Neuroprotective and Anti-Inflammatory Effect of Pterostilbene Against Cerebral Ischemia/Reperfusion Injury via Suppression of COX-2

Yan, Wenjun; Ren, Daoyuan; Feng, Xiaoxue; Huang, Jinwen; Wang, Da-Bin; Li, Ting; Zhang, Dong

doi:10.3389/fphar.2021.770329

Cited by 22 publications

(19 citation statements)

References 69 publications

(61 reference statements)

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“…The lack of any toxics effects of Ptb fluorescent derivatives ( 1 , 2 ) raised the question if these compounds still maintain some of neuro-protective effects ascribed to their precursor 50 , 51 . The discovery that high levels of neuroglobin (NGB), an endogenous neuroprotective globin, are active against several brain injuries, including neurodegeneration, hypoxia, ischaemia, toxicity, and nutrient deprivation prompted us to evaluate the effect of different concentrations of Ptb and their fluorescent derivatives in SH-SY5Y cells.…”

Section: Resultsmentioning

confidence: 99%

Pterostilbene fluorescent probes as potential tools for targeting neurodegeneration in biological applications

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Nencetti

Marino

et al. 2022

Journal of Enzyme Inhibition and Medicinal Chemistry

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Section: Resultsmentioning

confidence: 99%

Pterostilbene fluorescent probes as potential tools for targeting neurodegeneration in biological applications

Ciccone

Nencetti

Marino

et al. 2022

Journal of Enzyme Inhibition and Medicinal Chemistry

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“…The antioxidative enzymes that work to alleviate oxidative stress mainly include GSH and SOD. SOD prevents the formation of hydroxyl radicals by catalyzing the conversion of superradicals to H 2 O 2 (Yan et al., 2021 ). Accumulation of ROS and depletion of antioxidant enzymes may cause secondary brain damage (Chouchani et al., 2014 ).…”

Section: Discussionmentioning

confidence: 99%

Preparation of baicalin-loaded ligand-modified nanoparticles for nose-to-brain delivery for neuroprotection in cerebral ischemia

et al. 2022

Drug Delivery

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Neuroprotection in cerebral ischemia (CI) has received increasing attention. However, efficient delivery of therapeutic agents to the brain remains a major challenge due to the complex environment of the brain. Nose-to-brain-based delivery is a promising approach. Here, we optimized a nanocarrier formulation of neuroprotective agents that can be used for nose-to-brain delivery by obtaining RVG29 peptide-modified polyethylene glycol–polylactic acid-co-glycolic acid nanoparticles (PEG–PLGA RNPs) that have physicochemical properties that lead to stable and sustained drug release and thereby improve the bioavailability of neuroprotective agents. The brain-targeting ability of PEG–PLGA RNPs administered through nasal inhalation was verified in a rat model of CI. It was found that delivery to the whole brain can be achieved with little delivery to the peripheral circulation. Baicalin (BA) was selected as the neuroprotective agent for delivery. After intranasal administration of BA–PEG–PLGA RNPs, the neurological dysfunction of rats with ischemic brain injury was significantly alleviated, the cerebral infarction area was reduced, and nerve trauma and swelling were relieved. Furthermore, it was demonstrated that the neuroprotective effects of BA in a rat model of CI may be mediated by inhibition of inflammation and alleviation of oxidative stress. The immunohistochemical results obtained after treatment with nanoparticles loaded with BA showed that Nrf2/HO-1 was activated in the area in which ischemic brain damage had occurred and that its expression was significantly higher in the group treated with BA–PEG–PLGA RNPs than in the other groups. The ELISA results showed that the levels of IL-1β, IL-6, and TNF-α were abnormally increased in the serum of rats with cerebral ischemia. After treatment with BA-loaded nanoparticles, IL-1β, IL-6, and TNF-α levels decreased significantly. Oxidative stress was alleviated; the levels of glutathione and superoxide dismutase increased; and the levels of reactive oxygen species and malondialdehyde decreased, in animals to which BA–PEG–PLGA RNPs were delivered by intranasal inhalation. In conclusion, BA–PEG–PLGA RNPs can effectively deliver BA to rats and thereby exert neuroprotective effects against CI.

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“…PTE, a natural product with neuronal protection, has a chemical structure similar to that of RES and plays an important role in nervous system diseases. Evidence suggests that PTE can attenuate cerebral ischemia reperfusion injury by inhibiting oxidative stress and neuronal apoptosis ( Zhou et al, 2015 ), modulating microglial activation ( Liu J. et al, 2020 ), and suppressing cyclooxygenase-2 (COX2) ( Yan et al, 2021 ). It is reported that PTE alleviates Aβ 1–42 -induced cognitive dysfunction by inhibiting oxidative stress in SH-SY5Y cells ( Xu et al, 2020 ) and regulating the phosphatidylinositol 3-kinase (PI3K)/AKT pathway in PC12 cells ( Fu et al, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

SIRT1 Is Involved in the Neuroprotection of Pterostilbene Against Amyloid β 25–35-Induced Cognitive Deficits in Mice

Zhu

Zhang

et al. 2022

Front. Pharmacol.

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Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β (Aβ) deposits and neurofibrillary tangles. Pterostilbene (PTE), a bioactive component mainly in blueberries, is found to have neuroprotective properties. However, the specific underlying mechanisms of PTE in protecting AD remain unclear. Herein, we explored its effects on Aβ25–35-induced neuronal damage in vivo and in vitro and further compared the roles with its structural analog resveratrol (RES) in improving learning–memory deficits. We found that intragastric administration of PTE (40 mg/kg) displayed more effective neuroprotection on Aβ25–35-induced cognitive dysfunction assessed using the novel object test, Y-maze test, and Morris water maze test. Then, we found that PTE improved neuronal plasticity and alleviated neuronal loss both in vivo and in vitro. Additionally, PTE upregulated the expression of sirtuin-1 (SIRT1) and nuclear factor erythroid 2-related factor 2 (Nrf2) and the level of superoxide dismutase (SOD), and inhibited mitochondria-dependent apoptosis in the Aβ25–35-treated group. However, SIRT1 inhibitor EX527 reversed the neuroprotection and induced a drop in mitochondrial membrane potential in PTE-treated primary cortical neurons. Our data suggest that PTE’s enhancing learning–memory ability and improving neuroplasticity might be related to inhibiting mitochondria-dependent apoptosis via the antioxidant effect regulated by SIRT1/Nrf2 in AD.

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Neuroprotective and Anti-Inflammatory Effect of Pterostilbene Against Cerebral Ischemia/Reperfusion Injury via Suppression of COX-2

Cited by 22 publications

References 69 publications

Pterostilbene fluorescent probes as potential tools for targeting neurodegeneration in biological applications

Pterostilbene fluorescent probes as potential tools for targeting neurodegeneration in biological applications

Preparation of baicalin-loaded ligand-modified nanoparticles for nose-to-brain delivery for neuroprotection in cerebral ischemia

SIRT1 Is Involved in the Neuroprotection of Pterostilbene Against Amyloid β 25–35-Induced Cognitive Deficits in Mice

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