Hyperinflammation, apoptosis, and organ damage

Kuypers, Frans A.

doi:10.1177/15353702221090454

Cited by 14 publications

(9 citation statements)

References 154 publications

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“…Previous studies have shown that oxidative stress ultimately leads to apoptosis of neuronal cells . The cysteine protease family is the primary regulator of apoptosis. , The caspase-3 apoptosis pathway plays a key role in apoptosis . In the present study, immunofluorescence and Tunel assays showed that SeNPs-Met-MVs could significantly reduce the expression of apoptotic factors (cleaved caspase-3).…”

Section: Discussionsupporting

confidence: 59%

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: 59%

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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“…Oxidative stress and inflammation are important triggers of gastric ulcers [ 26 ]. Proinflammatory factors such as IL-1β, IL-6, TNF-α, and PEG2 play a crucial role in the inflammatory response [ 27 ]. TNF-α stimulates IL-1β production and cell apoptosis, leading to delayed ulcer healing [ 28 ].…”

Section: Resultsmentioning

confidence: 99%

Dendrobium officinale Polysaccharides as a Natural Functional Component for Acetic-Acid-Induced Gastric Ulcers in Rats

Zhang,

Xu,

Chen

et al. 2024

Molecules

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Dendrobium officinale is an important edible and medicinal plant, with the Dendrobium officinale polysaccharide (DOP) being its primary active constituent, known for its diverse biological activities. In this study, DOP was extracted and characterized for its structural properties. The potential of DOP to ameliorate gastric ulcers (GUs) was investigated using an acetic-acid-induced GU model in rats. The results demonstrated that DOP exerted a multifaceted protective effect against GU, mitigating the deleterious impact on food intake and body weight in rats. DOP exhibited its protective action by attenuating cellular damage attributed to oxidative stress and inflammatory reactions mediated by enhanced activities of SOD, GSH, and GSH-PX, coupled with a downregulation in the expression of pro-inflammatory cytokines, including IL-1β, IL-6, and TNF-α. Furthermore, DOP effectively inhibited apoptosis in gastric mucosa cells of acetic-acid-induced GU rat models and facilitated the self-repair of damaged tissues. Remarkably, the DOP-200 and DOP-400 groups outperformed omeprazole in reducing the expression of IL-6 and malondialdehyde (MDA) in tissues, as well as IL-1β, IL-6, and TNF-α in serum. These groups also exhibited an improved expression of SOD in tissues and SOD, GSH, and GSH-PX in serum. A Western blot analysis of gastric mucosa demonstrated that the DOP-200 and DOP-400 groups significantly reduced the expression of NF-κBp65, phosphorylated NF-κBp65, FoxO3a, and Bim. The observed antagonism to GU appeared to be associated with the NF-κB cell pathway. Additionally, qRT-PCR results indicate that DOP reduced the mRNA transcription levels of IL-6, and TNF-α, which shows that the healing of GU is related to the reduction in the inflammatory reaction by DOP. However, the expression of EGF and VEGF decreased, suggesting that the mechanism of DOP inhibiting GU may not be directly related to EGF and VEGF, or there is an uncertain competitive relationship between them, so further research is needed.

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“…A dysregulated inflammatory response can have several causes: excessively high pathogen load in the context of sepsis, inadequate sensing or triggering of the immune system without the presence of a pathogen at all (as occurs with Castleman’s disease), or inappropriate inflammasome activation due to genetic disease [ 36 , 37 , 38 ]. Further examples are the inability of the immune system to terminate an initially adequate immune response and return to baseline (e.g., primary hemophagocytic lymphohistiocytosis, HLH) or conditions with uncontrolled infection and persistent immune activation (e.g., macrophage activation syndrome (MAS)-HLH in, e.g., CMV, EBV, or Influenza) [ 39 ].…”

Section: Pathophysiology Of Csmentioning

confidence: 99%

Cytokine Storm—Definition, Causes, and Implications

Jarczak

Nierhaus

2022

IJMS

117

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The human innate and adaptive immune systems consist of effector cells producing cytokines (interleukins, interferons, chemokines, and numerous other mediators). Usually, a fragile equilibrium of pro- and anti-inflammation effects is maintained by complex regulatory mechanisms. Disturbances of this homeostasis can lead to intricate chain reactions resulting in a massive release of cytokines. This may result in a drastic self-reinforcement of various feedback mechanisms, which can ultimately lead to systemic damage, multi-organ failure, or death. Not only pathogens can initiate such disturbances, but also congenital diseases or immunomodulatory therapies. Due to the complex and diverse interactions within the innate and adaptive immune systems, the understanding of this important clinical syndrome is incomplete to date and effective therapeutic approaches remain scarce.

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Hyperinflammation, apoptosis, and organ damage

Cited by 14 publications

References 154 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

Dendrobium officinale Polysaccharides as a Natural Functional Component for Acetic-Acid-Induced Gastric Ulcers in Rats

Cytokine Storm—Definition, Causes, and Implications

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