scholarly journals Dexmedetomidine protects PC12 cells from ropivacaine injury through miR-381/LRRC4 /SDF-1/CXCR4 signaling pathway

2020 ◽  
Vol 14 ◽  
pp. 322-329
Author(s):  
Ying Xue ◽  
Tao Xu ◽  
Wei Jiang
Keyword(s):  
Signaling Pathway ◽  
Pc12 Cells ◽  
Cxcr4 Signaling

scholarly journals Resveratrol Protects PC12 Cell against 6-OHDA Damage via CXCR4 Signaling Pathway

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Jing Zhang ◽  
Wenchuang Fan ◽  
Hui Wang ◽  
Lihua Bao ◽  
Guibao Li ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Pc12 Cells ◽  
Molecular Mechanisms ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Immunofluorescent Staining ◽  
Double Staining ◽  
Polyphenolic Compound ◽  
Neuroprotective Effects ◽  
Cxcr4 Signaling

Resveratrol, herbal nonflavonoid polyphenolic compound naturally derived from grapes, has long been acknowledged to possess extensive biological and pharmacological properties including antioxidant and anti-inflammatory ones and may exert a neuroprotective effect on neuronal damage in neurodegenerative diseases. However, the underlying molecular mechanisms remain undefined. In the present study, we intended to investigate the neuroprotective effects of resveratrol against 6-OHDA-induced neurotoxicity of PC12 cells and further explore the possible mechanisms involved. For this purpose, PC12 cells were exposed to 6-OHDA in the presence of resveratrol (0, 12.5, 25, and 50 μM). The results showed that resveratrol increased cell viability, alleviated the MMP reduction, and reduced the number of apoptotic cells as measured by MTT assay, JC-1 staining, and Hoechst/PI double staining (allp<0.01). Immunofluorescent staining and Western blotting revealed that resveratrol averts 6-OHDA induced CXCR4 upregulation (p<0.01). Our results demonstrated that resveratrol could effectively protect PC12 cells from 6-OHDA-induced oxidative stress and apoptosis via CXCR4 signaling pathway.

Irisin Ameliorates Hypoxia/Reoxygenation-Induced Inflammation and Apoptosis in PC12 Cells by Inhibiting TLR4/MYD88 Signaling Pathway

2019 ◽  
Vol 17 (3) ◽  
pp. 329-336
Author(s):  
Wang Jinli ◽  
Xu Fenfen ◽  
Zheng Yuan ◽  
Cheng Xu ◽  
Zhang Piaopiao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Major Complication ◽  
Lactic Dehydrogenase ◽  
Dependent Manner ◽  
Cerebral Ischemic Stroke ◽  
Cerebral Ischemic ◽  
Myd88 Signaling ◽  
Hypoxia Reoxygenation

Cardiovascular disease including cerebral ischemic stroke is the major complication that increases the morbidity and mortality in patients with diabetes mellitus as much as four times. It has been well established that irisin, with its ability to regulate glucose and lipid homeostasis as well as anti-inflammatory and anti-apoptotic properties, has been widely examined for its therapeutic potentials in managing metabolic disorders. However, the mechanism of irisin in the regulation of cerebral ischemic stroke remains unclear. Using PC12 cells as a model, we have shown that hypoxia/reoxygenation inhibits cell viability and increases lactic dehydrogenase. Irisin, in a dose-dependent manner, reversed these changes. The increase in inflammatory mediators (IL-1β, IL-6, and TNF-α) by hypoxia/reoxygenation was reversed by irisin. Furthermore, the cell apoptosis promoted by hypoxia/reoxygenation was also inhibited by irisin. Irisin suppressed TLR4/MyD88 signaling pathway leading to amelioration of inflammation and apoptosis in PC12 cells. Thus, inhibition of TLR4/MyD88 signaling pathway via irisin could be an important mechanism in the regulation of hypoxia/reoxygenation-induced inflammation and apoptosis in PC12 cells.

Neuroprotective effect of NDEELNK from sea cucumber ovum against scopolamine-induced PC12 cells damage through enhancing energy metabolism and upregulation of PKA/BDNF/NGF signaling pathway

2021 ◽  
Author(s):  
Yue Zhao ◽  
Yifei Dong ◽  
Qi Ge ◽  
Pengbo Cui ◽  
Na Sun ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Sea Cucumber ◽  
Molecular Mechanisms ◽  
Neuroprotective Effect ◽  
Ngf Signaling ◽  
Neuroprotective Function

The aim of study was to evaluate the neuroprotective function of sea cucumber ovum peptides-derived NDEELNK and explore underlying molecular mechanisms. NDEELNK exerted neuroprotective effect by improving the acetylcholine (ACh)...

scholarly journals Isorhynchophylline Protects PC12 Cells Against Beta-Amyloid-Induced Apoptosis via PI3K/Akt Signaling Pathway

2013 ◽  
Vol 2013 ◽  
pp. 1-8 ◽  
Author(s):  
Yan-Fang Xian ◽  
Zhi-Xiu Lin ◽  
Qing-Qiu Mao ◽  
Jian-Nan Chen ◽  
Zi-Ren Su ◽  
...  
Keyword(s):  
Signaling Pathway ◽  
Pc12 Cells ◽  
Molecular Mechanisms ◽  
Glycogen Synthase ◽  
Neuroprotective Effect ◽  
Protective Action ◽  
Protective Effects ◽  
Phosphorylated Akt ◽  
Induced Apoptosis

The neurotoxicity of amyloid-β(Aβ) has been implicated as a critical cause of Alzheimer’s disease. Isorhynchophylline (IRN), an oxindole alkaloid isolated fromUncaria rhynchophylla,exerts neuroprotective effect againstAβ25–35-induced neurotoxicityin vitro. However, the exact mechanism for its neuroprotective effect is not well understood. The present study aimed to investigate the molecular mechanisms underlying the protective action of IRN againstAβ25–35-induced neurotoxicity in cultured rat pheochromocytoma (PC12) cells. Pretreatment with IRN significantly increased the cell viability, inhibited the release of lactate dehydrogenase and the extent of DNA fragmentation inAβ25–35-treated cells. IRN treatment was able to enhance the protein levels of phosphorylated Akt (p-Akt) and glycogen synthase kinase-3β(p-GSK-3β). Lithium chloride blockedAβ25–35-induced cellular apoptosis in a similar manner as IRN, suggesting that GSK-3βinhibition was involved in neuroprotective action of IRN. Pretreatment with LY294002 completely abolished the protective effects of IRN. Furthermore, IRN reversedAβ25–35-induced attenuation in the level of phosphorylated cyclic AMP response element binding protein (p-CREB) and the effect of IRN could be blocked by the PI3K inhibitor. These experimental findings unambiguously suggested that the protective effect of IRN againstAβ25–35-induced apoptosis in PC12 cells was associated with the enhancement of p-CREB expression via PI3K/Akt/GSK-3βsignaling pathway.

Abstract 17802: Ips Cells -derived Cardiac Progenitors Induce Dramatic Cardiac Regeneration and Improve Function by Cxcr4 Signaling Pathway in Infarcted Myocardium

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Zeshan Pasha ◽  
Romana Saeed ◽  
Muhammad Ashraf
Keyword(s):  
Stem Cells ◽  
Signaling Pathway ◽  
Small Molecule ◽  
In Vivo Studies ◽  
Immunofluorescent Staining ◽  
Concomitant Treatment ◽  
Post Transplantation ◽  
Cardiac Progenitors ◽  
Cxcr4 Signaling ◽  
Infarcted Myocardium

Background: The participation of endogenous cardiac stem/progenitor cells is limited in restoring cardiac structure and function in the ischemic myocardium which is further aggravated by poor survival and propagation of transplanted stem cells of different origin in the infarcted heart. The goal of this study was to explore the survival and engraftability of newly discovered induced pluripotent stem cells (IPS) in the myocardium following infarction (MI). Methods and Results: Integration free iPS were generated from myoblasts and characterized. Cardiac progenitors (CPs) were created by treatment with a small molecule. CPs proliferation was assessed by BrdU labeling; Differentiation by both RT-PCR and immunofluorescent staining for cardiac markers Nkx2.5, actinin, and -MHC. Gene expression profiling was performed using Affymetrix array. In vivo studies were carried out by injecting CPs or nontreated IPS (3x105), into mouse model of permanent LAD. Echocardiography, histological parameters, TUNEL assay and capillary vessel density were measured 6 weeks post transplantation. Treatment of IPS with a small molecule upregulated Nkx2.5 and maintained up to 4 weeks (p<0.01 vs nontreated IPS). Expression of actinin and -MHC was also detectable at 3 weeks. Increased proliferative activity (p<0.01) evaluated by cell proliferation and Brdu assay was observed. Significant CPs survival and reduced apoptosis were noticed in the small molecule treated iPSC compared to nontreated and/or saline group. Enhanced ejection fraction and fractional shortening (p< 0.05) was observed 6 weeks post transplantation. Interestingly there was 2-3 fold upregulation of chemokines including CCL7, CXCR2, CXCR5. miR Microarray analysis showed upregulation of cardiac specific mir-133,762. Western blot analysis showed increased phospho-Akt levels as compared to nontreated IPSC (p<0.01). Survival and differentiation properties of CPs were abolished by concomitant treatment of IPS with CXR4 blocker (p<0.05). Conclusion: This study provides a novel strategy for generating CPs and their enhanced survival, engraftment and differentiation with the treatment of cardiogenic small molecule post transplantation in the infarcted myocardium through CXCR4 signaling pathway.

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