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Magnolol Reduces Renal Ischemia and Reperfusion Injury via Inhibition of Apoptosis.

  • Tang, Chia-Yu1, 2
  • Lai, Chang-Chi1, 2, 3
  • Huang, Po-Hsun4, 2, 5
  • Yang, An-Han6
  • Chiang, Shu-Chiung7
  • Huang, Po-Chao8
  • Tseng, Kuo-Wei3
  • Huang, Cheng-Hsiung1
  • 1 * Division of Cardiovascular Surgery, Department of Surgery, Taipei Veterans General Hospital, Taipei, Taiwan. , (Taiwan)
  • 2 § Institute of Clinical Medicine, National Yang-Ming University, Taipei, Taiwan. , (Taiwan)
  • 3 ** Department of Exercise and Health Sciences, University of Taipei, Taipei, Taiwan. , (Taiwan)
  • 4 † Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan. , (Taiwan)
  • 5 ¶ Cardiovascular Research Center, National Yang-Ming University, Taipei, Taiwan. , (Taiwan)
  • 6 ‡ Department of Pathology and Laboratory Medicine, Taipei Veterans General Hospital, Taipei, Taiwan. , (Taiwan)
  • 7 ∥ Institute of Hospital and Health Care Administration, School of Medicine, National Yang-Ming University, Taipei, Taiwan. , (Taiwan)
  • 8 †† Department of Life Science, College of Life Science, National Taiwan University, Taipei, Taiwan. , (Taiwan)
Published Article
The American journal of Chinese medicine
Publication Date
Jan 01, 2017
DOI: 10.1142/S0192415X1750077X
PMID: 28946769


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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