scholarly journals Sodium ferulate attenuates high‑glucose‑induced oxidative injury in HT22 hippocampal cells

2019 ◽  
Author(s):  
Jiangpei Zhao ◽  
Lerong Liu ◽  
Lingxiao Zhang ◽  
Jing Lv ◽  
Xueli Guo ◽  
...  
Keyword(s):  
High Glucose ◽  
Oxidative Injury ◽  
Sodium Ferulate

scholarly journals Geranylgeranyl Transferase-I Knockout Inhibits Oxidative Injury of Vascular Smooth Muscle Cells and Attenuates Diabetes-Accelerated Atherosclerosis

2020 ◽  
Vol 2020 ◽  
pp. 1-14
Author(s):  
Guo-Ping Chen ◽  
Jian Yang ◽  
Guo-Feng Qian ◽  
Wei-Wei Xu ◽  
Xiao-Qin Zhang
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
High Glucose ◽  
Oxidative Injury ◽  
Accelerated Atherosclerosis ◽  
Vsmc Proliferation ◽  
Geranylgeranyl Transferase

The proliferation of vascular smooth muscle cells (VSMCs) induced by oxidative injury is one of the main features in diabetes-accelerated atherosclerosis. Geranylgeranyl transferase-I (GGTase-I) is an essential enzyme mediating posttranslational modification, especially the geranylgeranylation of small GTPase, Rac1. Our previous studies found that GGTase-I played an important role in diabetes-accelerated atherosclerosis. However, its exact role is largely unclear. In this study, mouse conditional knockout of VSMC GGTase-I (Pggt1bΔ/Δ mice) was generated using the CRISPR/Cas9 system. The mouse model of diabetes-accelerated atherosclerosis was induced by streptozotocin injections and an atherogenic diet. We found that GGTase-I knockout attenuated diabetes-accelerated atherosclerosis in vivo and suppressed high-glucose-induced VSMC proliferation in vitro. Moreover, after a 16-week duration of diabetes, Pggt1bΔ/Δ mice exhibited lower α-smooth muscle actin (α-SMA) and nitrotyrosine level, Rac1 activity, p47phox and NOXO1 expression, and phospho-ERK1/2 and phosphor-JNK content than wild-type mice. Meanwhile, the same changes were found in Pggt1bΔ/Δ VSMCs cultured with high glucose (22.2 mM) in vitro. In conclusion, GGTase-I knockout efficiently blocked diabetes-accelerated atherosclerosis, and this protective effect must be related to the inhibition of VSMC proliferation. The potential mechanisms probably involved interfering Rac1 geranylgeranylation, inhibiting the assembly of NADPH oxidase cytosolic regulatory subunits, reducing oxidative injury, and decreasing ERK1/2 and JNK phosphorylation.

scholarly journals Aloperine attenuates high glucose-induced oxidative injury in Schwann cells via activation of NRF2/HO-1 pathway

2020 ◽  
Vol 19 (6) ◽  
pp. 1147-1152
Author(s):  
Yiran Chen ◽  
Tieming Ma ◽  
Zhimin Wang ◽  
Lianqun Jia ◽  
Xiaoqing Zhang ◽  
...  
Keyword(s):  
Cell Viability ◽  
Schwann Cells ◽  
High Glucose ◽  
Cell Injury ◽  
Annexin V ◽  
Oxidative Injury ◽  
Heme Oxygenase 1 ◽  
Related Factor ◽  
Oxygen Species ◽  
Potent Drug

Purpose: To determine the involvement of nuclear factor erythroid 2-related factor 2 (NRF2) and heme oxygenase-1 (HO-1) in the action of aloperine on Schwann cell injury caused by high glucose (HG).Methods: Cell viability was determined using MTT assay while the release of lactate dehydrogenase (LDH) was determined by biochemical assay. Apoptosis was assessed using flow cytometry, while the levels of malondialdehyde (MDA) were determined by Annexin V-FIT staining. Glutathione Stransferase (GST), glutathione peroxidase (GPX), and reactive oxygen species (ROS) were determined using enzyme-linked immunosorbent assay.Results: Treatment with HG suppressed RSC96 cell viability and increased LDH release, while aloperine reversed these results (p < 0.05). Apoptosis of RSC96 cells was induced by HG stimulation, but was abolished by aloperine. The levels of ROS, MDA, and GST were enhanced in cells followingtreatment with HG, but was reversed by aloperine (p < 0.05). The decreased level of GPX caused by HG in RSC96 cells was elevated by aloperine. Moreover, aloperine upregulated NRF2 and HO-1 in RSC96 cells treated with HG (p < 0.05).Conclusion: Aloperine attenuates HG-induced oxidative injury in Schwann cells via activation of NRF2/HO-1 pathway, suggesting its potential as a potent drug for the management of diabetic peripheral neuropathy. Keywords: Aloperine, Schwann cells, High glucose, Oxidative stress, NRF2, HO-1

The Nrf2 activator MIND4‐17 protects retinal ganglion cells from high glucose‐induced oxidative injury

2020 ◽  
Vol 235 (10) ◽  
pp. 7204-7213 ◽  
Author(s):  
Nan Chen ◽  
Ya Li ◽  
Nan Huang ◽  
Jin Yao ◽  
Wei‐Feng Luo ◽  
...  
Keyword(s):  
Retinal Ganglion Cells ◽  
High Glucose ◽  
Ganglion Cells ◽  
Oxidative Injury ◽  
Retinal Ganglion ◽  
Nrf2 Activator

Paeoniflorin protects Schwann cells against high glucose induced oxidative injury by activating Nrf2/ARE pathway and inhibiting apoptosis

2016 ◽  
Vol 185 ◽  
pp. 361-369 ◽  
Author(s):  
Xinwei Yang ◽  
Weijie Yao ◽  
Haotian Shi ◽  
Haolong Liu ◽  
Yangfan Li ◽  
...  
Keyword(s):  
Schwann Cells ◽  
High Glucose ◽  
Oxidative Injury
Sign in / Sign up

Export Citation Format

Share Document