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[Display omitted] • sPlas significantly reduced cerebral ischemic infarction in mice at 5 d after tMCAO. • sPlas significantly alleviated neural oxidative stress in mice at 5 d after tMCAO. • sPlas significantly regulated neural inflammation in mice at 5 d after tMCAO. • sPlas significantly attenuated neurovascular unit damage in mice at 5 d after tMCAO. • sPlas may be a preventive and therapeutic candidate against ischemic stroke. Scallop-derived plasmalogen (sPlas) has both anti-oxidative and anti-inflammation activities, but its efficacy has not been investigated in ischemic stroke models where oxidative stress, inflammation, and neurovascular unit (NVU) damage accelerates pathophysiological progression. Therefore, in the present study, we aimed to assess the neuroprotective effects of sPlas in ischemic stroke by using a transient middle cerebral artery occlusion (tMCAO) mouse model. After the pretreatment of vehicle or sPlas (10 mg/kg/day) for 14 days, adult male mice were subjected to tMCAO for 60 min, then continuously treated with vehicle or sPlas during reperfusion and for an additional 5 days. The administration of sPlas significantly improved motor deficits (corner and rotarod tests, * p < 0.05 vs vehicle), enhanced serum antioxidative activity (OXY-adsorbent and d-ROMs tests, * p < 0.05 vs vehicle), reduced infarction volume (* p < 0.05 vs vehicle), decreased the expression of two oxidative stress markers, 4-HNE (* p < 0.05 vs vehicle) and 8-OHdG (* p < 0.05 vs vehicle), decreased the expression of pro-inflammatory markers Iba-1 (** p < 0.01 vs vehicle), IL-1β (** p < 0.01 vs vehicle), and TNF-α (** p < 0.01 vs vehicle), and alleviated NVU damage (collagen IV, MMP9, and GFAP/collagen IV, * p < 0.05 vs vehicle). Our present findings are the first to demonstrate the neuroprotective effects of sPlas on acute ischemic stroke mice at 5 d after tMCAO via anti-oxidative stress, anti-inflammation, and improvement of NVU damage, suggesting the potential of sPlas in preventing and treating ischemic stroke. [ABSTRACT FROM AUTHOR]

• Plasmalogen strongly attenuated the activation of pSTAT3/PIM1/NFATc1 axis. • Plasmalogen significantly suppressed NLRP3 inflammasome activation. • Plasmalogen tended to improve cerebral HP-enhanced cerebral vascular dysfunction. A strong relationship between Alzheimer's disease (AD) and vascular dysfunction has been the focus of increasing attention in aging societies. In the present study, we examined the long-term effect of scallop-derived plasmalogen (sPlas) on vascular remodeling-related proteins in the brain of an AD with cerebral hypoperfusion (HP) mouse model. We demonstrated, for the first time, that cerebral HP activated the axis of the receptor for advanced glycation endproducts (RAGE)/phosphorylated signal transducer and activator of transcription 3 (pSTAT3)/provirus integration site for Moloney murine leukemia virus 1 (PIM1)/nuclear factor of activated T cells 1 (NFATc1), accounting for such cerebral vascular remodeling. Moreover, we also found that cerebral HP accelerated pSTAT3-mediated astrogliosis and activation of the nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome, probably leading to cognitive decline. On the other hand, sPlas treatment attenuated the activation of the pSTAT3/PIM1/NFATc1 axis independent of RAGE and significantly suppressed NLRP3 inflammasome activation, demonstrating the beneficial effect on AD. [ABSTRACT FROM AUTHOR]

[Display omitted] • FGA, FGB, and FGG accumulation increased in the CNS in Alzheimer's disease. • Aβ deposition related to FGA, FGB, and FGG accumulated in neural cells and vessels. • FGA, FGB, and FGG are potential targets for AD diagnosis and therapy. Alzheimer's disease (AD) is a common neurodegenerative disease that is characterized by the abnormal accumulation of intracellular and extracellular amyloid-β (Aβ) as well as disruption of the blood brain barrier (BBB). Fibrinogen plays an essential role in regulating thrombosis, wound healing, and other biological functions. In the present study, we investigated the relationship between three polypeptide chains α, β, and γ (FGA, FGB, and FGG) and Aβ deposition in the APP23 plus chronic cerebral hypoperfusion (CCH) mice model as well as the human AD brain. FGA, FGB, and FGG accumulated when Aβ was deposited in neural cells and cerebral vessels. This deposition was significantly higher in AD plus CCH mice models relative to wild-type brains, and in human AD brains compared to control brains. The present study demonstrates that FGA, FGB, and FGG are associated with AD progress, and can thus be potential targets for the diagnosis and therapy of AD. [ABSTRACT FROM AUTHOR]