Hollow Prussian Blue Nanozymes Drive Neuroprotection against Ischemic Stroke via Attenuating Oxidative Stress, Counteracting Inflammation, and Suppressing Cell Apoptosis

Zhang, Kai; Tu, Mengjiao; Gao, Wei; Cai, Xiaojun; Song, Fahuan; Zheng, Chen; Zhang, Qian; Wang, Jing; Jin, Chentao; Shi, Jingjing; Xiang, Yang; Zhu, Yuankai; Gu, Weizhong; Hu, Bing; Zheng, Yuanyi; Zhang, Hong; Tian, Mei

doi:10.1021/acs.nanolett.8b04729

Cited by 237 publications

(222 citation statements)

References 73 publications

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“…Neuroinflammation is an important and harmful mechanism in cerebral ischemia-reperfusion injury [49,50]. It has been reported that the TLR4/NF-κB signaling pathway and the TLR4/MAPK signaling pathway has an important relationship with neuroinflammation in the MCAO/R model, which have the similar molecular mechanisms as the LPS-activated expression of proinflammatory factors in microglia.…”

Section: Discussionmentioning

confidence: 99%

Anti-Neuroinflammatory Effect of Alantolactone through the Suppression of the NF-κB and MAPK Signaling Pathways

Tan

Wang

et al. 2019

Cells

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Neuroinflammation is a major cause of central nervous system (CNS) damage and can result in long-term disability and mortality. Therefore, the development of effective anti-neuroinflammatory agents for neuroprotection is vital. To our surprise, the naturally occurring molecule alantolactone (Ala) was reported to significantly inhibit tumor growth and metastasis as a result of its excellent anti-inflammatory effects. Thus, we proposed that it could also act as an anti-neuroinflammatory agent. Thus, in this study, a coculture system of BV2 cells and PC12 cells were used as an in vitro neuroinflammatory model to investigate the anti-neuroinflammatory mechanism of Ala. The results indicated that Ala downregulated the expression of proinflammatory factors by suppressing the nuclear factor kappa light-chain enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways. Further evaluation using a middle cerebral artery occlusion and reperfusion (MCAO/R) rat model supported the conclusion that Ala could (1) alleviate cerebral ischemia-reperfusion injury; (2) reduce neurological deficits, cerebral infarct volume, and brain edema; and (3) attenuate the apoptosis and necrosis of neurons. In sum, Ala demonstrates anti-neuroinflammatory properties that contribute to the amelioration of CNS damage, and it could be a promising candidate for future applications in CNS injury treatment.

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Section: Discussionmentioning

confidence: 99%

Anti-Neuroinflammatory Effect of Alantolactone through the Suppression of the NF-κB and MAPK Signaling Pathways

Tan

Wang

et al. 2019

Cells

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“…Ischemic stroke occurs when the blood flow to a certain portion of the brain is obstructed secondary to occlusion of cerebral arteries. The following deprivation of oxygen and energy triggers an ischemic cascade, such as OS and inflammation, resulting in neuronal excitotoxicity and cell death ( Khoshnam et al, 2017 ; Li et al, 2019a ; Zhang K. et al, 2019 ). Before ferroptosis was defined, iron accumulation [for review see Selim and Ratan (2004) ] had been found in lesioned regions, such as the basal ganglia and the hippocampal area of the brain, and iron overload exaggerated neuronal damage during reperfusion ( Dietrich and Bradley, 1988 ; Kondo et al, 1995 ; Lipscomb et al, 1998 ; Park et al, 2011 ).…”

Section: The Role and Mechanism Of Ferroptosis In Acute Cns Injuriesmentioning

confidence: 99%

Ferroptosis in Acute Central Nervous System Injuries: The Future Direction?

Shen

Lin

et al. 2020

Front. Cell Dev. Biol.

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Acute central nervous system (CNS) injuries, such as stroke, traumatic brain injury (TBI), and spinal cord injury (SCI) present a grave health care challenge worldwide due to high morbidity and mortality, as well as limited clinical therapeutic strategies. Established literature has shown that oxidative stress (OS), inflammation, excitotoxicity, and apoptosis play important roles in the pathophysiological processes of acute CNS injuries. Recently, there have been many studies on the topic of ferroptosis, a form of regulated cell death characterized by the accumulation of iron-dependent lipid peroxidation. Some studies have revealed an emerging connection between acute CNS injuries and ferroptosis. Ferroptosis, induced by the abnormal metabolism of lipids, glutathione (GSH), and iron, can accelerate acute CNS injuries. However, pharmaceutical agents, such as iron chelators, ferrostatin-1 (Fer-1), and liproxstatin-1 (Lip-1), can inhibit ferroptosis and may have neuroprotective effects after acute CNS injuries. However, the specific mechanisms underlying this connection has not yet been clearly elucidated. In this paper, we discuss the general mechanisms of ferroptosis and its role in stroke, TBI, and SCI. We also summarize ferroptosis-related drugs and highlight the potential therapeutic strategies in treating various acute CNS injuries. Additionally, this paper suggests a testable hypothesis that ferroptosis may be a novel direction for further research of acute CNS injuries by providing corresponding evidence.

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“…Prussian blue nanozymes (HPBZs) possessed multienzyme activity assisted with Bi3 + and exerted antiapoptotic effects to protect cells from ischemia-induced injury by regulating the expression of anti-and pro-apoptotic proteins in vitro and vivo in a recent study [45]. Although the material structure of HPBZs did a little differ from PBNPs, the anti-apoptotic effects may be closely related to ROS scavenging.…”

Section: Discussionmentioning

confidence: 99%

A Treatment Combined Prussian Blue Nanoparticles With Low-intensity Pulsed Ultrasound Alleviates Cartilage Damage in Knee Osteoarthritis by Initiating PI3K/Akt/mTOR Pathway

Zuo

Tan

Jia

et al. 2020

Preprint

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Background: Reactive oxidative stress (ROS) related apoptosis in chondrocytes and extracellular matrix (ECM) degradation play crucial roles in the process of osteoarthritis (OA). Prussian blue nanoparticles (PBNPs) are known to scavenge ROS in cellular. Low-intensity pulsed ultrasound (LIPUS) has been used as a non-invasive modality for the is widely used in clinical rehabilitation management of OA. Methods: In this study, we aim to investigate the effects of PBNPs/LIPUS combined treatment on knee osteoarthritis (KOA) and to determine whether phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway mediates this process. Use LPS to process primary cells of knee joint cartilage to establish a cartilage knee arthritis model. After treated with LIPUS and PBNPs, cell viability was rated by CCK-8 and ROS levels were assessed by DCFH-DA. Cell apoptosis was estimated by flow cytometry and TUNEL staining. Articular pathological changes were observed by naked eyes, H&E, and Safranin O staining, then monitored by cartilage lesion grades and Mankin’s score. Protein levels of cleaved caspase-3, Bcl-2, Bax, p-PI3K, PI3K, p-Akt, Akt, p-mTOR, mTOR, IL-1β, MMP3, MMP13, p-JINK, JINK, p-c-Jun, and c-Jun were subjected to western blot. Results: Cellular ROS, apoptosis rate, and TUNEL staining of chondrocytes were fairly decreased in the PBNPs group and the LIPUS group but drastically down-regulated in the PBNPs/LIPUS combination treatment group when compared with the LPS group. Both PBNPs and LIPUS decreased the grades of cartilage lesions and Mankin scores of knee articular cartilage, while combined administration achieved more reduction. Western blot results showed that the cleaved caspase-3, Bax, IL-1β, MMP3 and MMP13 in the PBNPs and LIPUS groups slightly decreased, and Bcl2 increased slightly, while in the combination treatment group, the former was significantly decreased, and Bcl2 was Significantly increased. Conclusion: The PBNPs/LIPUS combination treatment increased protein levels of p-PI3K, p-Akt, and p-mTOR but decreased the protein levels of p-JINK and p-c-Jun, in vitro and vivo. The PBNPs/LIPUS combination treatment reduced cellular ROS, apoptosis, and matrix metalloproteinases (MMPs), as a consequence, alleviated articular cartilage damage in KOA. Moreover, the PBNPs/LIPUS combination treatment suppressed the JINK/c-Jun signal pathway.

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Hollow Prussian Blue Nanozymes Drive Neuroprotection against Ischemic Stroke via Attenuating Oxidative Stress, Counteracting Inflammation, and Suppressing Cell Apoptosis

Cited by 237 publications

References 73 publications

Anti-Neuroinflammatory Effect of Alantolactone through the Suppression of the NF-κB and MAPK Signaling Pathways

Anti-Neuroinflammatory Effect of Alantolactone through the Suppression of the NF-κB and MAPK Signaling Pathways

Ferroptosis in Acute Central Nervous System Injuries: The Future Direction?

A Treatment Combined Prussian Blue Nanoparticles With Low-intensity Pulsed Ultrasound Alleviates Cartilage Damage in Knee Osteoarthritis by Initiating PI3K/Akt/mTOR Pathway

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