scholarly journals Naofucong Ameliorates High Glucose Induced Hippocampal Neuron Injury Through Suppressing P2X7/NLRP1/Caspase-1 Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Guangchan Jing ◽  
Huanyuan Wang ◽  
Fengwei Nan ◽  
Yuqin Liu ◽  
Mengren Zhang
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Hippocampal Neurons ◽  
Hippocampal Neuron ◽  
Neuronal Injury ◽  
Protective Effects ◽  
Ht22 Cells ◽  
Caspase 1 ◽  
Neuron Injury ◽  
Cells Cultured

P2X7/NLRP1/caspase-1 mediated neuronal injury plays an important role in diabetic cognitive impairment and eventually inflammatory cascade reaction. Chinese herbal compound Naofucong has been mainly used to treat cognitive disorders in Traditional Chinese Medicine The present study aimed to investigate whether its neuroprotective effects might be related to the inhibition of P2X7R/NLRP1/caspase-1 mediated neuronal injury or not. In this study, high glucose-induced HT22 hippocampal neurons were used to determine Naofucong-containing serum neuronal protective effects. Lentiviruses knock out of TXNIP and P2X7R was used to determine that protective effects of Naofucong was related to inflammatory response and P2X7/NLRP1/caspase-1 mediated neuronal injury. NAC was also used to inhibit oxidative stress, so as to determine that oxidative stress is an important starting factor for neuronal injury of HT22 cells cultured with high glucose. Naofucong decreased apoptosis, IL-1β and IL-18 levels in high glucose-induced HT22 hippocampal neuron cells. Naofucong suppressed NLRP1/caspase-1 mediated neuronal injury, and P2X7 was involved in process. HT22 cells cultured in high glucose had an internal environment with elevated oxidative stress, which could promote neuronal injury. The current study demonstrated that Naofucong could significantly improve high glucose-induced HT22 hippocampal neuron injury, which might be related to suppress P2X7R/NLRP1/caspase-1 pathway, which provides novel evidence to support the future clinical use of Naofucong.

scholarly journals Norcepharadione B attenuates H2O2-induced neuronal injury by upregulating cellular antioxidants and inhibiting volume-sensitive Cl− channel

2019 ◽  
Vol 244 (16) ◽  
pp. 1463-1474 ◽  
Author(s):  
Xin Jia ◽  
Yan Liu ◽  
Xing Li ◽  
Cong Huo ◽  
Dongtao Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Apoptosis ◽  
Hippocampal Neurons ◽  
Chinese Herb ◽  
Neuronal Injury ◽  
Cell Swelling ◽  
Ht22 Cells ◽  
Aporphine Alkaloid ◽  
Houttuynia Cordata ◽  
Apoptotic Protein

Oxidative stress acts as an essential culprit factor in the development of stroke and Alzheimer’s disease. Norcepharadione B possesses various pharmacologic features as an extract obtained from Houttuynia cordata. Nevertheless, the anti-apoptotic and neuroprotective characteristics of norcepharadione B remain unclear. In this study, the neuronal protection effect provided by norcepharadione B against injury caused by hydrogen peroxide (H2O2) in HT22 cell as well as the fundamental mechanism was systematically explored. The neurotoxicity assays of hippocampal cells, which were co-cultured with H2O2, showed that norcepharadione B had the ability to insulate the toxicity induced by H2O2 with significant reduced cell apoptosis. Besides, norcepharadione B potentiated the activity of superoxide dismutase (SOD), increased the level of glutathione (GSH), and decreased malondialdehyde content. The H2O2-induced apoptotic protein Bax was suppressed, and the anti-apoptotic protein Bcl-2 was boosted by norcepharadione B. Norcepharadione B promoted Akt phosphorylation and further upregulated heme oxygenase (HO-1) in cells exposed to oxidative stress. However, the inductive effect of HO-1 by norcepharadione B was shut off via the PI3K/Akt inhibitor LY294002. Furthermore, 2-h incubation with H2O2 substantially increased cell volume in HT22 cells, while norcepharadione B effectively alleviated such effect by interrupting the activation of VSOR Cl− channel. Collectively, our data revealed protective properties of norcepharadione B in resisting oxidative stress induced by H2O2 through elevation of HO-1 in the dependence of PI3K/Akt and in inhibiting H2O2-induced cell swelling by VSOR Cl− channel obstruction in HT22 cells. Impact statement Norcepharadione B is an aporphine alkaloid compound extracted from Chinese herb Houttuynia cordata. It was well known for its anti-inflammatory, anti-cancer, and anti-platelet aggregation outcomes. Our study demonstrated that Norcepharadione B protected hippocampal neurons against oxidative stress and the resultant cell apoptosis upon H2O2 exposure. Meanwhile, Norcepharadione B also substantially reduced cell swelling induced by H2O2 via inhibiting VSOR Cl− channel in neurons. These findings uncovered the potential mechanisms of Norcepharadione B in protecting neuron apoptosis under oxidative stress and propose that Norcepharadione B may serve as a favorable herb medicine for restoring neuronal injury in the pathogenesis of stroke together with other neurodegenerative diseases.

scholarly journals Dexmedetomidine Reduces Propofol-Induced Hippocampal Neuron Injury by Modulating the miR-377-5p/Arc Pathway

2021 ◽  
Author(s):  
Zong Chen ◽  
Yong Ding ◽  
Ying Zeng ◽  
Xue-Ping Zhang ◽  
Jian-Yan Chen
Keyword(s):  
Promoter Region ◽  
Hippocampal Neurons ◽  
Hippocampal Neuron ◽  
Molecular Mechanisms ◽  
Expression Level ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Luciferase Reporter ◽  
Protective Effects ◽  
Expression Levels ◽  
Neuron Injury

Abstract BackgroundPropofol and dexmedetomidine (DEX) are widely used in general anesthesia, and exert toxic and protective effects on hippocampal neurons, respectively. The study sought to investigate the molecular mechanisms of DEX-mediated neuroprotection against propofol-induced hippocampal neuron injury in mouse brains.MethodsHippocampal neurons of mice were treated with propofol, DEX, and propofol+DEX in vitro and in vivo. Neuronal apoptosis was evaluated by a means of TUNEL (terminal deoxynucleotidyl transferase dUTP nick end labeling) or Hochest 33258 staining; Arc positive expression in hippocampus tissues was detected using a microscope in immunohistochemistry assays; miRNA-377-5p expression levels were quantified by RT-PCR; the protein levels of Arc, DNMT3A, and DNMT3B were determined using western blot; CCK-8 kit was used to evaluated neuron viability; methylation analysis in miR-377-5p promoter was performed through the methylated DNA immunoprecipitation (MeDIP) assay; luciferase reporter assay was performed to confirm whether Arc was under targeted regulation of miR-377-5p.Results In the current study, both in vitro and in vivo, propofol treatment induced hippocampal neuron apoptosis and suppressed cell viability. DNMT3A and DNMT3B expression levels were decreased following propofol treatment, resulting in lowered methylation in the miR-377-5p promoter region and then enhanced expression of miR-377-5p, leading to a decrease in the expression level of downstream Arc. Conversely, the expression levels of DNMT3A and DNMT3B were increased following DEX treatment, thus methylation in miR-377-5p promoter region was improved, and miR-377-5p expression levels were decreased, leading to an increase in the expression level of downstream Arc. Finally, DEX pretreatment protected hippocampal neurons against propofol-induced neurotoxicity by recover the expression levels of DNMT3A, miR-377-5p, and Arc to the normal levels.ConclusionsDEX reduced propofol-induced hippocampal neuron injury via the miR-377-5p/Arc signaling pathway.

Protective Effects of Chungkookjang Extract on High Glucose Induced Oxidative Stress in LLC-PK1Cells

2008 ◽  
Vol 13 (2) ◽  
pp. 84-89 ◽  
Author(s):  
Na-Ri Yi ◽  
Kyoung-Chun Seo ◽  
Ji-Myung Choi ◽  
Eun-Ju Cho ◽  
Young-Ok Song ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Protective Effects

Protective effects of andrographolide derivative AL-1 on high glucose-induced oxidative stress in RIN-m cells

2016 ◽  
Vol 22 (4) ◽  
pp. 499-505 ◽  
Author(s):  
Hui Yan ◽  
Yongmei Li ◽  
Yali Yang ◽  
Zaijun Zhang ◽  
Gaoxiao Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
M Cells ◽  
Protective Effects

scholarly journals Tetrahydrocurcumin Ameliorates Diabetic Cardiomyopathy by Attenuating High Glucose-Induced Oxidative Stress and Fibrosis via Activating the SIRT1 Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
Author(s):  
Kaifeng Li ◽  
Mengen Zhai ◽  
Liqing Jiang ◽  
Fan Song ◽  
Bin Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Signaling Pathway ◽  
Diabetic Cardiomyopathy ◽  
High Glucose ◽  
Therapeutic Potential ◽  
Ros Generation ◽  
Protective Effects ◽  
Collagen Iii

Hyperglycemia-induced oxidative stress and fibrosis play a crucial role in the development of diabetic cardiomyopathy (DCM). Tetrahydrocurcumin (THC), a major bioactive metabolite of natural antioxidant curcumin, is reported to exert even more effective antioxidative and superior antifibrotic properties as well as anti-inflammatory and antidiabetic abilities. This study was designed to investigate the potential protective effects of THC on experimental DCM and its underlying mechanisms, pointing to the role of high glucose-induced oxidative stress and interrelated fibrosis. In STZ-induced diabetic mice, oral administration of THC (120 mg/kg/d) for 12 weeks significantly improved the cardiac function and ameliorated myocardial fibrosis and cardiac hypertrophy, accompanied by reduced reactive oxygen species (ROS) generation. Mechanically, THC administration remarkably increased the expression of the SIRT1 signaling pathway both in vitro and in vivo, further evidenced by decreased downstream molecule Ac-SOD2 and enhanced deacetylated production SOD2, which finally strengthened antioxidative stress capacity proven by repaired activities of SOD and GSH-Px and reduced MDA production. Additionally, THC treatment accomplished its antifibrotic effect by depressing the ROS-induced TGFβ1/Smad3 signaling pathway followed by reduced expression of cardiac fibrotic markers α-SMA, collagen I, and collagen III. Collectively, these finds demonstrated the therapeutic potential of THC treatment to alleviate DCM mainly by attenuating hyperglycemia-induced oxidative stress and fibrosis via activating the SIRT1 pathway.

scholarly journals Neuroprotective Effects of Grape Seed Procyanidins on Ethanol-Induced Injury and Oxidative Stress in Rat Hippocampal Neurons

2020 ◽  
Vol 55 (4) ◽  
pp. 357-366
Author(s):  
Wenyang Jin ◽  
Mizhu Sun ◽  
Bingbing Yuan ◽  
Runzhi Wang ◽  
Hongtao Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hippocampal Neurons ◽  
Primary Cultures ◽  
Neuronal Injury ◽  
Grape Seed ◽  
Neuroprotective Effects ◽  
Dendritic Length ◽  
New Type ◽  
The Brain ◽  
And Oxidative Stress

Abstract Aims Ethanol is a small molecule capable of interacting with numerous targets in the brain, the mechanisms of which are complex and still poorly understood. Studies have revealed that ethanol-induced hippocampal neuronal injury is associated with oxidative stress. Grape seed procyanidin (GSP) is a new type of antioxidant that is believed to scavenge free radicals and be anti-inflammatory. This study evaluated the ability and mechanism by which the GSP improves ethanol-induced hippocampal neuronal injury. Methods Primary cultures of hippocampal neurons were exposed to ethanol (11, 33 and 66 mM, 1, 4, 8, 12 and 24 h) and the neuroprotective effects of GSP were assessed by evaluating the activity of superoxide dismutase (SOD), the levels of malondialdehyde (MDA) and lactate dehydrogenase (LDH) and cell morphology. Results Our results indicated that GSP prevented ethanol-induced neuronal injury by reducing the levels of MDA and LDH, while increasing the activity of SOD. In addition, GSP increased the number of primary dendrites and total dendritic length per cell. Conclusion Together with previous findings, these results lend further support to the significance of developing GSP as a therapeutic tool for use in the treatment of alcohol use disorders.

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