Tianma Gouteng Decoction Exerts Cardiovascular Protection by Upregulating OPG and TRAIL in Spontaneously Hypertensive Rats.
Tianma Gouteng Decoction Exerts Cardiovascular Protection by Upregulating OPG and TRAIL in Spontaneously Hypertensive Rats.
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DOI：
10.1155/2020/3439191
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发表时间：
2020
期刊：
影响因子：
--
通讯作者：
Liu W
中科院分区：
文献类型：
--
作者：
Deng LH;Li L;Zhai Y;Michael S;Yang CY;Guo R;Chen SF;Fan GW;Zhao YQ;Liu W
天麻勾藤汤（TGD）被广泛用于治疗高血压及其相关并发症，但其作用机制尚不完全明确。我们现在的目标是评估TGD对心血管损伤的保护作用，并研究其特征和潜在的机制。采用无创测量方法测定tgd治疗的自发性高血压大鼠（SHR）血压。超声心动图评价心脏功能和结构，天狼星红染色评价心脏纤维化，评价血管重构程度。ELISA法检测大鼠血管收缩因子和舒张因子的表达变化。western blot检测蛋白表达变化。与未治疗的SHR相比，tgd治疗的SHR表现出更接近于正常血压的Wistar Kyoto （WKY）大鼠的心血管特征。即舒张压、收缩压和平均血压降低，血管舒张因子表达增高。我们还发现，TGD可减少SHR患者的心室和血管重构，改善心功能。最后，我们测试了TGD在SHR中的抗凋亡作用，表面上是通过上调OPG、TRAIL和死亡受体5 （DR5）的表达，下调caspases 8、7和3的表达。TRAIL还可能通过上调AKT的表达而发挥抗凋亡和促存活的作用。因此，TGD可能通过上调OPG和TRAIL的表达，上调AKT，抑制细胞凋亡，至少在一定程度上逆转SHR的心血管重构。我们首次发现OPG和TRAIL在SHR中发挥互补的心脏保护作用。
Tianma Gouteng Decoction (TGD) is widely used in traditional Chinese medicine for the treatment of hypertension and its related complications, but its mechanisms remain incompletely defined. We now aim to assess the protective effect of TGD against cardiovascular damage and to investigate its characteristics and underlying mechanisms. Blood pressure was determined in TGD-treated spontaneously hypertensive rats (SHR) by noninvasive measurements. Echocardiography was performed to assess cardiac function and structure and sirius red staining to evaluate cardiac fibrosis, and the degree of vascular remodeling was evaluated. Additionally, vasoconstriction and relaxation factor expression changes were examined by means of ELISA. Protein expression changes were verified by western blot. Compared with untreated SHR, TGD-treated SHR exhibited cardiovascular traits more akin to those of the normotensive Wistar Kyoto (WKY) rats. That is, they had lower diastolic blood pressure, systolic blood pressure and mean BP, and increased expression of vasodilation factor. We also found that TGD reduces ventricular and vascular remodeling and improves cardiac function in SHR. Finally, we tested the antiapoptosis effect TGD exerts in SHR, ostensibly by upregulating the expression of OPG, TRAIL, and death receptor 5 (DR5) and downregulating caspases 8, 7, and 3. TRAIL may also exert antiapoptotic and prosurvival effects by upregulating AKT expression. Therefore, TGD may reverse cardiovascular remodeling in SHR by upregulating the expression of OPG and TRAIL, upregulating AKT, and inhibiting apoptosis, at least in part. For the first time, we have shown that OPG and TRAIL play complimentary cardioprotective roles in SHR.
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影响因子：
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