Piperine attenuates the inflammation, oxidative stress, and pyroptosis to facilitate recovery from spinal cord injury via autophagy enhancement

Zhang, Haojie; Wu, Chen‐Yu; Yu, Dongdong; Su, Haohan; Chen, Yanlin; Ni, Wen-Fei

doi:10.1002/ptr.7625

Cited by 12 publications

(6 citation statements)

References 55 publications

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“…Recent studies have shown that oxidative stress is involved in a series of neurological diseases, including cerebral ischemia, SCI, and Alzheimer’s disease. − Many studies have confirmed that excessive ROS can exacerbate SCI . Excessive ROS production can cause severe damage to proteins and DNA in spinal cord tissue, ultimately leading to increased inflammation and neuronal cell death. , ROS, GSH, SOD, and MDA are widely used as markers of oxidative stress after SCI. , In the present study, both in vitro and in vivo experiments showed that SeNPs-Met-MVs could be a key regulator of neuroprotection in response to oxidative stress.…”

Section: Discussionsupporting

confidence: 52%

Encapsulation of Selenium Nanoparticles and Metformin in Macrophage-Derived Cell Membranes for the Treatment of Spinal Cord Injury

Liu,

Sun,

et al. 2023

ACS Biomater. Sci. Eng.

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Spinal cord injury is an impact-induced disabling condition. A series of pathological changes after spinal cord injury (SCI) are usually associated with oxidative stress, inflammation, and apoptosis. These pathological changes eventually lead to paralysis. The short half-life and low bioavailability of many drugs also limit the use of many drugs in SCI. In this study, we designed nanovesicles derived from macrophages encapsulating selenium nanoparticles (SeNPs) and metformin (SeNPs-Met-MVs) to be used in the treatment of SCI. These nanovesicles can cross the blood–spinal cord barrier (BSCB) and deliver SeNPs and Met to the site of injury to exert anti-inflammatory and reactive oxygen species scavenging effects. Transmission electron microscopy (TEM) images showed that the SeNPs-Met-MVs particle size was approximately 125 ± 5 nm. Drug release assays showed that Met exhibited sustained release after encapsulation by the macrophage cell membrane. The cumulative release was approximately 80% over 36 h. In vitro cellular experiments and in vivo animal experiments demonstrated that SeNPs-Met-MVs decreased reactive oxygen species (ROS) and malondialdehyde (MDA) levels, increased superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities, and reduced the expression of inflammatory (TNF-α, IL-1β, and IL-6) and apoptotic (cleaved caspase-3) cytokines in spinal cord tissue after SCI. In addition, motor function in mice was significantly improved after SeNPs-Met-MVs treatment. Therefore, SeNPs-Met-MVs have a promising future in the treatment of SCI.

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Section: Discussionsupporting

confidence: 52%

Encapsulation of Selenium Nanoparticles and Metformin in Macrophage-Derived Cell Membranes for the Treatment of Spinal Cord Injury

Liu,

Sun,

et al. 2023

ACS Biomater. Sci. Eng.

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“…Previous studies have found that some CRMs, such as resveratrol and aspirin, inhibit oxidative stress and reduce ROS levels 78 , 79 . Activation of the antioxidative stress mechanism inhibits pyroptosis and necroptosis of neurocytes by regulating autophagy 80 . Whether 3,4-DC promotes autophagy and inhibits pyroptosis and necroptosis by inhibiting oxidative stress remains to be further studied.…”

Section: Discussionmentioning

confidence: 99%

3,4-Dimethoxychalcone, a caloric restriction mimetic, enhances TFEB-mediated autophagy and alleviates pyroptosis and necroptosis after spinal cord injury

Zhang¹,

Ni²,

Yu³

et al. 2023

Theranostics

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Background: Caloric restriction mimetics (CRMs) mimic the favourable effects of caloric restriction (CR) and have been shown to have therapeutic effects in neuroinflammatory disease. However, whether CRMs improve the functional recovery from spinal cord injury (SCI) and the underlying mechanism of action remain unclear. In this study, we used the CRMs 3,4-dimethoxychalcone (3,4-DC) to evaluate the therapeutic value of CRMs for SCI. Methods: HE, Masson and Nissl staining; footprint analysis; and the Basso mouse scale were used to determine the functional recovery from SCI after 3,4-DC treatment. RNA sequencing was used to identify the mechanisms of 3,4-DC in SCI. Western blotting, qPCR and immunofluorescence were used to detect the levels of pyroptosis, necroptosis, autophagy and the AMPK-TRPML1-calcineurin signalling pathway. We employed a dual-luciferase reporter assay in vitro and applied AAV vectors to inhibit TFEB in vivo to explore the mechanism of 3,4-DC. Results: 3,4-DC reduced glial scar area and motor neuron death and improved functional recovery after SCI. RNA-sequencing results indicated that oxidative stress, pyroptosis, necroptosis, and autophagy may be involved in the ability of 3,4-DC to improve functional recovery. Furthermore, 3,4-DC inhibited pyroptosis and necroptosis by enhancing autophagy. We also found that 3,4-DC enhances autophagy by promoting TFEB activity. A decrease in the TFEB level abolished the protective effect of 3,4-DC. In addition, 3,4-DC partially regulated TFEB activity through the AMPK-TRPML1-calcineurin signalling pathway. Conclusions: 3,4-DC promotes functional recovery by upregulating TFEB-mediated autophagy and inhibiting pyroptosis and necroptosis after SCI, which may have potential clinical application value.

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“…Recent studies have shown that increased autophagy can reduce inflammation and pyroptosis ( 107 , 108 ). In the context of alleviating SCI, betulinic acid (BA) and piperine have been found to activate autophagy, leading to a decrease in ROS formation and NLRP3/GSDMD-mediated pyroptosis ( 75 , 109 ). Specifically, BA activates macroautophagy through the AMPK-mTOR-TFEB pathway, which in turn reduces ROS accumulation by enhancing mitophagy, thereby inhibiting pyroptosis ( 75 ).…”

Section: Ros In Pyroptosismentioning

confidence: 99%

ROS: Executioner of regulating cell death in spinal cord injury

Yin,

Wan,

Gong

et al. 2024

Front. Immunol.

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The damage to the central nervous system and dysfunction of the body caused by spinal cord injury (SCI) are extremely severe. The pathological process of SCI is accompanied by inflammation and injury to nerve cells. Current evidence suggests that oxidative stress, resulting from an increase in the production of reactive oxygen species (ROS) and an imbalance in its clearance, plays a significant role in the secondary damage during SCI. The transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial regulatory molecule for cellular redox. This review summarizes recent advancements in the regulation of ROS-Nrf2 signaling and focuses on the interaction between ROS and the regulation of different modes of neuronal cell death after SCI, such as apoptosis, autophagy, pyroptosis, and ferroptosis. Furthermore, we highlight the pathways through which materials science, including exosomes, hydrogels, and nanomaterials, can alleviate SCI by modulating ROS production and clearance. This review provides valuable insights and directions for reducing neuronal cell death and alleviating SCI through the regulation of ROS and oxidative stress.

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Piperine attenuates the inflammation, oxidative stress, and pyroptosis to facilitate recovery from spinal cord injury via autophagy enhancement

Cited by 12 publications

References 55 publications

Encapsulation of Selenium Nanoparticles and Metformin in Macrophage-Derived Cell Membranes for the Treatment of Spinal Cord Injury

Encapsulation of Selenium Nanoparticles and Metformin in Macrophage-Derived Cell Membranes for the Treatment of Spinal Cord Injury

3,4-Dimethoxychalcone, a caloric restriction mimetic, enhances TFEB-mediated autophagy and alleviates pyroptosis and necroptosis after spinal cord injury

ROS: Executioner of regulating cell death in spinal cord injury

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