MiR-582-5p attenuates neonatal hypoxic-ischemic encephalopathy by targeting high mobility group box 1 (HMGB1) through inhibiting neuroinflammation and oxidative stress

2021 ◽  
Vol 18 ◽  
Author(s):  
Guang Yang ◽  
Zhimin Xue ◽  
Yuan Zhao
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Pc12 Cells ◽  
Pc12 Cell ◽  
Cell Injury ◽  
High Mobility ◽  
High Mobility Group ◽  
Hypoxic Ischemic Encephalopathy ◽  
And Oxidative Stress ◽  
Ischemic Encephalopathy

Background: MiR-582-5p has been demonstrated to protect against ischemic stroke. However, its implication in the progression of neonatal hypoxic-ischemic encephalopathy (HIE) has not been explored. Methods: In this study, we used an in vitro model of oxygen-glucose deprivation (OGD) to investigate the protective effect of miR-582-5p on PC12 cells. OGD-induced inhibition of cell viability and promotion of cell death was assessed by CCK-8 assay and flow cytometry. Real-time PCR and enzyme-linked immunosorbent assay (ELISA) were utilized to examine the levels of inflammatory cytokines. The effects of miR-582-5p on OGD-induced oxidative injury were assessed by the determination of oxidative stress indicators. Furthermore, dual-luciferase reporter assay and gain-offunction assay were used to determine the mechanism of miR-582-5p in OGD-induced cell injury. Results : The expression of miR-582-5p was reduced upon OGD treatment in PC12 cells. Overexpression of miR-582-5p inhibited OGD-induced PC12 cell injury by regulating cell viability, apoptosis, inflammatory responses, and oxidative stress. MiR-582-5p targeted and negatively regulated high mobility group box 1 (HMGB1). MiR-582-5p presented protective effects on OGD-induced PC12 cell injury by targeting HMGB1. Conclusion: Our results indicated that miR-582-5p ameliorates neuronal injury by inhibiting apoptosis, inflammation, and oxidative stress through targeting HMGB1.

scholarly journals Brain Hypothermic Therapy Dramatically Decreases Elevated Blood Concentrations of High Mobility Group Box 1 in Neonates with Hypoxic-Ischemic Encephalopathy

2013 ◽  
Vol 35 ◽  
pp. 327-330 ◽  
Author(s):  
Toshihiko Nakamura ◽  
Shingo Yamada ◽  
Toshirou Yoshioka
Keyword(s):  
Reference Values ◽  
Early Stage ◽  
High Mobility ◽  
High Mobility Group ◽  
Hypoxic Ischemic Encephalopathy ◽  
Hmgb1 Level ◽  
Blood Concentrations ◽  
Successful Resuscitation ◽  
Significant Difference ◽  
Ischemic Encephalopathy

Background. According to the Consensus 2010 of the International Liaison Committee on Resuscitation (ILCOR), children with moderate to severe hypoxic-ischemic encephalopathy (HIE) should receive brain hypothermic therapy (BHT) after successful resuscitation. Elevated high mobility group box 1 (HMGB1) in the blood at the early stage of brain ischemia-reperfusion injury has been suggested to be involved in the release of various inflammatory cytokines.Methods. In total, 21 neonates plasma HMGB1 concentration was measured. These neonates included 8 with HIE in whom BHT was indicated, 5 controls diagnosed as having HIE but who were not suitable candidates for BHT, and 8 normal controls.Results. The umbilical artery HMGB1 (UA-HMGB1) level before undergoing BHT significantly exceeded reference values. The UA-HMGB1 level in the BHT (−) group did not differ significantly from reference values, but was significantly increased 24 hours after birth. Repeated measure ANOVA showed a significant difference in time course changes between the BHT (+) and BHT (−) groups (P=0.0002).Conclusions. This study demonstrated hypothermic therapy to significantly decrease HMGB1. Furthermore, HMGB1 is a useful index of the inhibition of early stage inflammation.

Protective effect of dexmedetomidine on neuronal hypoxic injury through inhibition of miR-134

2021 ◽  
pp. 096032712110237
Author(s):  
Y-J Li ◽  
D-Z Zhang ◽  
Y Xi ◽  
C-A Wu
Keyword(s):  
Oxidative Stress ◽  
Cell Viability ◽  
Pc12 Cells ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Cell Damage ◽  
Annexin V ◽  
Protective Effects ◽  
Gene And Protein Expression ◽  
And Oxidative Stress

Objective: To explore the mechanism of dexmedetomidine (DEX)-mediated miR-134 inhibition in hypoxia-induced damage in PC12 cells. Methods: Hydrogen peroxide (H2O2)-stimulated PC12 cells were divided into control, H2O2, DEX + H2O2, miR-NC/inhibitor + H2O2, and miR-NC/ mimic + DEX + H2O2 groups. Cell viability and apoptosis were assessed by the 3-(4,5-dimethylthiazol(-2-y1)-2,5-diphenytetrazolium bromide (MTT) assay and Annexin V-FITC/PI staining, while gene and protein expression levels were detected by qRT-PCR and western blotting. Reactive oxygen species (ROS) levels were tested by 2′,7′-dichlorodihydrofluorescein diacetate (DCFH-DA) staining, and malondialdehyde (MDA) content was determined with a detection kit. Results: DEX treatment decreased H2O2-elevated miR-134 expression. H2O2-induced PC12 cell damage was improved by DEX and miR-134 inhibitor; additionally, cell viability was increased, while cell apoptosis was reduced. In addition, both DEX and miR-134 inhibitor reduced the upregulated expression of cleaved caspase-3 and increased the downregulated expression of Bcl-2 in H2O2-induced PC12 cells. However, compared to that in the DEX + H2O2 group, cell viability in the mimic + DEX + H2O2 group was decreased, and the apoptotic rate was elevated with increased cleaved caspase-3 and decreased Bcl-2 expression. Inflammation and oxidative stress were increased in H2O2-induced PC12 cells but improved with DEX or miR-134 inhibitor treatment. However, this improvement of H2O2-induced inflammation and oxidative stress induced by DEX in PC12 cells could be reversed by the miR-134 mimic. Conclusion: DEX exerts protective effects to promote viability and reduce cell apoptosis, inflammation, and oxidative stress in H2O2-induced PC12 cells by inhibiting the expression of miR-134.

scholarly journals 1,8-Cineol Attenuated AΒ25-35-Induced PC12 Cell Injury through Reducing Caspase 3 Expression and NO Production

2019 ◽  
Vol 1 (1) ◽  
pp. 12-17
Author(s):  
Ze-qin Zhang ◽  
Hai-jian Li ◽  
Wan-zhong Li ◽  
Lin Wang ◽  
Zhen-zhen Li ◽  
...  
Keyword(s):  
Protein Expression ◽  
Cell Viability ◽  
Pc12 Cells ◽  
Pc12 Cell ◽  
Caspase 3 ◽  
Cell Injury ◽  
Control Group ◽  
No Production ◽  
Detection Assay

Objective To investigate the effect of 1,8-cineol on caspase 3 expression and NO production induced by Aβ25-35 in PC12 cells. Methods PC12 cells were cultured in vitro, and cell injury was induced by Aβ25-35 with a concentration of 20 μM. 1,8-cineol (1, 3, 10 μM) was pretreated before Aβ25-35 treatment. PC12 cell viability was evaluated by MTT detection assay. Caspase 3 protein expression was detected by Western blotting. The level of NO production in PC12 cells was measured using ELISA detection assay kit. Results In cultured PC12 cells in vitro, MTT results showed that 20 μM of Aβ25-35 reduced cell viability significantly compared with control group. The cell viability was increased by pretreatment with 1,8-cineol with concentrations of 3 and 10 μM compared with Aβ25-35 only group. Western blotting results showed compared with control group, caspase 3 expression was increased significantly in 20 μM Aβ25-35 group. Compared with Aβ25-35 group, 1,8-cineol of 3 and 10 μM group reduced caspase 3 protein expression significantly. The level of NO production in PC12 cells was increased significantly, which was decreased by pretreatment with 3 and 10 μM of 1,8-cineol. Conclusions: Our results revealed a protective effect of 1,8-cineol on Aβ25-35 induced PC12 cell injury through inhibition of caspase 3 expression and NO production.

The Effect of Ethyl Pyruvate on High Mobility Group Box I and Oxidative Stress in Induced Rheumatoid Arthritis in Rats

2019 ◽  
Vol 87 (June) ◽  
pp. 2547-2554
Author(s):  
HADEER S. SALAH, M.Sc. OMNIA S. EL-DEEB, M.D. ◽  
SAAD EL-DEEN A. ABO EL-NOEMAN, M.D NAGAH K. GAAFAR, M.D.
Keyword(s):  
Rheumatoid Arthritis ◽  
Oxidative Stress ◽  
Ethyl Pyruvate ◽  
High Mobility ◽  
High Mobility Group ◽  
And Oxidative Stress

microRNA-218 Inhibits Lipopolysaccharide-Induced Bronchial Epithelial Cell Injury by Targeting E2F2

2020 ◽  
Vol 10 (8) ◽  
pp. 1161-1169
Author(s):  
Min Gong ◽  
Zhongmei Mao ◽  
Jinni Chen ◽  
Xin Ye ◽  
Xiaobing Zhou
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Bronchial Epithelial Cell ◽  
Stress Injury ◽  
Bronchial Epithelial ◽  
Oxidative Stress Injury ◽  
And Oxidative Stress

Acute bronchopneumonia is a common hospitalization disease in children and serious acute bronchopneumonia will lead to death of children. MicroRNAs (miRNAs) have been thought to be related to inflammation in many diseases. The present study aimed to investigate the relation between miR218 and E2F2 and the effect of miR-218 overexpression and E2F2 inhibition on the improvement of inflammation in LPS-induced bronchial epithelial cell. BEAS-2B cells were induced by LPS for 0, 6, 12, 24 and 48 h which the cell viability was analyzed by CCK-8 assay. The expression of miR-218 in LPS-induced bronchial epithelial cell and cell transfection was detected by RT-qPCR analysis. The levels of TNF-α, IL-1α, and IL-6 in BEAS2B cells were detected using commercially-available ELISA kits. The levels of ROS, MDA, SOD and LDH were detected by ROS assay kit and oxidative stress assay kit. The cell apoptosis was analyzed by flow cytometry analysis and DAPI and hochest staining. As a result, miR-218 was decreased in LPS-induced bronchial epithelial cell. With the time of LPS treatment extends, the cell viability was decreased. Overexpression of miR-218 reduced the expression of inflammatory cytokines and oxidative stress injury in LPS-induced BEAS2B cells. Overexpression of miR-218 reduced apoptosis of LPS-induced BEAS2B cells. E2F2 was demonstrated be a target of miR-218 which miR-218 overexpression could inhibit the expression of E2F2. E2F2 inhibition could reverse the inflammatory and oxidative stress injury of LPS-induced BEAS2B cells caused by miR-218 inhibition. E2F2 inhibition could reverse the apoptosis of LPS-induced BEAS2B cells caused by miR-218 inhibition. In addition, E2F2 inhibition could reverse the expression of p-STAT1, cleaved-caspase3 and cleaved-caspase9 in LPS-induced BEAS2B cells caused by miR-218 inhibition. In conclusion, this study indicated that miR-218 overexpression and E2F2 inhibition can alleviate the inflammation in LPS-induced bronchial epithelial cell, thereby decreasing the oxidative stress and cell apoptosis.

scholarly journals Typhae pollen polysaccharides protect hypoxia-induced PC12 cell injury via regulation of miR-34a/SIRT1

2020 ◽  
Vol 34 ◽  
pp. 205873842091000
Author(s):  
Shichun Wang ◽  
Qianqian Tang ◽  
Fuchao Ge ◽  
Qing Guo
Keyword(s):  
Western Blot ◽  
Cell Viability ◽  
Pc12 Cells ◽  
Pc12 Cell ◽  
Cell Injury ◽  
Cell Model ◽  
Luciferase Assay ◽  
Signal Pathways ◽  
Qrt Pcr

This current research was performed to investigate the role of typhae pollen polysaccharides (TPP) in hypoxia-treated PC12 cell which was an in vitro cell model of cerebral ischemia. Hypoxia-treated cells were treated with TPP for 12 h. Cell viability and apoptosis were detected by 3-(4,5-dimethylthiazol-2-yl)-2 5-diphenyl-2H-tetrazolium bromide (MTT) assay and flow cytometry, respectively. Cell apoptotic proteins and PI3K/AKT and Ras/Raf/MEK/ERK signal pathway–associated proteins were also examined by western blot. Furthermore, abnormal expression of miR-34a and silent information regulator 1 (SIRT1) was achieved by transfection. Besides, the expression of miR-34a and SIRT1 was examined by quantitative real-time polymerase chain reaction (qRT-PCR). The expression of SIRT1 was detected by qRT-PCR and western blot. The relationship between miR-34a and SIRT1 was verified by luciferase assay. We found that TPP enhanced cell viability and inhibited apoptosis in hypoxia-treated PC12 cells. Moreover, TPP increased the accumulated levels of Bcl-2 while decreased expression of Bax, cleaved Caspase-3, and cleaved PARP. TPP downregulated miR-34a expression while induced by hypoxia. Further results showed that miR-34a overexpression reversed the results led by TPP in cell viability, apoptosis, and its related proteins. In addition, SIRT1 was upregulated by TPP and was verified to be a target of miR-34a. Silence of SIRT1 led to the opposite results led by TPP. In the end, TPP activated PI3K/AKT and Ras/Raf/MEK/ERK signal pathways. In conclusion, TPP plays important roles in regulating cell viability and apoptosis in hypoxia-treated PC12 cells via modulating miR-34a/SIRT1, as well as activating PI3K/AKT and Ras/Raf/MEK/ERK signal pathways.

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