Duraplasty of PHBV/PLA/Col membranes promotes axonal regeneration by inhibiting NLRP3 complex and M1 macrophage polarization in rats with spinal cord injury

Zhao, Tengfei; Xu, Kan; Wu, Qionghua; Wang, Chenggui; Xiao, Shining; Li, Heyangzi; Teng, Hui; Wang, Linlin; Li, Fangcai; Chen, Qixin

doi:10.1096/fj.202000190rr

Cited by 9 publications

(4 citation statements)

References 49 publications

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“…Therefore, the abuse of N2O may cause long-term and irreversible damage to neurons and movement. Lately, two studies have shown that the depression of the activation of NLRP3 inflammasomes can be beneficial for axonal regeneration of nerve cells [ 35 , 36 ]. This suggests that the therapeutic effect of TXNIP/NLRP3 knockdown on N2O-induced nerve injury may be connected with axonal regeneration, which needs to be further explored in the future.…”

Section: Discussionmentioning

confidence: 99%

Activation of NLR family, domain of pyrin containing 3 inflammasome by nitrous oxide through thioredoxin-interacting protein to induce nerve cell injury

et al. 2021

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Nitrous Oxide (N 2 O) has been shown to be neurotoxic, but its specific mechanism is still unclear. The purpose of this work is to probe into the impact of N 2 O on nerve cell injury through regulating thioredoxin-interacting protein (TXNIP)/the NOD-like receptor domain of pyrin containing 3 (NLRP3) pathway. The results indicated that, N 2 O exposure elevated TXNIP/NLRP3 expression in vivo and in vitro, led to declined learning and memory capabilities in mice, reduced apoptosis rate in hippocampal neuron and Nissl bodies, elevated inflammatory factors TNF-α, IL-1β and IL-6 levels, as well as cleaved caspase-3 and Bax expressions, and reduced Bcl-2 expression. Overexpressing TXNIP or NLRP3 further aggravated these injuries, but knocking down TXNIP or NLRP3 improved them. CO-IP indicated that TXNIP and NLRP3 can be combined, with interaction relationship. All in all, the results manifested that N 2 O is available to promote nerve cell inflammation and apoptosis through activating the TXNIP/NLRP3 pathway that can be used as a potential target for N 2 O-induced nerve damage in the future.

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Section: Discussionmentioning

confidence: 99%

Activation of NLR family, domain of pyrin containing 3 inflammasome by nitrous oxide through thioredoxin-interacting protein to induce nerve cell injury

et al. 2021

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“…The results demonstrated that duroplasty with PHBV/PLA/Collagen membranes reduced glial scar formation and promoted axonal growth by inhibiting inflammasome activation and modulating macrophage polarization in acute SCI. Functional locomotor recovery improved 8 weeks after injury [82].…”

Section: Phbv Composites For Tissue Engineering Applicationsmentioning

confidence: 91%

Biomedical Applications of the Biopolymer Poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV): Drug Encapsulation and Scaffold Fabrication

Rodríguez-Cendal,

Gómez-Seoane,

de Toro-Santos

et al. 2023

IJMS

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Poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV) is a biodegradable and biocompatible biopolymer that has gained popularity in the field of biomedicine. This review provides an overview of recent advances and potential applications of PHBV, with special emphasis on drug encapsulation and scaffold construction. PHBV has shown to be a versatile platform for drug delivery, offering controlled release, enhanced therapeutic efficacy, and reduced side effects. The encapsulation of various drugs, such as anticancer agents, antibiotics, and anti-inflammatory drugs, in PHBV nanoparticles or microspheres has been extensively investigated, demonstrating enhanced drug stability, prolonged release kinetics, and increased bioavailability. Additionally, PHBV has been used as a scaffold material for tissue engineering applications, such as bone, cartilage, and skin regeneration. The incorporation of PHBV into scaffolds has been shown to improve mechanical properties, biocompatibility, and cellular interactions, making them suitable for tissue engineering constructs. This review highlights the potential of PHBV in drug encapsulation and scaffold fabrication, showing its promising role in advancing biomedical applications.

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“…For example, it has been shown that poly(3-hydroxybutyrate-co-3-hydroxyvalerate)/ collagen (PHBV/Col) nanofibers are promising substrates as bioengineered grafts for the regeneration of neural tissue [ 137 , 138 ]. Zhao and his colleagues found that the use of poly(hydroxybutyrate-co-hydroxyvalerate)/polylactic acid/ collagen (PHBV/PLA/Col) membranes for duralplasty reduced glial scar formation and promoted axonal regeneration after acute SCI by suppressing NLRP3 inflammasome activation and M1 macrophage polarization [ 139 ]. In addition, ceria nanoparticle (CeNP) has been shown to attenuate WMI after ICH, and the mechanisms may be related to the involvement of microglia and astrocytes in myelin regeneration [ 71 ].…”

Section: Targeting Nlrp3 In the Pathogenesis Of Secondary Wmi After Ichmentioning

confidence: 99%

Secondary White Matter Injury Mediated by Neuroinflammation after Intracerebral Hemorrhage and Promising Therapeutic Strategies of Targeting the NLRP3 Inflammasome

Wang

Sun

Xiao

et al. 2023

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Intracerebral hemorrhage (ICH) is a neurological disease with high mortality and disability. Recent studies showed that white matter injury (WMI) plays an important role in motor dysfunction after ICH. WMI includes WMI proximal to the lesion and WMI distal to the lesion, such as corticospinal tract injury located at the cervical enlargement of the spinal cord after ICH. Previous studies have tended to focus only on gray matter (GM) injury after ICH, and fewer studies have paid attention to WMI, which may be one of the reasons for the poor outcome of previous drug treatments. Microglia and astrocyte-mediated neuroinflammation are significant mechanisms responsible for secondary WMI following ICH. The NOD-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome activation, has been shown to exacerbate neuroinflammation and brain injury after ICH. Moreover, NLRP3 inflammasome is activated in microglia and astrocytes and exerts a vital role in microglia and astrocytes-mediated neuroinflammation. We speculate that NLRP3 inflammasome activation is closely related to the polarization of microglia and astrocytes and that NLRP3 inflammasome activation may exacerbate WMI by polarizing microglia and astrocytes to the pro-inflammatory phenotype after ICH, while NLRP3 inflammasome inhibition may attenuate WMI by polarizing microglia and astrocytes to the anti-inflammatory phenotype following ICH. Therefore, NLRP3 inflammasome may act as leveraged regulatory fulcrums for microglia and astrocytes polarization to modulate WMI and WM repair after ICH. This review summarized the possible mechanisms by which neuroinflammation mediated by NLRP3 inflammasome exacerbates secondary WMI after ICH and discussed the potential therapeutic targets.

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Duraplasty of PHBV/PLA/Col membranes promotes axonal regeneration by inhibiting NLRP3 complex and M1 macrophage polarization in rats with spinal cord injury

Cited by 9 publications

References 49 publications

Activation of NLR family, domain of pyrin containing 3 inflammasome by nitrous oxide through thioredoxin-interacting protein to induce nerve cell injury

Activation of NLR family, domain of pyrin containing 3 inflammasome by nitrous oxide through thioredoxin-interacting protein to induce nerve cell injury

Biomedical Applications of the Biopolymer Poly(3-hydroxybutyrate-co-3-hydroxyvalerate) (PHBV): Drug Encapsulation and Scaffold Fabrication

Secondary White Matter Injury Mediated by Neuroinflammation after Intracerebral Hemorrhage and Promising Therapeutic Strategies of Targeting the NLRP3 Inflammasome

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