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Anti-apoptosis effects of codonolactone on cerebral ischemia-reperfusion injury
  1. Feichi Chen1,
  2. Weiqian Lin2
  1. 1Department of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China
  2. 2Department of Cardiology, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China
  1. Correspondence to Dr Feichi Chen, Department of Neurology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang Province, China; feichichenfree{at}163.com

Abstract

Codonolactone is the main biologically active ingredient in Atractylodes lancea. Studies have shown various functions of codonolactone, while its protective effect against neurotoxicity caused by ischemic stroke is unclear. This study investigated the roles of codonolactone in inflammation, oxidative stress and apoptosis after cerebral ischemia-reperfusion (I/R) injury. Rats with codonolactone treatment, I/R treatment and the sham operation group were used in this study. After reperfusion for 24 hours, nerve damage was detected by nerve staining, and the neurological deficits of the rats were analyzed. The contents of superoxide dismutase (SOD), malondialdehyde (MDA), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) in rat brain tissues were also determined. Western blot analysis was performed to determine the expression levels of Akt/Nrf2 pathway-associated proteins. Compared with the I/R group, the cerebral blood flow, infarct volume, brain water content, coronary blood flow and neurological deficits in the codonolactone treatment group, especially with the 80 mg/kg dosage, were significantly reduced. Codonolactone could significantly reduce the expression levels of caspase-3 and Bax, and significantly increase the expression levels of Bcl-2 after I/R. In addition, codonolactone could significantly reduce MDA content and the expression levels of TNF-α and IL-1β in ischemic brain tissues. It also significantly increased SOD activity, the expression levels of heme oxygenase-1 (HO-1) and the phosphorylation of Akt and Nrf2. Codonolactone ameliorated the cerebral I/R injury by improving anti-oxidant, anti-inflammatory activities and reducing apoptosis. Besides, the Akt/Nrf2 pathway was involved in the pharmacological action of the codonolactone.

  • inflammation

Data availability statement

Data are available on reasonable request. The datasets used and/or analyzed during the current study is available from the corresponding author on reasonable request.

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Data availability statement

Data are available on reasonable request. The datasets used and/or analyzed during the current study is available from the corresponding author on reasonable request.

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Footnotes

  • Contributors FC: experimental design, literature review, experiments, data analysis and manuscript preparation. WL: definition of intellectual content, literature research experimental studies, manuscript preparation and editing. All authors read and approved the final manuscript. FC is responsible for the overall content as the guarantor.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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