scholarly journals RNA-Seq Based Transcriptome Analysis of Ethanol Extract of Saffron Protective Effect Against Corticosterone-Induced PC12 Cell Injury

2021 ◽  
Author(s):  
Xi Chen ◽  
Ting Yang ◽  
Cong' en Zhang ◽  
Zhijie Ma
Keyword(s):  
Protective Effect ◽  
Pc12 Cells ◽  
Pc12 Cell ◽  
Cell Injury ◽  
Ethanol Extract ◽  
Mapk Signaling ◽  
Cell Counting ◽  
Rna Seq ◽  
Traditional Chinese Herbal Medicine ◽  
Water Test

Abstract Background Saffron is a traditional Chinese herbal medicine, which is typically used in clinical to regulate anxiety, tension, and other depression-related conditions. The study aimed to explore the neuroprotective effect of ethanol extract of saffron (EES) on corticosterone (CORT)-induced injury in PC12 cells and further explored its potential mechanism. Methods The authenticity of saffron and the active components of EES were identified by a water test and ultra-performance liquid chromatography-time of flight mass spectrometry system. The screening of cytotoxicity for PC12 cells was incubated with EES in different concentrations for 24 h, and the protective efficacy of EES on CORT (500 µM) induced PC12 cell injury, cell viability was assessed by Cell Counting Kit-8 (CCK-8) assay. The DEGs of EES-protected PC12 cells were analyzed using the RNA-seq method, and the results were analyzed for GO and KEGG enrichment. The results of RNA-seq were verified by qPCR analysis. Results The saffron was initially identified as authentic in the water test and 10 compounds were identified by UPLC-MS. The results of CCK-8 demonstrated that EES at concentrations above 640 µg/mL exerted a certain cytotoxic effect, and PC12 cells pretreated with EES (20, 40, and 80 µg/mL) significantly reversed the 500 µM CORT-induced cell death. RNA-seq analysis showed that EES regulated 246 differential genes, which were mainly enriched in the MAPK signaling pathway. Dusp5, Dusp6, Gadd45b, Gadd45G, and Pdgfc were further validated by qPCR. Experimental data showed that the results of qPCR were consistent with RNA-seq. Conclusions These findings provide an innovative understanding of the molecular mechanism of the protective effect of EES on PC12 cells at the molecular transcription level, and the above molecules may be potential novel targets for antidepressant treatment.

scholarly journals NLRC5 alleviated OGD/R-induced PC12-cell injury by inhibiting activation of the TLR4/MyD88/NF-κB pathway

2020 ◽  
Vol 48 (8) ◽  
pp. 030006052094045
Author(s):  
Zhen Zhang ◽  
Yuhan Sun ◽  
Xin Chen
Keyword(s):  
Cerebral Ischemia ◽  
Oxidative Damage ◽  
Pc12 Cells ◽  
Pc12 Cell ◽  
Cell Injury ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Apoptosis Rate

Objective To assess the role of NOD-like receptor C5 (NLRC5; a major NLRC family protein that regulates immunity, inflammation and tissue fibrosis), in cerebral ischemia-reperfusion injury, characterized by inflammation and oxidative damage. Methods Blood NLRC5 levels were assessed in neonates with cerebral ischemia and in healthy controls. A stable PC12 cell line was established that overexpressed or knocked down NLRC5. Inflammatory responses, apoptosis rate and oxidative damage in PC12 cells under oxygen-glucose deprivation/reperfusion (OGD/R) conditions were evaluated using enzyme-linked immunosorbent assay (ELISA), terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) and reactive oxygen species (ROS) assay. Results Blood NLRC5 levels were suppressed in neonates with cerebral ischemia. ELISAs showed that NLRC5 suppressed levels of tumour necrosis factor-α, interleukin (IL)-6, IL-1β, ROS and superoxide dismutase in OGD/R-treated PC12 cells. Furthermore, NLRC5 overexpression was associated with reduced apoptosis rate in PC12 cells treated by OGD/R. Overexpression of NLRC5 also inhibited levels of toll-like receptor (TLR)4, myeloid differentiation primary response protein MyD88 (MyD88) and phosphorylated nuclear factor kappa B-transcription factor p65 (NF-κB p-p65) in PC12 cells, and decreased nuclear levels of NF-κB p-p65. Conclusion NLRC5 alleviated inflammatory responses, oxidative damage and apoptosis in PC12 cells under OGD/R conditions by suppressing activation of the TLR4/MyD88/NF-κB pathway.

scholarly journals Suppression of Nitric Oxide Implicated in the Protective Effect of Echinacoside on H2O2-Induced PC12 Cell Injury

2010 ◽  
Vol 5 (4) ◽  
pp. 1934578X1000500 ◽  
Author(s):  
Rong Kuang ◽  
Yiguo Sun ◽  
Xiaoxiang Zheng
Keyword(s):  
Nitric Oxide ◽  
Protective Effect ◽  
Pc12 Cells ◽  
Laser Scanning ◽  
Cell Injury ◽  
Inhibitory Effect ◽  
Pcr Analysis ◽  
Inos Mrna ◽  
Rt Pcr ◽  
Pheochromocytoma Cell

We investigated whether suppression of nitric oxide (NO) implicated in the protective effect of echinacoside (ECH), a phenylethanoid glycoside, on H2O2-induced injury to the rat pheochromocytoma cell line (PC12 cells). Data show that application of ECH to H2O2-injured PC12 cells (HIPCs) increased cell viability and decreased the necrotic ratio. Laser scanning confocal microscopic (LSCM) analysis suggested that ECH exerted an inhibitory effect on the formation of NO. In addition, RT-PCR analysis revealed that ECH down-regulated p65 and iNOS mRNA expressions in HIPCs. In summary, suppression of NO is related to the protective effect of ECH on HIPCs.

scholarly journals Protective effect of HAMI 3379 against high glucose-induced PC12 cell injury

2015 ◽  
Vol 6 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Zhao Chunzhen ◽  
Wang Lin ◽  
Li Wanzhong
Keyword(s):  
Protective Effect ◽  
Pc12 Cell ◽  
High Glucose ◽  
Cell Injury

scholarly journals Protective effect of resveratrol against corticosterone-induced neurotoxicity in PC12 cells

2019 ◽  
Vol 10 (1) ◽  
pp. 235-240 ◽  
Author(s):  
Ye Zhang ◽  
Yun He ◽  
Ning Deng ◽  
Yan Chen ◽  
Jiecong Huang ◽  
...  
Keyword(s):  
Protein Expression ◽  
Protective Effect ◽  
Cell Viability ◽  
Pc12 Cells ◽  
Caspase 3 ◽  
Annexin V ◽  
Cell Counting ◽  
Depressant Effect ◽  
Protective Efficiency ◽  
Related Proteins

Abstract Objective Resveratrol(RES) is a natural polyphenol which possesses an anti-depressant effect. However, the mechanisms of its anti-depressant effect remain unclear. The aim of the study is to investigate the potential mechanisms in the neuro-protective efficiency in the corticosterone-induced pheochromacytoma 12 (PC12) cells. Methods PC12 cells were treated with 200 μM of corticosterone in the absence or presence of different concentrations of RES for 24 h. Then, cell viability was measured by Cell Counting Kit-8 assay. Apoptosis of PC12 cells was measured by Annexin V-FITC and Propidium iodide (PI) labelling. The expression of apoptosis-related proteins including Bax, Bcl-2, caspase-3 was determined by western blotting. Results The results showed that treatment with 200 μM of corticosterone induced cytotoxicity in PC12 cells. However, different concentrations of RES (2.5μmol/L, 5μmol/L and 10 μmol/L) significantly increased the cell viability, suppressed the apoptosis of PC12 cells, down-regulated Bax and caspase-3 protein expression, and up-regulated Bcl-2 protein expression, compared to the model group (p<0.05). Conclusion Resveratrol has a protective effect on corticosterone-induced neurotoxicity in PC12 cells, which may be related to the apoptosis via inhibition of apoptosis-related proteins and displays the antidepressant-like effect.

scholarly journals Exocyst Sec10 protects renal tubule cells from injury by EGFR/MAPK activation and effects on endocytosis

2014 ◽  
Vol 307 (12) ◽  
pp. F1334-F1341 ◽  
Author(s):  
Ben Fogelgren ◽  
Xiaofeng Zuo ◽  
Janine M. Buonato ◽  
Aleksandr Vasilyev ◽  
Jeong-In Baek ◽  
...  
Keyword(s):  
Acute Kidney Injury ◽  
Protective Effect ◽  
Cell Injury ◽  
Renal Tubule ◽  
Mapk Pathway ◽  
Kidney Injury ◽  
Mapk Signaling ◽  
Mitogen Activated Protein Kinase ◽  
Zebrafish Model ◽  
Tubule Cells

Acute kidney injury is common and has a high mortality rate, and no effective treatment exists other than supportive care. Using cell culture models, we previously demonstrated that exocyst Sec10 overexpression reduced damage to renal tubule cells and speeded recovery and that the protective effect was mediated by higher basal levels of mitogen-activated protein kinase (MAPK) signaling. The exocyst, a highly-conserved eight-protein complex, is known for regulating protein trafficking. Here we show that the exocyst biochemically interacts with the epidermal growth factor receptor (EGFR), which is upstream of MAPK, and Sec10-overexpressing cells express greater levels of phosphorylated (active) ERK, the final step in the MAPK pathway, in response to EGF stimulation. EGFR endocytosis, which has been linked to activation of the MAPK pathway, increases in Sec10-overexpressing cells, and gefitinib, a specific EGFR inhibitor, and Dynasore, a dynamin inhibitor, both reduce EGFR endocytosis. In turn, inhibition of the MAPK pathway reduces ligand-mediated EGFR endocytosis, suggesting a potential feedback of elevated ERK activity on EGFR endocytosis. Gefitinib also decreases MAPK signaling in Sec10-overexpressing cells to levels seen in control cells and, demonstrating a causal role for EGFR, reverses the protective effect of Sec10 overexpression following cell injury in vitro. Finally, using an in vivo zebrafish model of acute kidney injury, morpholino-induced knockdown of sec10 increases renal tubule cell susceptibility to injury. Taken together, these results suggest that the exocyst, acting through EGFR, endocytosis, and the MAPK pathway is a candidate therapeutic target for acute kidney injury.

scholarly journals Seven Novel Genes Related to Cell Proliferation and Migration of VHL-Mutated Pheochromocytoma

2021 ◽  
Vol 12 ◽  
Author(s):  
Shuai Gao ◽  
Longfei Liu ◽  
Zhuolin Li ◽  
Yingxian Pang ◽  
Jiaqi Shi ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Pc12 Cells ◽  
Pc12 Cell ◽  
Collagen Type ◽  
Tissue Growth ◽  
Cell Counting ◽  
Type I ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

Pheochromocytoma, as a neuroendocrine tumor with the highest genetic correlation in all types of tumors, has attracted extensive attention. Von Hipper Lindau (VHL) has the highest mutation frequency among the genes associated with pheochromocytoma. However, the effect of VHL on the proteome of pheochromocytoma remains to be explored. In this study, the VHL knockdown (VHL-KD) PC12 cell model was established by RNA interference (shRNA). We compared the proteomics of VHL-KD and VHL-WT PC12 cell lines. The results showed that the expression of 434 proteins (VHL shRNA/WT &gt; 1.3) changed significantly in VHL-KD-PC12 cells. Among the 434 kinds of proteins, 83 were involved in cell proliferation, cell cycle and cell migration, and so on. More importantly, among these proteins, we found seven novel key genes, including Connective Tissue Growth Factor (CTGF), Syndecan Binding Protein (SDCBP), Cysteine Rich Protein 61 (CYR61/CCN1), Collagen Type III Alpha 1 Chain (COL3A1), Collagen Type I Alpha 1 Chain (COL1A1), Collagen Type V Alpha 2 Chain (COL5A2), and Serpin Family E Member 1 (SERPINE1), were overexpressed and simultaneously regulated cell proliferation and migration in VHL-KD PC12 cells. Furthermore, the abnormal accumulation of HIF2α caused by VHL-KD significantly increased the expression of these seven genes during hypoxia. Moreover, cell-counting, scratch, and transwell assays demonstrated that VHL-KD could promote cell proliferation and migration, and changed cell morphology. These findings indicated that inhibition of VHL expression could promote the development of pheochromocytoma by activating the expression of cell proliferation and migration associated genes.

Protective effect of hydrogen against ischemia-reperfusion induced spinal nerve cell apoptosis

2021 ◽  
Author(s):  
Yanqing Sun ◽  
Wei Shi ◽  
Bo Yuan ◽  
Zhiwei Wang ◽  
Shengyuan Zhou ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Protective Effect ◽  
Cell Viability ◽  
Signaling Pathway ◽  
Pc12 Cells ◽  
Pc12 Cell ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
Ischemia Reperfusion ◽  
Caspase 12

Abstract Background: This study aims to explore the protective effect of hydrogen against oxygen-glucose-serum deprivation/restoration (OGSD/R)-induced PC12 cell apoptosis in vitro and the possible underlying mechanism. Methods: A normal control (NC) group was set where PC12 cells were cultured normal, while a positive control (PC) group, where PC12 cells were exposed to OGSD 12h/R1h without intervention, and a hydrogen intervention (HI) group, where PC12 cells were exposed to OGSD 12h/R1h plus HI, were conducted at the same time. At OGSD 12h/R 1h, cells were DAPI stained to detect viability and changes in the expression of apoptosis-associated proteins caspase-3, caspase-12 and CHOP/GADD153, and the endoplasmic reticulum-related signaling pathway protein PERK-eIF2α-ATF4. At the same time, the effect of HI was observed. Results: The result revealed that compared with NC group, cell apoptosis was more severe and cell viability was reduced significantly in PC group, while cell apoptosis was ameliorated and cell viability was increased significantly in HI as compared with PC group. In addition, the content of caspase-3 and caspase-12 in HI group was decreased significantly as compared with that in PC group. During this process, the endoplasmic reticulum-related signaling pathway protein PERK-eIF2α-ATF4 was activated. In HI group, the expression of this protein was decreased and cell viability was increased significantly as compared with those in PC group. Conclusions: Hydrogen was able to inhibit OGSD/R-induced PC12 cell apoptosis and exert a protective effect against ischemia-repurfusion injury (IRI) to nerve cells, probably through inhibiting the endoplasmic reticulum-related signaling pathway protein.

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