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Punicalagin attenuated cerebral ischemia–reperfusion insult via inhibition of proinflammatory cytokines, up-regulation of Bcl-2, down-regulation of Bax, and caspase-3
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  • 作者:Lavanya Yaidikar ; Santhrani Thakur
  • 关键词:Cerebral ischemia–reperfusion injury ; Punicalagin ; Neuroprotection ; Anti ; inflammatory action ; Anti ; apoptotic activity
  • 刊名:Molecular and Cellular Biochemistry
  • 出版年:2015
  • 出版时间:April 2015
  • 年:2015
  • 卷:402
  • 期:1-2
  • 页码:141-148
  • 全文大小:547 KB
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  • 刊物类别:Biomedical and Life Sciences
  • 刊物主题:Life Sciences
    Biochemistry
    Medical Biochemistry
    Oncology
    Cardiology
  • 出版者:Springer Netherlands
  • ISSN:1573-4919
文摘
Punicalagin (PG) is a hydrolysable tannin compound found in Punica granatum L. The purpose of the present work is to explore the neuroprotective mechanism of PG against ischemia–reperfusion (I/R) injury in rat model of middle cerebral artery occlusion (MCAO). Rats were randomly divided into sham, MCAO, and PG-treated groups. PG (15 and 30?mg/kg), the vehicle was administered orally for 7?days prior to MCAO. Rats were anesthetised with ketamine (100?mg/kg/im), xylazine (10?mg/kg/im) and subjected to 2?h occlusion and 22?h reperfusion. The effects of PG on behavioral deficit and infarct volume, the levels of glutamate and calcium as well as the levels of inflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) were evaluated. Moreover, the expressions of caspase-3, Bcl-2, and Bax were detected by Western blotting. As compared with MCAO group, PG-treated rats showed dose-dependent reduction in infarct volume and substantial improvement in behavioral deficit. The levels of glutamate, calcium, TNF-α, IL-1β, and IL-6 were restored significantly. The Western blotting results revealed that the expression of Bcl-2 was up-regulated and that of caspase-3, Bax were down-regulated when exposed to PG. From our results, it can be concluded that PG showed an ameliorative effect against cerebral I/R injury in rats through its anti-inflammatory, antioxidant actions besides it inhibits excitotoxicity. It also suppresses apoptosis through regulating, Bcl-2, caspase-3, and Bax protein expressions, perhaps another mechanism by which PG employs its neuroprotective action.

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