N-Butyrylated Hyaluronic Acid Achieves Anti-Inflammatory Effects In Vitro and in Adjuvant-Induced Immune Activation in Rats

Xue, Liyan; Cong, Zhongcheng; Anastassiades, Tassos; Gao, Yin

doi:10.3390/molecules27103267

Cited by 9 publications

(8 citation statements)

References 46 publications

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“…Moreover, these derivatives have superior antioxidant properties compared to native HA, thereby inhibiting the activation of NF-κB signaling. 24 However, it should be noted that immune regulation in the human skin involves complex cellular interactions, including the roles of Langerhans cells and macrophages, both of which are critical in anti-inflammatory processes. In addition, the nervous and endocrine systems contribute to the modulation of the immune system.…”

Section: Discussionmentioning

confidence: 99%

“…This allows HA to persist in the extracellular matrix and sustain receptor binding for an extended period. Moreover, these derivatives have superior antioxidant properties compared to native HA, thereby inhibiting the activation of NF‐κB signaling 24 …”

Section: Discussionmentioning

confidence: 99%

“…Moreover, these derivatives have superior antioxidant properties compared to native HA, thereby inhibiting the activation of NF‐κB signaling. 24 …”

Section: Discussionmentioning

confidence: 99%

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Glutamic‐acid grafted hyaluronic acid inhibits inflammatory factors via fibroblast and skin model tests

Jiang,

Wang,

Han

et al. 2024

Skin Research and Technology

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BackgroundExcessive inflammation may cause tissue damage and disrupt the function of the skin barrier. Hyaluronic acid (HA), an endogenous component, was found to regulate multiple inflammatory factors for skin health. This work aims to further enhance its efficacy by grafting amino acid onto its molecule.MethodsGlutamic acid (Glu) was selected as the ligand to react with low‐molecular‐weight HA. Fibroblast tests and a 3D skin model were used to investigate the anti‐inflammation efficacy of HA‐Glu.ResultsFor IL‐1α, IL‐6 and TNF‐α, the grafted compound presents stronger inhibition ability versus native HA. Moreover, HA‐Glu could promote the repair of damaged skin by improving the compactness of the stratum corneum and increasing the thickness of the living cell layer.ConclusionThe application of HA‐Glu compound in skin care formulas would be effective to alleviate inflammation‐induced skin symptoms and skin aging.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Glutamic‐acid grafted hyaluronic acid inhibits inflammatory factors via fibroblast and skin model tests

Jiang,

Wang,

Han

et al. 2024

Skin Research and Technology

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“…Previous studies have shown that inflammatory signaling pathways, such as NF-κB and JAKs/STATs, can interact with one another and play critical roles in triggering, promoting, and regulating inflammatory responses [ 46 ]. NF-κB can induce STAT1 synthesis and promote STAT1 activation.…”

Section: Discussionmentioning

confidence: 99%

Abrocitinib Attenuates Microglia-Mediated Neuroinflammation after Traumatic Brain Injury via Inhibiting the JAK1/STAT1/NF-κB Pathway

Peng

et al. 2022

Cells

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Background and Purpose: Neuroinflammation has been shown to play a critical role in secondary craniocerebral injury, leading to poor outcomes for TBI patients. Abrocitinib, a Janus kinase1 (JAK1) selective inhibitor approved to treat atopic dermatitis (AD) by the Food and Drug Administration (FDA), possesses a novel anti-inflammatory effect. In this study, we investigated whether abrocitinib could ameliorate neuroinflammation and exert a neuroprotective effect in traumatic brain injury (TBI) models. Methods: First, next-generation sequencing (NGS) was used to select genes closely related to neuroinflammation after TBI. Then, magnetic resonance imaging (MRI) was used to dynamically observe the changes in traumatic focus on the 1st, 3rd, and 7th days after the induction of fluid percussion injury (FPI). Moreover, abrocitinib’s effects on neurobehaviors were evaluated. A routine peripheral blood test was carried out and Evans blue dye extravasation, cerebral cortical blood flow, the levels of inflammatory cytokines, and changes in the numbers of inflammatory cells were evaluated to investigate the function of abrocitinib on the 1st day post-injury. Furthermore, the JAK1/signal transducer and activator of transcription1 (STAT1)/nuclear factor kappa (NF-κB) pathway was assessed. Results: In vivo, abrocitinib treatment was found to shrink the trauma lesions. Compared to the TBI group, the abrocitinib treatment group showed better neurological function, less blood-brain barrier (BBB) leakage, improved intracranial blood flow, relieved inflammatory cell infiltration, and reduced levels of inflammatory cytokines. In vitro, abrocitinib treatment was shown to reduce the pro-inflammatory M1 microglia phenotype and shift microglial polarization toward the anti-inflammatory M2 phenotype. The WB and IHC results showed that abrocitinib played a neuroprotective role by restraining JAK1/STAT1/NF-κB levels after TBI. Conclusions: Collectively, abrocitinib treatment after TBI is accompanied by improvements in neurological function consistent with radiological, histopathological, and biochemical changes. Therefore, abrocitinib can indeed reduce excessive neuroinflammation by restraining the JAK1/STAT1/NF-κB pathway.

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“…In another animal model focused on acute gouty arthritis and hyperuricemia, N-butylated-HA exerted anti-inflammatory and antioxidative properties. The study underlines that the anti-inflammation properties of HA are linked to its antioxidative ones [ 120 ].…”

Section: Ros-generated Ha In Inflammationmentioning

confidence: 99%

Hyaluronan and Reactive Oxygen Species Signaling—Novel Cues from the Matrix?

et al. 2023

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Hyaluronan (HA) is a naturally occurring non-sulfated glycosaminoglycan (GAG) localized to the cell surface and the tissue extracellular matrix (ECM). It is composed of disaccharides containing glucuronic acid and N-acetylglucosamine, is synthesized by the HA synthase (HAS) enzymes and is degraded by hyaluronidase (HYAL) or reactive oxygen and nitrogen species (ROS/RNS) actions. HA is deposited as a high molecular weight (HMW) polymer and degraded to low molecular weight (LMW) fragments and oligosaccharides. HA affects biological functions by interacting with HA-binding proteins (hyaladherins). HMW HA is anti-inflammatory, immunosuppressive, and antiangiogenic, whereas LMW HA has pro-inflammatory, pro-angiogenetic, and oncogenic effects. ROS/RNS naturally degrade HMW HA, albeit at enhanced levels during tissue injury and inflammatory processes. Thus, the degradation of endothelial glycocalyx HA by increased ROS challenges vascular integrity and can initiate several disease progressions. Conversely, HA exerts a vital role in wound healing through ROS-mediated HA modifications, which affect the innate immune system. The normal turnover of HA protects against matrix rigidification. Insufficient turnover leads to increased tissue rigidity, leading to tissue dysfunction. Both endogenous and exogenous HMW HA have a scavenging capacity against ROS. The interactions of ROS/RNS with HA are more complex than presently perceived and present an important research topic.

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N-Butyrylated Hyaluronic Acid Achieves Anti-Inflammatory Effects In Vitro and in Adjuvant-Induced Immune Activation in Rats

Cited by 9 publications

References 46 publications

Glutamic‐acid grafted hyaluronic acid inhibits inflammatory factors via fibroblast and skin model tests

Glutamic‐acid grafted hyaluronic acid inhibits inflammatory factors via fibroblast and skin model tests

Abrocitinib Attenuates Microglia-Mediated Neuroinflammation after Traumatic Brain Injury via Inhibiting the JAK1/STAT1/NF-κB Pathway

Hyaluronan and Reactive Oxygen Species Signaling—Novel Cues from the Matrix?

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