Magnolol Reduces Renal Ischemia and Reperfusion Injury via Inhibition of Apoptosis

厚朴 标记法 厚朴酚 肌酐 细胞凋亡 医学 内分泌学 末端脱氧核苷酸转移酶 激酶 p38丝裂原活化蛋白激酶 药理学 缺血 再灌注损伤 血尿素氮 内科学 化学 MAPK/ERK通路 生物化学 病理 替代医学 中医药
作者
Chia‐Yu Tang,Chang‐Chi Lai,Po‐Hsun Huang,An-Han Yang,Shu‐Chiung Chiang,Po‐Chao Huang,Kuo-Wei Tseng,Cheng-Hsiung Huang
出处
期刊:The American Journal of Chinese Medicine [World Scientific]
卷期号:45 (07): 1421-1439 被引量:26
标识
DOI:10.1142/s0192415x1750077x
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.
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