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6-Gingerol attenuates microglia-mediated neuroinflammation and ischemic brain injuries through Akt-mTOR-STAT3
Ying Liu1, ShiJi Deng2, Zhi Zhang2
1Department of Neurology, Affiliated Drum Tower Hospital of Medical School, And The State Key Laboratory of Pharmaceutical Biotechnology, Nanjing University, Nanjing, Jiangsu, PR China; Jiangsu Key Laboratory for Molecular Medicine, Nanjing University Medical School, Nanjing, Jiangsu, PR China; Nanjing Clinic Medicine Center for Neurological and Psychiatric Diseases, Nanjing, Jiangsu, PR China.
Abstract:
Neuroinflammation is critical for the pathogenesis of ischemia brain damage. Over-activated microglia-mediated inflammation plays a very important role in ischemia cerebral injuries. 6-Gingerol, obtained from edible ginger (Zingiber Officinale) exhibits protective effects against inflammation. In this study, we found that 6-Gingerol could reduce the size of infarction (P = 0.0184) and improve neurological functions (P = 0.04) at the third day after ischemic brain injury in vivo. Since 6-Gingerol has the anti-inflammatory effects, we further investigated its impacts on neuroinflammation mediated by microglia both in vivo and in vitro. We found that the levels of pro-inflammatory cytokines Interleukin-1 beta (IL-1β, P = 0.0213), Interleukin-6 (IL-6, P = 0.0316), and inducible NO synthase (iNOS, P = 0.0229) in the infarct penumbra were lower in 6-Gingerol treated groups. Furthermore, microglia induced pro-inflammatory cytokines, such as IL-6, IL-1β, incremental intercellular nitric oxide (NO), as well as iNOS were blocked by the treatment of 6-Gingerol in lipopolysaccharide (LPS) stimulated microglia. In terms of mechanism, 6-Gingerol potently suppressed phosphorylation of serine-threonine protein kinase (Akt) - mammalian target of rapamycin (mTOR) - signal transducer and activator of transcription 3 (STAT3) in LPS-treated microglia. Taken together, the present study suggested that 6-Gingerol improved cerebral ischemia injury by suppressing microglia-mediated neuroinflammation by down-regulating Akt-mTOR-STAT3 pathway.
Insights
6-Gingerol from ginger reduces brain damage and improves function after ischemic stroke by reducing neuroinflammation. It suppresses microglia activation and the Akt-mTOR-STAT3 pathway, offering a potential therapeutic strategy.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Neuroinflammation, particularly from over-activated microglia, is key in ischemic brain damage.
- 6-Gingerol, derived from ginger (Zingiber Officinale), possesses known anti-inflammatory properties.
Purpose of the Study:
- To investigate the neuroprotective effects of 6-Gingerol in ischemic brain injury.
- To elucidate the mechanisms underlying 6-Gingerol's action on microglia-mediated neuroinflammation.
Main Methods:
- In vivo studies assessing infarct size and neurological function post-ischemia in 6-Gingerol treated subjects.
- In vitro studies using lipopolysaccharide (LPS)-stimulated microglia to analyze cytokine and nitric oxide production.
- Western blot analysis to examine the Akt-mTOR-STAT3 signaling pathway.
Main Results:
- 6-Gingerol significantly reduced infarct size (P=0.0184) and improved neurological function (P=0.04) in vivo.
- Treatment with 6-Gingerol decreased levels of pro-inflammatory cytokines (IL-1β, IL-6) and iNOS in the infarct penumbra.
- 6-Gingerol inhibited LPS-induced pro-inflammatory cytokine release and nitric oxide production in microglia, down-regulating the Akt-mTOR-STAT3 pathway.
Conclusions:
- 6-Gingerol demonstrates significant neuroprotective effects against ischemic brain injury.
- The compound exerts its benefits by suppressing microglia-mediated neuroinflammation.
- Down-regulation of the Akt-mTOR-STAT3 pathway is a key mechanism for 6-Gingerol's therapeutic action.
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