Open Access

Effect of β‑patchoulene on cerebral ischemia‑reperfusion injury and the TLR4/NF‑κB signaling pathway

  • Authors:
    • Fu‑Bo Zhang
    • Jian‑Ping Wang
    • Hong‑Xia Zhang
    • Gui‑Mei Fan
    • Xin Cui
  • View Affiliations

  • Published online on: March 12, 2019     https://doi.org/10.3892/etm.2019.7374
  • Pages: 3335-3342
  • Copyright: © Zhang et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

β‑patchoulene (β‑PAE), an active constituent of the Pogostemon cablin, is well known for its anti‑inflammatory and antioxidative functions in various diseases. However, little is known about the impact of β‑PAE on the cerebral ischemia‑reperfusion (I/R) injury. The current study aimed to determine the neuroprotective effect of β‑PAE and the underlying mechanisms on cerebral I/R injury. Following pretreatment with β‑PAE (10 mg/kg body weight) by tail intravenous injection for 1 h, Sprague‑Dawley rats were subjected to middle cerebral artery occlusion for 2 h and reperfusion for 24 h. The results indicated that pretreatment with β‑PAE could diminish the infarct volume, decrease the brain water content, reduce the neurological deficit score and restore the mitochondrial membrane potential, compared with the untreated I/R injury group. Furthermore, cell apoptosis was markedly suppressed by β‑PAE, and this effect was associated with the decreased apoptosis regulator BAX/apoptosis regulator Bcl‑2 expression ratio and caspase‑3 activity. In addition, β‑PAE significantly inhibited the release of proinflammatory factors, including tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6. Superoxide generation and malondialdehyde levels were reduced while the levels of glutathione peroxidase and superoxide dismutase were elevated following treatment with β‑PAE, indicating the antioxidative role of β‑PAE in cerebral I/R injury. Furthermore, the Toll‑like receptor 4 (TLR4)/nuclear factor‑κB (NF‑κB) signaling pathway was inhibited by β‑PAE, as demonstrated by the decreased TLR4 expression and nuclear translocation of p65, and increased IκBα level. Taken together, the results suggested that β‑PAE may exhibit a neuroprotective effect on cerebral I/R injury in rats through inactivating the TLR4/NF‑κB signaling pathway.
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May-2019
Volume 17 Issue 5

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Spandidos Publications style
Zhang FB, Wang JP, Zhang HX, Fan GM and Cui X: Effect of β‑patchoulene on cerebral ischemia‑reperfusion injury and the TLR4/NF‑κB signaling pathway. Exp Ther Med 17: 3335-3342, 2019
APA
Zhang, F., Wang, J., Zhang, H., Fan, G., & Cui, X. (2019). Effect of β‑patchoulene on cerebral ischemia‑reperfusion injury and the TLR4/NF‑κB signaling pathway. Experimental and Therapeutic Medicine, 17, 3335-3342. https://doi.org/10.3892/etm.2019.7374
MLA
Zhang, F., Wang, J., Zhang, H., Fan, G., Cui, X."Effect of β‑patchoulene on cerebral ischemia‑reperfusion injury and the TLR4/NF‑κB signaling pathway". Experimental and Therapeutic Medicine 17.5 (2019): 3335-3342.
Chicago
Zhang, F., Wang, J., Zhang, H., Fan, G., Cui, X."Effect of β‑patchoulene on cerebral ischemia‑reperfusion injury and the TLR4/NF‑κB signaling pathway". Experimental and Therapeutic Medicine 17, no. 5 (2019): 3335-3342. https://doi.org/10.3892/etm.2019.7374