Abstract TP97: Korean Red Ginseng Ameliorates Cerebral Hypoxic-Ischemic Damage Through the Activation of the Nrf2 Pathway by Preferentially Altering Reactive Astrogliosis

Stroke ◽  
2017 ◽  
Vol 48 (suppl_1) ◽  
Author(s):  
Lei Liu ◽  
Mary K. Vollmer ◽  
Morgan W. Carson ◽  
Todd J. Sahagian ◽  
Hocheol Kim ◽  
...  

Introduction: Endogenous defense mechanisms by which the brain protects itself against noxious stimuli and recovers from ischemic damage are key targets of stroke research that may ultimately facilitate functional recovery. Multiple evidences indicate that the transcriptional factor Nrf2 plays a vital role in cellular defense against oxidative stress and inflammation, and consequently, targeting Nrf2 has emerged as a promising therapeutic strategy for disease prevention. Korean Red Ginseng (Ginseng), one of the most widely used herbal medicines in the world, has been suggested as one of the most potent Nrf2 activators, thereby making it efficacious against various acute neurological disorders, including stroke. Hypothesis: To evaluate whether Ginseng could exert protective effects against hypoxic-ischemic brain damage and whether Nrf2 activation is pivotal to the various neuroprotective effects of Ginseng. Methods: C57BL/6 WT and Nrf2 knockout mice (10-18 weeks old, n=12-16) were orally administered Ginseng (100mg/kg/d) or vehicle 7d prior to cerebral hypoxic-ischemic damage. At 6 and 24h after stroke, mice were neurologically scored. Brain lesion size and edema formation were measured at 24h. Using immunostaining, we examined which cells appeared to be most preferentially activated in a spatiotemporal pattern by this Nrf2 pathway, in particular, in the early stage of ischemic injury. Based on the results, we are further evaluating the efficacy of inducing the Nrf2 pathway and assess the extended neuroprotective effects of Ginseng at 7d after stroke. Results: Ginseng treatment significantly reduced cerebral infarct size, neuronal death, edema formation and the resultant functional neurological deficits at 24h after stroke (P<0.001); whereas, Nrf2 ablation remarkably attenuated all benefits. Notably, the above protective effects of Ginseng were significantly attenuated in Nrf2 knockouts (P<0.05). In addition, Ginseng treated mice also exhibited reduced neuronal death and delayed severe reactive astrogliosis at 6 and 12h (P<0.05). Conclusion: Our findings indicate a neuroprotective effect of Ginseng against hypoxic-ischemic brain damage, and that Nrf2-dependent cytoprotective responses appear to be more prominent in astrocytes.

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Changjun Yang ◽  
Brian D Sanz ◽  
Kelly M DeMars ◽  
Andrew A Butler ◽  
Eduardo Candelario-Jalil

Adropin is an endogenous peptide highly expressed in the brain and is encoded by the energy homeostasis-associated gene, Enho . We recently found that treatment with synthetic adropin peptide reduces infarct volume in ischemic stroke. This protection by exogenous adropin is associated with a significant increase in endothelial nitric oxide synthase (eNOS) phosphorylation (Ser 1176 ) and reduction of blood-brain barrier (BBB) permeability. However, it is not known whether endogenous adropin modulates ischemic brain damage. We hypothesize that lack of brain adropin increases stroke damage by exacerbating neurovascular dysfunction, while overexpression of this peptide decreases ischemic brain injury. We measured infarct size and BBB damage in male and female adropin overexpressing transgenics (AdrTg), adropin knockout ( Enho -/- ), and corresponding wild-type (WT) control mice subjected to permanent middle cerebral artery occlusion (pMCAO). At 48h after stroke, infarct volume was significantly smaller in AdrTg mice of both sexes compared to WT controls, while stroke resulted in a much larger infarction in both male and female Enho -/- compared to Enho +/+ mice. Brain levels of IgG and albumin, two sensitive markers of BBB disruption, were significantly reduced in AdrTg mice compared to the WT group, while the levels of these two plasma proteins in the ischemic brain of Enho -/- mice were dramatically increased compared to Enho +/+ animals after stroke. Latex vessel casting showed no differences in cerebrovascular anatomy or the diameter of the main brain arteries between Enho -/- , AdrTg and their respective WT controls. In AdrTg mice, we found a positive correlation between brain adropin levels and eNOS phosphorylation. These data suggest that increased eNOS phosphorylation by adropin is a potential mechanism underlying its protective effects in stroke. Consistent with this hypothesis, the protective effects of adropin were completely abolished in eNOS knockout (eNOS -/- ) mice subjected to pMCAO. Taken together, our findings show for the first time that endogenous adropin is a neuroprotective peptide in ischemic stroke. Understanding adropin signaling and function could offer a novel therapeutic strategy for the treatment of ischemic brain damage.


2021 ◽  
Vol 12 ◽  
Author(s):  
Wei Wei ◽  
Min Lu ◽  
Xiao-bing Lan ◽  
Ning Liu ◽  
Wei-ke Su ◽  
...  

Oxymatrine (OMT), a quinolizidine alkaloid extracted from traditional Chinese herb Sophora flavescens Ait, has drawn attention because of its beneficial bioactivities against hypoxic–ischemic brain damage (HIBD). However, the underlying molecular mechanism remains unclear. In this study, we determined the in vivo and in vitro effects of OMT on seven-day old Sprague–Dawley rats with HIBD and in a rat model of primary hippocampal neuron oxygen glucose deprivation reoxygenation (OGD/R). This study was aimed to evaluate whether OMT exerted neuroprotective effects mediated by the (phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin) PI3K/Akt/mTOR pathway after HIBD. Experimental results showed that the alkaloid significantly improved the early neurofunctional development, brain water content, abnormal pathological changes, and necrosis of neurons after HIBD. Moreover, OMT enhanced the cell viability and stabilized the mitochondrial permeability transition pore in the primary hippocampal neurons after OGD/R. OMT significantly decreased the autophagosome generation, elevated the expression of PI3K, Akt, and mTOR, and simultaneously reversed the mRNA expression of microtubule-associated protein 1-light chain 3 (LC3), Beclin-1, and sequestosomel (P62) induced by hypoxia and ischemia. However, these protective effects against HIBD could be suppressed when rapamycin, a specific inhibitor of mTOR, was included. Hence, the OMT exerted neuroprotective effects against HIBD by attenuating excessive autophagy by mediating the PI3K/Akt/mTOR pathway.


FEBS Journal ◽  
2008 ◽  
Vol 276 (1) ◽  
pp. 2-12 ◽  
Author(s):  
Domenico E. Pellegrini-Giampietro ◽  
Guido Mannaioni ◽  
Giacinto Bagetta

Antioxidants ◽  
2019 ◽  
Vol 8 (8) ◽  
pp. 273 ◽  
Author(s):  
Lei Liu ◽  
Marie G. Kelly ◽  
Erika L. Wierzbicki ◽  
Iana C. Escober-Nario ◽  
Mary K. Vollmer ◽  
...  

Cerebral ischemia is a devastating disease with a high incidence of death and disability; however, effective therapeutics remain limited. The transcriptional factor Nrf2 has been shown to play a pivotal role in the endogenous defense against brain oxidative stress and inflammation, and therefore represents a promising target for stroke intervention. However, the long-term effects of Nrf2 and the standardized Korean red ginseng (ginseng), a potent Nrf2 natural inducer, on permanent cerebral ischemic damage have not yet been reported. Wildtype (WT) and Nrf2-/- adult mice were pretreated with either vehicle or ginseng, and were subjected to permanent distal middle cerebral artery occlusion (pdMCAO). The infarct volume, the reactive astrocytes and microglia, and the water regulatory protein aquaporin 4 (AQP4) were examined at 28 days after stroke. When compared with the WT matched controls, the Nrf2 disruption significantly enlarged the infarct volume (40.4 ± 10.1%) and exacerbated the progression of reactive gliosis and AQP4 protein levels after pdMCAO. In contrast, ginseng significantly reduced the infarct volume and attenuated the reactive gliosis and AQP4 in the ischemic WT mice (47.3 ± 6.9%), but not in the Nrf2-/- mice (25.5 ± 5.6%). In conclusion, Nrf2 plays an important role in the long-term recovery of permanent cerebral ischemic damage and the neuroprotection of ginseng.


Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1805
Author(s):  
Chan-Min Liu ◽  
Zhi-Kai Tian ◽  
Yu-Jia Zhang ◽  
Qing-Lei Ming ◽  
Jie-Qiong Ma ◽  
...  

Gastrodin (GAS), the main phenolic glycoside extracted from Gastrodia elata Blume, exhibited potential neuroprotective properties. Here we examined the protective effects of GAS against lead(Pb)-induced nerve injury in mice, and explores its underlying mechanisms. Our research findings revealed that GAS improved behavioral deficits in Pb-exposed mice. GAS reduced the accumulation of p-tau and amyloid-beta (Aβ). GAS inhibited Pb-induced inflammation in the brain, as indicated by the decreased levels of pro-inflammatory cytokines, including tumor necrosis factor-a (TNF-α), cyclooxygenase-2 (COX-2). GAS increased the expression levels of NR2A and neurotrophin brain-derived neurotrophic factor (BDNF). GAS inhibited Pb-induced apoptosis of neurons in hippocampus tissue, as indicated by the decreased levels of pro-apoptotic proteins Bax and cleaved caspase-3. Furthermore, the neuroprotective effects of GAS were associated with inhibiting oxidative stress by modulating nuclear factor-erythroid 2-related factor 2 (Nrf2)-mediated antioxidant signaling. GAS supplement activated the Wnt/β-catenin signaling pathway and reduced the expression of Wnt inhibitor Dickkopf-1 (Dkk-1). Collectively, this study clarified that GAS exhibited neuroprotective property by anti-oxidant, anti-inflammatory and anti-apoptosis effects and its ability to regulate the Wnt/Nrf2 pathway.


2011 ◽  
Vol 60 (4) ◽  
pp. 674-682 ◽  
Author(s):  
Elisa Landucci ◽  
Tania Scartabelli ◽  
Elisabetta Gerace ◽  
Flavio Moroni ◽  
Domenico E. Pellegrini-Giampietro

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