1. Academic Validation
  2. Effect of β-patchoulene on cerebral ischemia-reperfusion injury and the TLR4/NF-κB signaling pathway

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

  • Exp Ther Med. 2019 May;17(5):3335-3342. doi: 10.3892/etm.2019.7374.
Fu-Bo Zhang 1 Jian-Ping Wang 1 Hong-Xia Zhang 1 Gui-Mei Fan 1 Xin Cui 2
Affiliations

Affiliations

  • 1 Department of Neurology, Cangzhou Central Hospital, Cangzhou, Hebei 061001, P.R. China.
  • 2 Department of Rheumatology, Cangzhou Central Hospital, Cangzhou, Hebei 061001, P.R. China.
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.

Keywords

anti-inflammatory; antioxidative; cerebral ischemia-reperfusion injury; toll like receptor 4/nuclear factor-ĸB pathway; β-patchoulene.

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