Dioscin alleviates Alzheimer's disease through regulating RAGE/NOX4 mediated oxidative stress and inflammation

Guan, Linshu; Zhang, Mao; Yang, Sen; Wu, Guanlin; Chen, Yurong; Yin, Lianhong; Yan, Qi; Han, Lei; Xu, Lina

doi:10.1016/j.biopha.2022.113248

Cited by 33 publications

(17 citation statements)

References 79 publications

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“…SH-SY5Y cells have obvious protrusions in morphology, and their physiological and biochemical functions are similar to those of normal nerve cells. After spinal cord injury, the body accumulates a large number of free radicals and the tissue clearance ability is reduced, which leads to a large number of neuronal apoptosis, 37 Our findings in the SH-SY5Y and BV2 cell lines should be verified and extended using more realistic preclinical models.…”

Section: Resultsmentioning

confidence: 60%

“…H 2 O 2 is a neurotoxic reactive oxygen species, which increases significantly after spinal cord injury. Therefore, in this study, H 2 O 2 was used to stimulate SH-SY5Y cells to construct an in vitro nerve cell damage model, to characterize the neuroprotective effect of drugs . Our findings in the SH-SY5Y and BV2 cell lines should be verified and extended using more realistic preclinical models.…”

Section: Resultsmentioning

confidence: 90%

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Injectable Hydrogel To Deliver Bone Mesenchymal Stem Cells Preloaded with Azithromycin To Promote Spinal Cord Repair

Wan,

Lin,

Tan

et al. 2024

ACS Nano

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Spinal cord injury is a disease that causes severe damage to the central nervous system. Currently, there is no cure for spinal cord injury. Azithromycin is commonly used as an antibiotic, but it can also exert anti-inflammatory effects by down-regulating M1-type macrophage genes and up-regulating M2-type macrophage genes, which may make it effective for treating spinal cord injury. Bone mesenchymal stem cells possess tissue regenerative capabilities that may help promote the repair of the injured spinal cord. In this study, our objective was to explore the potential of promoting repair in the injured spinal cord by delivering bone mesenchymal stem cells that had internalized nanoparticles preloaded with azithromycin. To achieve this objective, we formulated azithromycin into nanoparticles along with a trans-activating transcriptional activator, which should enhance nanoparticle uptake by bone mesenchymal stem cells. These stem cells were then incorporated into an injectable hydrogel. The therapeutic effects of this formulation were analyzed in vitro using a mouse microglial cell line and a human neuroblastoma cell line, as well as in vivo using a rat model of spinal cord injury. The results showed that the formulation exhibited anti-inflammatory and neuroprotective effects in vitro as well as therapeutic effects in vivo. These results highlight the potential of a hydrogel containing bone mesenchymal stem cells preloaded with azithromycin and trans-activating transcriptional activator to mitigate spinal cord injury and promote tissue repair.

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Section: Resultsmentioning

confidence: 60%

Section: Resultsmentioning

confidence: 90%

Injectable Hydrogel To Deliver Bone Mesenchymal Stem Cells Preloaded with Azithromycin To Promote Spinal Cord Repair

Wan,

Lin,

Tan

et al. 2024

ACS Nano

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“…The Nissl damage was considerably improved in the Bor-Sch B-Ms therapy group compared to the Sch B-Ms group; the free Sch B group showed the least impact (Figure B). Moreover, immunofluorescence labeling was used to study the expression of the neuronal protein NeuN in order to further assess the degree of neuronal injury . In Figure C, the highest expression of NeuN was identified in the cortex, hippocampus, and CA1 of the blank group, indicating that the neurons were in good condition.…”

Section: Resultsmentioning

confidence: 99%

“…Moreover, immunofluorescence labeling was used to study the expression of the neuronal protein NeuN in order to further assess the degree of neuronal injury. 52 In Figure 8C Numerous studies have found that oxidative stress plays a crucial role in the onset and progression of Alzheimer's disease. As a result, increasing cellular antioxidant capability is critical for preventing oxidative stress.…”

Section: Neuroprotective Effect Of Bor-sch B-ms On D-gal-induced Mode...mentioning

confidence: 99%

Borneol-Modified Schisandrin B Micelles Cross the Blood–Brain Barrier To Treat Alzheimer’s Disease in Aged Mice

Li,

Yu,

et al. 2024

ACS Chem. Neurosci.

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Objective: Schisandrin B (Sch B) is a bioactive dibenzocyclooctadiene derizative that is prevalent in the fruit of Schisandra chinensis. Numerous studies have demonstrated that Sch B has a neuroprotective action by reducing oxidative stress and effectively preventing inflammation. It follows that Sch B is a potential treatment for Alzheimer's disease (AD). However, the drug's solubility, bioavailability, and lower permeability of the blood−brain barrier (BBB) can all reduce its efficacy during the therapy process. Therefore, this study constructed borneolmodified schisandrin B micelles (Bor-Sch B-Ms), which increase brain targeting by accurately delivering medications to the brain, effectively improving bioavailability. High therapeutic efficacy has been achieved at the pathological site. Methods: Bor-Sch B-Ms were prepared using the thin film dispersion approach in this article. On the one hand, to observe the targeting effect of borneol, we constructed a blood−brain barrier (BBB) model in vitro and studied the ability of micelles to cross the BBB. On the other hand, the distribution of micelle drugs and their related pharmacological effects on neuroinflammation, oxidative stress, and neuronal damage were studied through in vivo administration in mice. Results: In vitro studies have demonstrated that the drug uptake of bEnd.3 cells was increased by the borneol alteration on the surface of the nano micelles, implying that Bor-Sch B-Ms can promote the therapeutic effect of N 2 a cells. This could result in more medicines entering the BBB. In addition, in vivo studies revealed that the distribution and circulation time of medications in the brain tissue were significantly higher than those in other groups, making it more suitable for the treatment of central nervous system diseases. Conclusion: As a novel nanodrug delivery system, borneol modified schisandrin B micelles have promising research prospects in the treatment of Alzheimer's disease.

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“…The receptor for advanced glycation end products ( RAGE ), which belongs to the immunoglobulin superfamily, acts as a critical player under physiological and pathological conditions ( 13 ). Moreover, it is believed that RAGE is not only an inflammatory intermediary but also a key inducer of oxidative stress ( 14 ). It was reported previously that RAGE regulation is important for the improvement of sepsis-associated lung injury.…”

Section: Introductionmentioning

confidence: 99%

Idebenone reduces sepsis-induced oxidative stress and apoptosis in hepatocytes via RAGE/p38 signaling

Gou¹,

Jin²,

Xia³

2022

Ann Transl Med

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Background: Sepsis-induced liver dysfunction is believed to be an independent risk factor for multiple organ dysfunction and death. Idebenone (IDE), a synthetic analog of coenzyme Q10 (CoQ10), possesses an antioxidizing property. The present study aimed to investigate the efficacy of IDE on sepsis-induced liver injury and discuss its reaction mechanism in vivo and in vitro. Methods:To establish an in vivo model of sepsis-induced liver injury, rats were treated with highgrade cecal ligation and puncture (CLP). Hematoxylin-eosin staining was applied to observe the liver pathological changes, and liver function was examined using alanine aminotransferase (ALT) and aspartate aminotransferase (AST) assay kits. Enzyme-linked immunosorbent assay (ELISA) kits were employed to assess the levels of inflammatory cytokines in serum and tissues. The activities of malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were analyzed using MDA, SOD, and GSH-Px assay kits, respectively. The apoptosis of liver tissues was measured by terminal deoxynucleotidyl transferase-mediated nick-end labeling (TUNEL) staining, and western blot was employed to estimate apoptosis-related proteins. In vitro, 0.5 μg/mL lipopolysaccharide (LPS) was adopted to administrate primary hepatocytes. The expressions of receptor for advanced glycation end products (RAGE)/p38-related proteins were evaluated by western blot. Cell counting kit-8 (CCK-8) and dichloro-dihydro-fluorescein diacetate (DCFH-DA) assays were utilized to estimate cell viability and reactive oxygen species (ROS) content.Moreover, the transfection efficacy of overexpression (Ov)-RAGE in primary hepatocytes was tested by realtime quantitative polymerase chain reaction (RT-qPCR) and western blot.Results: IDE could improve liver function and reduce sepsis-induced pathological damage. The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) in the serum and liver tissue of sepsis rats were suppressed by IDE. Additionally, IDE repressed the oxidative stress and apoptosis of liver tissues in sepsis-induced rats. IDE also inhibited RAGE/p38 signaling. Furthermore, IDE revived the decreased viability in LPS-induced hepatocytes concentration-dependently. After overexpressing RAGE, RAGE expression in hepatocytes was significantly elevated. Further functional experiments revealed that IDE attenuated cell viability injury, apoptosis, oxidative stress, and inflammatory damage in LPS-induced hepatocytes via RAGE/p38 signaling.Conclusions: IDE helped to protect against sepsis-induced liver injury via the regulation of RAGE/p38 signaling.

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Dioscin alleviates Alzheimer's disease through regulating RAGE/NOX4 mediated oxidative stress and inflammation

Cited by 33 publications

References 79 publications

Injectable Hydrogel To Deliver Bone Mesenchymal Stem Cells Preloaded with Azithromycin To Promote Spinal Cord Repair

Injectable Hydrogel To Deliver Bone Mesenchymal Stem Cells Preloaded with Azithromycin To Promote Spinal Cord Repair

Borneol-Modified Schisandrin B Micelles Cross the Blood–Brain Barrier To Treat Alzheimer’s Disease in Aged Mice

Idebenone reduces sepsis-induced oxidative stress and apoptosis in hepatocytes via RAGE/p38 signaling

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