Lycium ruthenicum Murr polysaccharide protects cortical neurons against oxygen-glucose deprivation/reperfusion in neonatal hypoxic-ischemic encephalopathy

Deng, Kewei; Li, Yanling; Xiao, Mei; Wang, Fanghui; Zhou, Ping; Zhang, Wei; Heep, Axel; Li, Xiaoquan

doi:10.1016/j.ijbiomac.2020.04.122

Cited by 36 publications

(24 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Therefore, by regulating Nrf2 levels, the downstream cascade is activated to relieve the body's oxidative stress and in ammation [39]. In recent years, some anti-oxidative stress and anti-in ammatory drugs such as licochalcone A, Lycium ruthenicum polysaccharide 3 (LRP3) have been revealed to up-regulate Nrf2 intranuclear metastasis to exert neuroprotective effects, which is consistent with our present ndings [40,41]. NF-kB is an important nuclear transcription factor in cells.…”

Section: Discussionsupporting

confidence: 89%

Chlorogenic Acid Exerts Neuroprotective Effect Against Hypoxia-Ischemia Brain Injury in Neonatal Rats by activating Sirt1 to Regulate the Nrf2-NF-κB Signaling Pathway

Zheng

Lin

et al. 2021

Preprint

View full text Add to dashboard Cite

Background: Neonatal hypoxic-ischemic brain injury (HIE) is caused by perinatal asphyxia, which is associated with various confounding factors. Although studies on the pathogenesis and treatment of HIE have matured, sub-hypothermia is the only clinical treatment available for HIE. Previous evidence indicates that chlorogenic acid (CGA) exerts a potential neuroprotective effect on brain injury. However, the role of CGA on neonatal HI brain damage and the exact mechanism remains elusive. Here, we investigate the effects of CGA on HI models in vivo and in vitro and explore the underlying mechanism. Methods: In the in vivo experiment, we ligated the left common carotid artery of 7-day-old rats and placed the rats in a hypoxic box for 2 hours. We did not ligate the common carotid artery of the pups in the sham group since they did not have hypoxia. Brain atrophy and infarct size were evaluated by Nissl staining, HE staining and 2,3,5-triphenyltetrazolium chloride monohydrate (TTC) staining. Morris Water Maze test (MWM) was used to evaluate neurobehavioral disorders. Western-blotting and immunofluorescence were used to detect the cell signaling pathway. Malondialdehyde (MDA) content test, catalase (CAT) activity detection and Elisa Assay was used to detect levels of inflammation and oxidative stress. In vitro experiments were performed on isolated primary neurons.Result: In our study, pretreatment with CGA significantly decreased the infarct volume of neonatal rats after HI, alleviated brain edema, and improved tissue structure in vivo. Moreover, we used the Morris water maze to verify CGA’s effects on enhancing the learning and cognitive ability and helping to maintain the long-term spatial memory after HI injury. However, Sirt1 inhibitor EX-527 partially reversed these therapeutic effects. CGA pretreatment inhibited neuronal apoptosis induced by HI by reducing inflammation and oxidative stress. The findings suggest that CGA potentially activates Sirt1 to regulate the Nrf2-NF-κB signaling pathway by forming complexes thereby protecting primary neurons from oxygen-glucose deprivation (OGD) damage. Also, CGA treatment significantly suppresses HI-induced proliferation of glial.Conclusion: Collectively, this study uncovered the underlying mechanism of CGA on neonatal HI brain damage. CGA holds promise as an effective neuroprotective agent to promote neonatal brain recovery from HI-induced injury.

show abstract

Section: Discussionsupporting

confidence: 89%

Chlorogenic Acid Exerts Neuroprotective Effect Against Hypoxia-Ischemia Brain Injury in Neonatal Rats by activating Sirt1 to Regulate the Nrf2-NF-κB Signaling Pathway

Zheng

Lin

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…Gao et al reported that upregulation of Nrf2 and HO-1 expression relieves oxidative stress and alleviates HIE in neonatal rats ( 37 ). Results from Deng group also showed that lycium ruthenicum polysaccharide 3 (LRP3) protects cortical neurons against neonatal HIE via activation of Nrf2/HO-1 pathway ( 38 ). In addition, Nrf2/HO-1 pathway plays an important role in ferroptosis.…”

Section: Discussionmentioning

confidence: 99%

Vitamin D suppresses ferroptosis and protects against neonatal hypoxic-ischemic encephalopathy by activating the Nrf2/HO-1 pathway

Cai¹,

Li²,

Tan³

et al. 2022

Transl Pediatr

View full text Add to dashboard Cite

Background: Hypoxic-ischemic encephalopathy (HIE) is a major cause of neonatal death, and vitamin D (VD) is a neuroprotection nutrition whose deficiency is associated with its risk. However, the mechanism of VD involved in neonatal HIE is not well known. Methods:In this experiment a hypoxic-ischemic brain damage (HIBD) model was established by using the Rice-Vannucci method, rats were intraperitoneally injected with 0.1 μg/kg VD every day for two weeks. The brain damage and mitochondria injury were examined by hematoxylin-eosin (HE) staining and transmission electron microscope (TEM), respectively. The oxidation response and inflammatory factors were determined by enzyme-linked immunosorbent assay (ELISA), and the cell viability was determined by Cell Counting Kit-8 (CCK-8). mRNA and protein expression were detected by quantitative real real-time PCR (qRT-PCR), Western blot, and immunofluorescence. Results:The results showed VD effectively ameliorated brain histologic damage and mitochondria injury induced by hypoxic ischemia (HI). VD elevated the expression of Nrf2 and HO-1, which resulted in increased levels of GPX4, superoxide dismutase (SOD), and glutathione (GSH) and reduced content of malondialdehyde (MDA) and reactive oxygen species (ROS), resulting in decreased ferroptosis in HItreated rats. Moreover, VD reduced the secretion of inflammatory factors, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β.Conclusions: VD suppresses ferroptosis through activation of the Nrf2/HO-1 signaling pathway and exerts a protective role in neonatal HIE.

show abstract

“…The cells were routinely cultured in Ham's F-12K (Kaighn's) medium, containing 15% fetal bovine serum (FBS), at 37°C in 95% air and 5% CO 2 . To mimic the hypoxic-ischemic conditions of the LIRI in vitro experiment, we subjected NR8383 cells to OGD/R as described [29]. Brie y, NR8383 cells were washed three times with pre-warmed (37°C) glucose-free balanced salt solution (PBS), fed serum-free and glucose-free Ham's F-12K medium, and then cultured for 1 h at 37°C in a Whitley H35 Hypoxystation (Don Whitley Scienti c, West Yorkshire, UK) in a hypoxic atmosphere of 1% O 2 , 5% CO 2 , and 94% N 2 .…”

Section: Ams Model Of Ogd/rmentioning

confidence: 99%

PD-1 induced-alveolar macrophages M1 polarization contributes to lung ischemia-reperfusion injury via SHP1/2-PI3K/Akt signaling

Lin

Xiao

et al. 2022

Preprint

View full text Add to dashboard Cite

Background: Lung ischemia-reperfusion injury (LIRI) is a common and complex pathophysiological process. Activation of alveolar macrophages (AMs) is involved in the inflammatory response and tissue damage during LIRI. Programmed cell death factor-1 (PD-1) plays an important role in immunomodulatory participants in diseases progression by regulating apoptosis and polarization of macrophages. In this study, we investigated the function of PD-1 on macrophage polarization during pulmonary ischemia-reperfusion.Methods: We conducted experiments both in a rat model of lung ischemia/reperfusion injury and in NR8383 cells (a rat alveolar macrophage line) model of oxygen-glucose deprivation-reoxygenation (OGD/R). The extent of lung injury was measured by pathohistological lung tissue damage, wet/dry ratios of pulmonary tissue, levels of inflammatory factors. Western blot was used to detect the relative expression of PD-1, SHP1, SHP2, p-Akt, and Akt. Expression of surface markers on macrophages was measured by immunohistochemistry, flow cytometry, and immunofluorescence staining.Results: The results showed that the expression of PD-1 increased in both in vivo and in vitro models, which promoted the polarization of M1 macrophages, resulting in the aggravation of the pulmonary ischemia-reperfusion injury. These effects were at least partially attributable to PD-1 inhibiting the PI3K/Akt pathway by regulating SHP1/2. Conclusion: PD-1 may exacerbate LIRI by promoting macrophage polarization, and inhibition of PD-1 may be an important role and therapeutic target of acute lung injury.

show abstract

Lycium ruthenicum Murr polysaccharide protects cortical neurons against oxygen-glucose deprivation/reperfusion in neonatal hypoxic-ischemic encephalopathy

Cited by 36 publications

References 26 publications

Chlorogenic Acid Exerts Neuroprotective Effect Against Hypoxia-Ischemia Brain Injury in Neonatal Rats by activating Sirt1 to Regulate the Nrf2-NF-κB Signaling Pathway

Chlorogenic Acid Exerts Neuroprotective Effect Against Hypoxia-Ischemia Brain Injury in Neonatal Rats by activating Sirt1 to Regulate the Nrf2-NF-κB Signaling Pathway

Vitamin D suppresses ferroptosis and protects against neonatal hypoxic-ischemic encephalopathy by activating the Nrf2/HO-1 pathway

PD-1 induced-alveolar macrophages M1 polarization contributes to lung ischemia-reperfusion injury via SHP1/2-PI3K/Akt signaling

Contact Info

Product

Resources

About