Piceatannol alleviate ROS‐mediated PC‐12 cells damage and mitochondrial dysfunction through SIRT3/FOXO3a signaling pathway

2021 ◽  
Author(s):  
Wei Yang ◽  
Yu Wang ◽  
Yiming Hao ◽  
Ziyuan Wang ◽  
Jie Liu ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Pc 12 Cells

scholarly journals Transcriptional Profiling and Biological Pathway(s) Analysis of Type 2 Diabetes Mellitus in a Pakistani Population

2020 ◽  
Vol 17 (16) ◽  
pp. 5866
Author(s):  
Zarish Noreen ◽  
Christopher A. Loffredo ◽  
Attya Bhatti ◽  
Jyothirmai J. Simhadri ◽  
Gail Nunlee-Bland ◽  
...  
Keyword(s):  
Gene Expression ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Health Concern ◽  
Receptor Signaling ◽  
Small Pilot Study

The epidemic of type 2 diabetes mellitus (T2DM) is an important global health concern. Our earlier epidemiological investigation in Pakistan prompted us to conduct a molecular investigation to decipher the differential genetic pathways of this health condition in relation to non-diabetic controls. Our microarray studies of global gene expression were conducted on the Affymetrix platform using Human Genome U133 Plus 2.0 Array along with Ingenuity Pathway Analysis (IPA) to associate the affected genes with their canonical pathways. High-throughput qRT-PCR TaqMan Low Density Array (TLDA) was performed to validate the selected differentially expressed genes of our interest, viz., ARNT, LEPR, MYC, RRAD, CYP2D6, TP53, APOC1, APOC2, CYP1B1, SLC2A13, and SLC33A1 using a small population validation sample (n = 15 cases and their corresponding matched controls). Overall, our small pilot study revealed a discrete gene expression profile in cases compared to controls. The disease pathways included: Insulin Receptor Signaling, Type II Diabetes Mellitus Signaling, Apoptosis Signaling, Aryl Hydrocarbon Receptor Signaling, p53 Signaling, Mitochondrial Dysfunction, Chronic Myeloid Leukemia Signaling, Parkinson’s Signaling, Molecular Mechanism of Cancer, and Cell Cycle G1/S Checkpoint Regulation, GABA Receptor Signaling, Neuroinflammation Signaling Pathway, Dopamine Receptor Signaling, Sirtuin Signaling Pathway, Oxidative Phosphorylation, LXR/RXR Activation, and Mitochondrial Dysfunction, strongly consistent with the evidence from epidemiological studies. These gene fingerprints could lead to the development of biomarkers for the identification of subgroups at high risk for future disease well ahead of time, before the actual disease becomes visible.

Cr(VI) induces cytotoxicity in vitro through activation of ROS-mediated endoplasmic reticulum stress and mitochondrial dysfunction via the PI3K/Akt signaling pathway

2017 ◽  
Vol 41 ◽  
pp. 232-244 ◽  
Author(s):  
Yujing Zhang ◽  
Fang Xiao ◽  
Xinmin Liu ◽  
Kaihua Liu ◽  
Xiaoxin Zhou ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Signaling Pathway

scholarly journals Polyphyllin I induces G2/M phase arrest and apoptosis in U251 human glioma cells via mitochondrial dysfunction and the JNK signaling pathway

2017 ◽  
Vol 49 (6) ◽  
pp. 479-486 ◽  
Author(s):  
Jiaxin Liu ◽  
Yueting Zhang ◽  
Li Chen ◽  
Fei Yu ◽  
Xiaojin Li ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Glioma Cells ◽  
Human Glioma ◽  
Human Glioma Cells ◽  
Jnk Signaling ◽  
Phase Arrest ◽  
M Phase ◽  
Jnk Signaling Pathway

scholarly journals Naringin inhibits high glucose-induced cardiomyocyte apoptosis by attenuating mitochondrial dysfunction and modulating the activation of the p38 signaling pathway

2013 ◽  
Vol 32 (2) ◽  
pp. 396-402 ◽  
Author(s):  
HAILI HUANG ◽  
KENG WU ◽  
QIONG YOU ◽  
RUINA HUANG ◽  
SHANGHAI LI ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
High Glucose ◽  
Cardiomyocyte Apoptosis

Quercetin attenuates mitochondrial dysfunction and biogenesis via upregulated AMPK/SIRT1 signaling pathway in OA rats

2018 ◽  
Vol 103 ◽  
pp. 1585-1591 ◽  
Author(s):  
Linan Qiu ◽  
Yuju Luo ◽  
Xiaojuan Chen
Keyword(s):  
Mitochondrial Dysfunction ◽  
Signaling Pathway

Liensinine perchlorate inhibits colorectal cancer tumorigenesis by inducing mitochondrial dysfunction and apoptosis

2018 ◽  
Vol 9 (11) ◽  
pp. 5536-5546 ◽  
Author(s):  
Yang Wang ◽  
Yang-Jia Li ◽  
Xiao-Hui Huang ◽  
Can-Can Zheng ◽  
Xing-Feng Yin ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Cell Apoptosis ◽  
Quantitative Proteomics ◽  
Food Source ◽  
Colorectal Cancer Cell ◽  
Functional Screen ◽  
Cancer Cell Apoptosis

Functional screen and quantitative proteomics reveal that food-source liensinine induces colorectal cancer cell apoptosisviathe JNK-mitochondrial dysfunction signaling pathway.

PM2.5 induces male reproductive toxicity via mitochondrial dysfunction, DNA damage and RIPK1 mediated apoptotic signaling pathway

2018 ◽  
Vol 634 ◽  
pp. 1435-1444 ◽  
Author(s):  
Jin Zhang ◽  
Jianhui Liu ◽  
Lihua Ren ◽  
Jialiu Wei ◽  
Junchao Duan ◽  
...  
Keyword(s):  
Dna Damage ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Reproductive Toxicity ◽  
Apoptotic Signaling

scholarly journals Emodin Alleviates Hydrogen Peroxide-Induced Inflammation and Oxidative Stress via Mitochondrial Dysfunction by Inhibiting the PI3K/mTOR/GSK3β Pathway in Neuroblastoma SH-SY5Y Cells

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Rui Li ◽  
Wenzhou Liu ◽  
Li Ou ◽  
Feng Gao ◽  
Min Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Molecular Mechanisms ◽  
Cell Damage ◽  
Neuroblastoma Cells ◽  
Inflammatory Factors ◽  
Protective Mechanism ◽  
Human Neuroblastoma ◽  
Induced Apoptosis

Emodin is an active monomer extracted from rhubarb root, which has many biological functions, including anti-inflammation, antioxidation, anticancer, and neuroprotection. However, the protective effect of emodin on nerve injury needs to be further elucidated. The purpose of this study is to investigate the effect of emodin on the neuroprotection and the special molecular mechanism. Here, the protective activity of emodin inhibiting H2O2-induced apoptosis and neuroinflammation as well as its molecular mechanisms was examined using human neuroblastoma cells (SH-SY5Y cells). The results showed that emodin significantly enhanced cell viability, reduced cell apoptosis and LDH release. Simultaneously, emodin downregulated H2O2-induced inflammatory factors, including IL-6, NO, and TNF-α, and alleviated H2O2-induced oxidative stress and mitochondrial dysfunction in SH-SY5Y cells. In addition, emodin inhibited the activation of the PI3K/mTOR/GSK3β signaling pathway. What is more, the PI3K/mTOR/GSK3β pathway participated in the protective mechanism of emodin on H2O2-induced cell damage. Collectively, it suggests that emodin alleviates H2O2-induced apoptosis and neuroinflammation potentially by regulating the PI3K/mTOR/GSK3β signaling pathway.

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