頁籤選單縮合
題名 | Protective Effect of Tongxinluo on Oxidative Injury Induced by Angiotensin Ⅱ in Rats= |
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作者 | Xu, Danling; Fang, Cheng; Su, Wei; Yuan, Lingyan; Yang, Lin; Jia, Jianguo; Wang, Keqiang; Zhang, Hongqi; |
期刊 | Acta Cardiologica Sinica |
出版日期 | 20110900 |
卷期 | 27:3 2011.09[民100.09] |
頁次 | 頁189-196 |
分類號 | 418.22 |
語文 | eng |
關鍵詞 | Angiotensin Ⅱ; Anti-oxidative; Aorta; Tongxinluo; |
英文摘要 | Purpose: To investigate the effect of Tongxinluo (TXL), a traditional Chinese herbal medicine, on aortic biological variation after angiotensin II (Ang II)-induced vascular oxidative injury. Methods: Randomly, 50 Sprague-Dawley (SD) rats were divided into three groups: sham, Ang II, and Ang II+TXL. A pump with Ang II was embedded in the rat backs in the Ang II and Ang II+TXL groups, whereas a pump containing physiological saline was emplaced in the sham group. TXL was delivered through a gastric tube in the Ang II+TXL group. Endothelin-1 (ET-1), tumor necrosis factor-α (TNF-α) and nitric oxide (NO) in the plasma were examined 14 days later; the aortic endothelial cells were observed under a scanning electron microscope (SEM); the expressions of endothelial nitric oxide synthase (eNOS), nuclear factor-κB (NF-κB), and vascular cell adhesion molecule-l. (VCAM-1) were measured via immunohistochemistry assays; apoptotic cells were investigated with DeadEndTM colorimetric TUNEL System; and the NAD(P)H oxidase subunit P22phox mRNA was examined through reverse transcription polymerase chain reaction. Results: The plasma concentrations of ET-1 and TNF-α increased significantly in the Ang II group in comparison with the sham one, but decreased in the Ang II+TXL group. The same observations occurred regarding NF-κB, VCAM-1, apoptosis and P22phox mRNA expressions in the aortic tissues. However, eNOS expression in the aorta produced a reverse response, which was ameliorated significantly by TXL. Conclusion: The findings suggested that TXL could play a potential role in inhibiting the oxidative injury induced by Ang II by reducing the inflammation and the apoptotic process via the P22phox pathway. |
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