关蛋白的功能抑制,肾小管上皮对钙的重吸收障碍,可能是糖皮质激素诱导肾虚骨质疏松症的病理机制之一。
5.模型大鼠骨组织TRPV5、CaBP-D28k、NCX1基因和蛋白表达的升高,提示TRPV5介导的骨钙转运通路相关蛋白的功能活跃,从而致骨吸收增强,骨密度降低,可能是糖皮质激素诱导肾虚骨质疏松症的病理机制之一。
6.补肾中药通过提高肾钙转运通路相关蛋白的表达水平,降低骨钙转运通路相关蛋白的表达水平,发挥促进肾钙吸收和抑制骨钙释放的作用,从而减少骨质的丢失,达到防治骨质疏松的目的。
Purpose:
In this study, the pathway of Ca2+ transport was mainly investigated. To observe the gene and protein expression of Ca2+ transport associated protein TRPV5, CaBP-D28k、NCX1 and PMCA1b in nephridial tissue and bone tissue of rats which had kidney-deficiency osteoporosis induced by dexamethasone, then to reveal the molecular mechanism of dexamethasone-induced kidney-deficiency osteoporosis, and to explain the curative mechanism of tonifying-kidney herbs.
Materials and methods:
In this study, we used dexamethasone 2.5mg/kg intramuscular injection twice in a week in rats to induce kidney-deficiency osteoporosis, at the same time used tonifying-kidney herbs to prevent and treat. The normal rats were as standard control, model rats were as blank control and positive control were GUSHUKANG granules, and to compare the therapeutic effect of invigorate-spleen herbs and promoting-blood flow herbs. Above process were 9 weeks. After 9 weeks, killed the rats to collect serum,femoral bone and nephridial tissue to detect. Using dual-energy X-ray absorptiometry (DEXA) to detect BMD of femoral bone upper 1/3. Detected serum Ca, P and ALP levels by biochemistry method. Enzyme linked immunosorbent assay (ELISA) were used to detect the serum TRAP level. Real-Time Quantitative PCR and Western Blotting were used to detect the gene and protein expressions of TRPV5、CaBP-D28k、NCX1、PMCA1b in nephridial tissue and bone tissue of rats.
Results:
1. Results of femoral bone upper 1/3 BMD of rats: Compared with normal group, BMD of blank group were obviously decreased(P<0.01). Compared with bland group, in each medication groups, femoral bone upper 1/3 BMD were all increased, and tonifying-kidney group were most obviously, statistical significance were predominant(P<0.01).
2. Results of bone metabolism markers: Compared with normal group, TRAP of blank group were obviously increased(P<0.01). Compared with bland group, TRAP were all decreased in each medication groups(P<0.01), and tonifying-kidney group and GUSHUKANG granules were most obviously, to approach to the level of normal group. Compared with normal group, blood calcium level had no obviously variation. Compared with blank group, blood calcium level of each medication groups were increased(P<0.05). Blood phosphonium level had no obviously variation. Compared with blank group, only GUSHUKANG granules group increased(P<0.01).
3.TRPV5 mRNA and protein expression of nephridial tissue: Compared with normal group, TRPV5 mRNA and protein expression of blank group were obviously decreased(P<0.01). Compared with blank group, TRPV5 mRNA and protein expression of each medication groups were all up-regulated in different degree, and tonifying-kidney group were most obviously(P<0.01).
4. CaBP-D28k protein expression of nephridial tissue: CaBP-D28k protein was expressed in nephridial tissue of all groups. Compared with normal group, CaBP-D28k protein expression of blank group were obviously decreased(P<0.01). Compared with blank group, CaBP-D28k protein expression of each medication groups were all up-regulated in different degree, and tonifying-kidney group were most obviously(P<0.01).
5. NCX1、PMCA1b mRNA and protein expression of nephridial tissue: Compared with normal group, NCX1 mRNA and protein expression of blank group were obviously decreased(P<0.01). Compared with blank group, NCX1 mRNA and protein expression of each medication groups were all up-regulated in different degree, and tonifying-kidney group were most obviously(P<0.01). PMCA1b protein was expressed in nephridial tissue of all groups. Compared with normal group, PMCA1b protein expression of blank group were obviously decreased(P<0.01). Compared with blank group, PMCA1b protein expression of each medication groups were all up-regulated in different degree, and tonifying-kidney group were most obviously(P<0.01).
6. TRPV5 mRNA and protein expression of bone tissue: Compared with normal group, TRPV5 mRNA and protein expression of blank group were obviously increased(P<0.01). Compared with blank group, TRPV5 mRNA and protein expression of each medication groups were all down-regulated in different degree, and tonifying-kidney group were most obviously(P<0.01).
7.CaBP-D28k protein expression of bone tissue: CaBP-D28k protein was expressed in bone tissue of all groups’rats. Compared with normal group, CaBP-D28k protein expression of blank group were obviously increased(P<0.01). Compared with blank group, CaBP-D28k protein expression of each medication groups were all down-regulated in different degree, and tonifying-kidney group were most obviously(P<0.01).
8. NCX1 mRNA and protein expression of bone tissue: Compared with normal group, NCX1 mRNA and protein expression of blank group were obviously increased(P<0.01). Compared with blank group, NCX1 mRNA and protein expression of each medication groups were all down-regulated in different degree, and tonifying-kidney group were most obviously(P<0.01).
Conclusions:
1. Used dexamethasone 2.5mg/kg intramuscular injection twice in a week for continuous 9 weeks, kidney-deficiency osteoporosis rat model can be induced.
2. TRPV5 and NCX1 are expressed in nephridial tissue of normal rats in gene and protein level, CaBP-D28k and PMCA1b are expressed in protein level, indicate that renal tubule of normal rats exist calcium transport pathway mediated by TRPV5, which can contribute to maintain the stability of calcium metabolism in the body.
3. TRPV5 and NCX1 are expressed in bone tissue of normal rats in gene and protein level, CaBP-D28k are expressed in protein level, indicate that osteoclast of normal rats exist calcium transport pathway mediated by TRPV5, which can contribute to bone metabolism and maintain the stability of calcium metabolism in the body.
4.The down-regulation of mRNA and protein expression of TRPV5、CaBP-D28k、NCX1 and PMCA1b in nephridial tissue of blank group indicate the function inhibition of calcium transport pathway associated proteins in kidney, and malabsorption of calcium in renal tubule epithelium, which maybe the one of pathomechanism of kidney-deficiency osteoporosis induced by glucocorticoid.
5. The up-regulation of mRNA and protein expression of TRPV5、CaBP-D28k、NCX1 in bone tissue of blank group indicate the active function of calcium transport pathway associated proteins in bone, so result in enhancement of bone resorption and decreased BMD, which maybe the one of pathomechanism of kidney-deficiency osteoporosis induced by glucocorticoid.
6. Tonifying-kidney herbs can boost the expression of calcium transport pathway associated proteins in kidney, inhibit expression of calcium transport pathway associated proteins in bone resorption process, from which to reinforce calcium absorption in kidney and inhibit bone resorption to reduce the loss of bone content,thereby to prevention and cure osteoporosis.
本研究从钙转运通路入手,通过观察地塞米松诱导的肾虚骨质疏松症大鼠肾组织及骨组织钙转运通路相关蛋白TRPV5、CaBP-D28k、NCX1及PMCA1b基因和蛋白的表达,从分子水平揭示糖皮质激素诱导的肾虚骨质疏松症的病理机制,以及补肾中药的疗效机理。
材料与方法:
本实验采用地塞米松(2.5mg/kg,周两次)肌肉注射的方法复制肾虚骨质疏松症大鼠模型,同时以补肾中药对模型大鼠进行防治。正常大鼠作为标准对照组,模型大鼠作为空白对照组,以骨疏康颗粒作为阳性对照药,同时与健脾中药及活血中药作疗效比较。造模及给药时间为9周。9周后处死动物并取血清、股骨、肾组织等进行下列指标检测:应用双能X线吸收法检测大鼠离体股骨上1/3骨密度(BMD);用生化方法检测血清钙、磷、碱性磷酸酶(ALP)的含量;酶联免疫吸附法(ELISA)检测血清抗酒石酸酸性磷酸酶(TRAP)的含量;用实时定量PCR法(Real-Time Quantitative PCR)及蛋白免疫印迹法(Western Blotting)法检测各组大鼠肾、骨组织TRPV5、CaBP-D28k、NCX1、PMCA1b mRNA和蛋白的表达。
结果:
1.大鼠离体股骨上1/3骨密度(BMD)结果显示:与正常组比较,模空组大鼠BMD明显下降(P<0.01);与模空组比较,各用药组大鼠股骨上1/3 BMD均升高,其中以补肾中药组升高程度最显著,有统计学意义(P<0.01)。
2.大鼠骨代谢生化指标结果显示:与正常组比较,模空组大鼠血清抗酒石酸酸性磷酸酶(TRAP)含量明显升高(P<0.01);与模空组比较,各用药组大鼠血清TRAP含量均有不同程度的下降,以补肾组和骨疏康组降低作用最明显(P<0.01),接近正常组水平。与正常组比较,模空组大鼠血清ALP含量升高,但无统计学意义;与模空组比较,各用药组大鼠血清ALP含量均上升,以补肾中药组和活血中药组升高程度最为显著,但统计学差异不明显。与正常组比较,模空组大鼠血钙含量升高,但无统计学意义;与模空组比较,各治疗组大鼠血钙含量均升高,其中补肾中药组和骨疏康组血钙升高较其他组明显(P<0.01)。各组大鼠血磷变化不明显,仅骨疏康组血磷水平升高,与正常组比较(P<0.01)。
3.大鼠肾组织TRPV5 mRNA和蛋白表达结果显示:与正常组比较,模空组TRPV5 mRNA和蛋白表达水平均明显下降(P<0.01);与模空组比较,除活血组外,各治疗组TRPV5 mRNA和蛋白表达水平均有不同程度的上调,其中补肾组上调趋势最显著(P<0.01)。
4.大鼠肾组织CaBP-D28k蛋白表达结果显示:各组大鼠肾组织均可检测到CaBP-D28k蛋白的表达,与正常组比较,模空组CaBP-D28k蛋白表达量明显降低(P<0.01);与模空组比较,各治疗组CaBP-D28k蛋白表达显示出不同程度的升高,其中补肾组升高趋势最明显(P<0.01)。
5.大鼠肾组织NCX1、PMCA1b mRNA和蛋白表达结果显示:与正常组比较,模空组NCX1 mRNA和蛋白表达水平明显下降(P<0.01);与模空组比较,各治疗组均可不同程度的上调NCX1 mRNA和蛋白表达水平,其中以补肾组上调作用最为显著(P<0.01)。各组大鼠肾组织均可检测到PMCA1b蛋白的表达,与正常组比较,模空组PMCA1b蛋白表达量明显降低(P<0.01);与模空组比较,各治疗组PMCA1b蛋白表达显示出不同程度的升高,其中补肾组升高趋势最为显著(P<0.01)。
6.大鼠骨组织TRPV5 mRNA和蛋白表达结果显示:与正常组比较,模空组骨组织TRPV5 mRNA和蛋白表达水平均明显升高(P<0.01);与模空组比较,各治疗组均可不同程度的下调TRPV5 mRNA和蛋白表达水平,以补肾中药组下调作用最显著(P<0.01)。
7.大鼠骨组织CaBP-D28k蛋白表达结果显示:各组大鼠骨组织均可检测到CaBP-D28k蛋白的表达,与正常组比较,模空组CaBP-D28k蛋白表达量明显升高(P<0.01);与模空组比较,各治疗组CaBP-D28k蛋白表达量均明显降低,其中补肾中药组的下调作用最显著(P<0.01)。
8.大鼠骨组织NCX1 mRNA和蛋白表达结果显示:与正常组比较,模空组骨组织NCX1 mRNA和蛋白表达水平均明显升高(P<0.01);与模空组比较,各治疗组均可不同程度的下调NCX1 mRNA和蛋白表达水平,其中补肾组下调作用最为显著(P<0.01)。
结论:
1.采用地塞米松肌肉注射法(2.5mg/kg,周两次),连续9周,可以成功诱导肾虚骨质疏松症大鼠模型。
2.正常大鼠肾组织可以在基因、蛋白水平表达TRPV5和NCX1,蛋白水平表达CaBP-D28k和PMCA1b,表明正常大鼠肾组织存在TRPV5介导的钙转运通路,在维持机体钙代谢稳定方面起重要作用。
3.正常大鼠骨组织可以在基因、蛋白水平表达TRPV5和NCX1,蛋白水平表达CaBP-D28k,表明正常大鼠骨组织存在TRPV5介导的钙转运通路,在骨代谢及机体钙稳态的调节方面起重要作用。
4.模型大鼠肾组织TRPV5、CaBP-D28k、NCX1和PMCA1b基因和蛋白表达的下降,提示TRPV5介导的肾钙转运通路相关蛋白的功能抑制,肾小管上皮对钙的重吸收障碍,可能是糖皮质激素诱导肾虚骨质疏松症的病理机制之一。
5.模型大鼠骨组织TRPV5、CaBP-D28k、NCX1基因和蛋白表达的升高,提示TRPV5介导的骨钙转运通路相关蛋白的功能活跃,从而致骨吸收增强,骨密度降低,可能是糖皮质激素诱导肾虚骨质疏松症的病理机制之一。
6.补肾中药通过提高肾钙转运通路相关蛋白的表达水平,降低骨钙转运通路相关蛋白的表达水平,发挥促进肾钙吸收和抑制骨钙释放的作用,从而减少骨质的丢失,达到防治骨质疏松的目的。
Purpose:
In this study, the pathway of Ca2+ transport was mainly investigated. To observe the gene and protein expression of Ca2+ transport associated protein TRPV5, CaBP-D28k、NCX1 and PMCA1b in nephridial tissue and bone tissue of rats which had kidney-deficiency osteoporosis induced by dexamethasone, then to reveal the molecular mechanism of dexamethasone-induced kidney-deficiency osteoporosis, and to explain the curative mechanism of tonifying-kidney herbs.
Materials and methods:
In this study, we used dexamethasone 2.5mg/kg intramuscular injection twice in a week in rats to induce kidney-deficiency osteoporosis, at the same time used tonifying-kidney herbs to prevent and treat. The normal rats were as standard control, model rats were as blank control and positive control were GUSHUKANG granules, and to compare the therapeutic effect of invigorate-spleen herbs and promoting-blood flow herbs. Above process were 9 weeks. After 9 weeks, killed the rats to collect serum,femoral bone and nephridial tissue to detect. Using dual-energy X-ray absorptiometry (DEXA) to detect BMD of femoral bone upper 1/3. Detected serum Ca, P and ALP levels by biochemistry method. Enzyme linked immunosorbent assay (ELISA) were used to detect the serum TRAP level. Real-Time Quantitative PCR and Western Blotting were used to detect the gene and protein expressions of TRPV5、CaBP-D28k、NCX1、PMCA1b in nephridial tissue and bone tissue of rats.
Results:
1. Results of femoral bone upper 1/3 BMD of rats: Compared with normal group, BMD of blank group were obviously decreased(P<0.01). Compared with bland group, in each medication groups, femoral bone upper 1/3 BMD were all increased, and tonifying-kidney group were most obviously, statistical significance were predominant(P<0.01).
2. Results of bone metabolism markers: Compared with normal group, TRAP of blank group were obviously increased(P<0.01). Compared with bland group, TRAP were all decreased in each medication groups(P<0.01), and tonifying-kidney group and GUSHUKANG granules were most obviously, to approach to the level of normal group. Compared with normal group, blood calcium level had no obviously variation. Compared with blank group, blood calcium level of each medication groups were increased(P<0.05). Blood phosphonium level had no obviously variation. Compared with blank group, only GUSHUKANG granules group increased(P<0.01).
3.TRPV5 mRNA and protein expression of nephridial tissue: Compared with normal group, TRPV5 mRNA and protein expression of blank group were obviously decreased(P<0.01). Compared with blank group, TRPV5 mRNA and protein expression of each medication groups were all up-regulated in different degree, and tonifying-kidney group were most obviously(P<0.01).
4. CaBP-D28k protein expression of nephridial tissue: CaBP-D28k protein was expressed in nephridial tissue of all groups. Compared with normal group, CaBP-D28k protein expression of blank group were obviously decreased(P<0.01). Compared with blank group, CaBP-D28k protein expression of each medication groups were all up-regulated in different degree, and tonifying-kidney group were most obviously(P<0.01).
5. NCX1、PMCA1b mRNA and protein expression of nephridial tissue: Compared with normal group, NCX1 mRNA and protein expression of blank group were obviously decreased(P<0.01). Compared with blank group, NCX1 mRNA and protein expression of each medication groups were all up-regulated in different degree, and tonifying-kidney group were most obviously(P<0.01). PMCA1b protein was expressed in nephridial tissue of all groups. Compared with normal group, PMCA1b protein expression of blank group were obviously decreased(P<0.01). Compared with blank group, PMCA1b protein expression of each medication groups were all up-regulated in different degree, and tonifying-kidney group were most obviously(P<0.01).
6. TRPV5 mRNA and protein expression of bone tissue: Compared with normal group, TRPV5 mRNA and protein expression of blank group were obviously increased(P<0.01). Compared with blank group, TRPV5 mRNA and protein expression of each medication groups were all down-regulated in different degree, and tonifying-kidney group were most obviously(P<0.01).
7.CaBP-D28k protein expression of bone tissue: CaBP-D28k protein was expressed in bone tissue of all groups’rats. Compared with normal group, CaBP-D28k protein expression of blank group were obviously increased(P<0.01). Compared with blank group, CaBP-D28k protein expression of each medication groups were all down-regulated in different degree, and tonifying-kidney group were most obviously(P<0.01).
8. NCX1 mRNA and protein expression of bone tissue: Compared with normal group, NCX1 mRNA and protein expression of blank group were obviously increased(P<0.01). Compared with blank group, NCX1 mRNA and protein expression of each medication groups were all down-regulated in different degree, and tonifying-kidney group were most obviously(P<0.01).
Conclusions:
1. Used dexamethasone 2.5mg/kg intramuscular injection twice in a week for continuous 9 weeks, kidney-deficiency osteoporosis rat model can be induced.
2. TRPV5 and NCX1 are expressed in nephridial tissue of normal rats in gene and protein level, CaBP-D28k and PMCA1b are expressed in protein level, indicate that renal tubule of normal rats exist calcium transport pathway mediated by TRPV5, which can contribute to maintain the stability of calcium metabolism in the body.
3. TRPV5 and NCX1 are expressed in bone tissue of normal rats in gene and protein level, CaBP-D28k are expressed in protein level, indicate that osteoclast of normal rats exist calcium transport pathway mediated by TRPV5, which can contribute to bone metabolism and maintain the stability of calcium metabolism in the body.
4.The down-regulation of mRNA and protein expression of TRPV5、CaBP-D28k、NCX1 and PMCA1b in nephridial tissue of blank group indicate the function inhibition of calcium transport pathway associated proteins in kidney, and malabsorption of calcium in renal tubule epithelium, which maybe the one of pathomechanism of kidney-deficiency osteoporosis induced by glucocorticoid.
5. The up-regulation of mRNA and protein expression of TRPV5、CaBP-D28k、NCX1 in bone tissue of blank group indicate the active function of calcium transport pathway associated proteins in bone, so result in enhancement of bone resorption and decreased BMD, which maybe the one of pathomechanism of kidney-deficiency osteoporosis induced by glucocorticoid.
6. Tonifying-kidney herbs can boost the expression of calcium transport pathway associated proteins in kidney, inhibit expression of calcium transport pathway associated proteins in bone resorption process, from which to reinforce calcium absorption in kidney and inhibit bone resorption to reduce the loss of bone content,thereby to prevention and cure osteoporosis.
引文
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