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  2. Ginkgetin exerts anti-inflammatory effects on cerebral ischemia/reperfusion-induced injury in a rat model via the TLR4/NF-κB signaling pathway

Ginkgetin exerts anti-inflammatory effects on cerebral ischemia/reperfusion-induced injury in a rat model via the TLR4/NF-κB signaling pathway

  • Biosci Biotechnol Biochem. 2019 Apr;83(4):675-683. doi: 10.1080/09168451.2018.1553608.
Qin Li 1 Tao Ye 2 Ting Long 3 Xuemei Peng 1
Affiliations

Affiliations

  • 1 a Department of Neurology , Chongqing General Hospital , Chongqing City , PR China.
  • 2 b Department of Clinical Laboratory , Chongqing General Hospital , Chongqing City , PR China.
  • 3 c Department of Neurology , The First Affiliated Hospital of Chongqing Medical University , Chongqing City , PR China.
Abstract

Ginkgo biloba, a natural biflavonoid isolated from Ginkgo biloba leaves, is reported to have strong anti-inflammatory and immunosuppressive properties. The aim of this study is to investigate the potential anti-inflammatory mechanisms of ginkgo Flavonoids on cerebral ischemia/reperfusion (I/R) injury. Inflammatory-associated cytokines in cerebral ischemic hemispheres were determined by immunohistochemical staining, Western blot and enzyme-like immunosorbent assay (ELISA). Our results indicated that treatment with Ginkgetin significantly restored rat brain I/R-induced neurological deficit scores. Inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) expression in Ginkgetin treatment group (100 mg/kg) also significantly reduced. The expression inflammation-related protein prostaglandin E2 (PGE2), tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and interleukin-8 (IL-8) was also decreased in Ginkgetin treatment group. However, the expression of interleukin-10 (IL-10) was remarkably increased. Thus, this study demonstrates that Ginkgetin protects neurons from I/R-induced rat injury by down-regulating pro-inflammatory cytokines and blocking the TLR4/NF-κB pathway.

Keywords

Ginkgetin; Ginkgo flavonoid; TLR4/NF-κB; anti-inflammatory; cerebral ischemia/reperfusion (I/R) injury.

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