https://scholars.lib.ntu.edu.tw/handle/123456789/633449
標題: | Magnolol Reduces Renal Ischemia and Reperfusion Injury via Inhibition of Apoptosis | 作者: | Tang, Chia-Yu Lai, Chang-Chi Huang, Po-Hsun Yang, An-Han Chiang, Shu-Chiung PO-CHAO HUANG Tseng, Kuo-Wei Huang, Cheng-Hsiung |
關鍵字: | Acute Kidney Injury; Apoptosis; Inflammatory Cytokines; Magnolol; Mitogen-Activated Protein Kinases; Prosurvival Kinases; Renal Ischemia and Reperfusion | 公開日期: | 2017 | 卷: | 45 | 期: | 7 | 來源出版物: | The American journal of Chinese medicine | 摘要: | Magnolol, a constituent of the bark of Magnolia officinalis, has been reported to decrease myocardial stunning and infarct size. In this study, we investigated whether magnolol can reduce renal ischemia and reperfusion (I/R) injury. Renal I/R, induced by a 60-min occlusion of bilateral renal arteries and a 24-h reperfusion, significantly increased blood urea nitrogen (BUN) and creatinine levels, and caused histological damage to the kidneys of rats. Apoptosis, as evaluated by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining and caspase-3 activation, was significantly increased in the kidneys. Furthermore, serum levels of tumor necrosis factor-[Formula: see text] (TNF-[Formula: see text]), interleukin-1β (IL-1β), and interleukin-6 (IL-6) were significantly elevated, while the interleukin-10 (IL-10) level was suppressed. However, intravenous pretreatment with magnolol at doses of 0.003[Formula: see text]mg/kg and 0.006[Formula: see text]mg/kg 10[Formula: see text]min before renal I/R significantly limited the increases of BUN, creatinine, the histological damage, and apoptosis in the kidneys. The increases in TNF-[Formula: see text], IL-1β, and IL-6, and the decrease in IL-10 were also significantly inhibited. Additionally, magnolol increased Bcl-2 and decreased Bax in the kidneys. Phosphorylation of the prosurvival kinases, including Akt and extracellular signal-regulated kinases 1 and 2 (ERK1/2), was elevated, while phosphorylation of the pro-apoptotic mitogen-activated protein kinases, including p38 and c-Jun N-terminal kinase (JNK), was suppressed. In conclusion, magnolol reduces renal I/R injury. The underlying mechanisms for this effect might be related to the prevention of apoptosis, possibly via the inhibition of both extrinsic and intrinsic apoptotic pathways, including the reduction of TNF-[Formula: see text] production and the modulation of pro- and anti-apoptotic signaling elements. |
URI: | https://scholars.lib.ntu.edu.tw/handle/123456789/633449 | ISSN: | 0192415X | DOI: | 10.1142/S0192415X1750077X |
顯示於: | 生物化學暨分子生物學科研究所 |
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