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Drug: Acetylcysteine
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Total 193 results found since Jan 2013.
Chlorpyrifos induces neuronal cell death via both oxidative stress and Akt activation downstream-regulated CHOP-triggered apoptotic pathways
In this study, CPF exposure (10-400 μM) significantly reduced Neuro-2a cell viability and induced apoptotic events, including the increase in caspase-3 activity, apoptotic cell population, and cleavage of caspase-3/-7 and PARP. Exposure of Neuro-2a cells to CPF also triggered CHOP activation. Transfection with CHOP-specific siRNA markedly suppressed the expression of CHOP, and attenuated cytotoxicity and apoptotic events in CPF-exposed Neuro-2a cells. Furthermore, CPF exposure obviously evoked the phosphorylation of Akt as well as ROS generation in a time-dependent manner. Pretreatment with LY294002 (an Akt inhibitor) eff...
Source: Toxicology in Vitro - October 17, 2022 Category: Toxicology Authors: Jhe-Wei Lin Shih-Chang Fu Jui-Ming Liu Shing-Hwa Liu Kuan-I Lee Kai-Min Fang Ren-Jun Hsu Chun-Fa Huang Kun-Min Liu Kai-Chih Chang Chin-Chuan Su Ya-Wen Chen Source Type: research
ROS induced the Rab26 promoter hypermethylation to promote cigarette smoking-induced airway epithelial inflammation of COPD through activation of MAPK signaling
In this study, we explore the role of Rab26 in CS exposure modulating the inflammatory response of airway epithelium and the novel mechanism of CS exposure regulation Rab26. These data showed that CS exposure and H2O2 (a type of ROS) suppressed the expression of Rab26 and increased the expression of DNMT3b in vivo and in vitro. GEO data analysis found the level of Rab26 was decreased in the lung tissue of COPD patients. CSE-induced ROS promoted DNA methylation of the Rab26 promoter and inhibited its promoter activity by elevating the DNMT3b level. Antioxidants N-Acetyl-l-cysteine (NAC), 5-Aza-2'-deoxycytidine (5-AZA) (DNA ...
Source: Free Radical Biology and Medicine - January 7, 2023 Category: Biology Authors: Bin-Feng He Yi-Xing Wu Wei-Ping Hu Jian-Lan Hua Yaoping Han Jing Zhang Source Type: research
DBP induced autophagy and necrotic apoptosis in HepG2 cells via the mitochondrial damage pathway
In this study, HepG2 cells were treated with 0.0625, 0.125, 0.25, 0.5 and 1 mM Dibutyl phthalate (DBP) for 48 h to investigate mitochondrial toxicity. The results showed that DBP caused mitochondrial damage, autophagy, apoptosis and necroptosis; Transcriptomics analysis identified that MAPK and PI3K were significant factors in the cytotoxic changes induced by DBP; N-Acetyl-L-cysteine (NAC), SIRT1 activator, ERK inhibitor, p38 inhibitor and ERK siRNA treatments counteracted the changes of SIRT1/PGC-1α and Nrf2 pathway-related proteins, autophagy and necroptotic apoptosis proteins induced by DBP. While PI3K and Nrf2 inhibit...
Source: Food and Chemical Toxicology - April 14, 2023 Category: Food Science Authors: Huan Liu Linjing Xu Lizi Zhou Wenna Han Zhongyi Li Chunhong Liu Source Type: research
ROS and DRP1 interactions accelerate the mitochondrial injury induced by polystyrene nanoplastics in human liver HepG2 cells
Chem Biol Interact. 2023 Apr 19:110502. doi: 10.1016/j.cbi.2023.110502. Online ahead of print.ABSTRACTMicroplastics have become a serious environmental pollutant and subsequently have harmful effects on human health. Thus, the impacts of microplastics on human cells need to be explored. In the present study, the cytotoxic effects at the subcellular-organelle levels to polystyrene nanoplastics (PS-NPs, diameter 21.5 ± 2.7 nm) were investigated in the human hepatocellular carcinoma (HepG2) cell line. The cell viability exposed to PS-NPs at the concentrations of 6.25, 12.5, 25 and 50 μg/mL for 24 h diminished in a concentra...
Source: Chemico-Biological Interactions - April 19, 2023 Category: Molecular Biology Authors: Yunjing Li Menghao Guo Shuyan Niu Mengting Shang Xiaoru Chang Zuoyi Sun Rui Zhang Xin Shen Yuying Xue Source Type: research
TCF12 regulates exosome release from epirubicin-treated CAFs to promote ER+ breast cancer cell chemoresistance
In this study, we showed that epirubicin (EPI) treatment triggered ROS which initiated autophagy in CAFs, TCF12 inhibited autophagy flux and further promoted exosome secretion. Inhibition of EPI-induced reactive oxygen species (ROS) production with N-acetyl-L-cysteine (NAC) or suppression of autophagic initiation with short interfering RNA (siRNA) against ATG5 blunted exosome release from CAFs. Furthermore, exosome secreted from EPI-treated CAFs not only prevented ROS accumulation in CAFs but also upregulated the CXCR4 and c-Myc protein levels in recipient ER+ breast cancer cells, thus promoting EPI resistance of tumor cel...
Source: Biochimica et Biophysica Acta - May 3, 2023 Category: Biochemistry Authors: Yuxiang Qiu Xing Wang Yan Sun Yan-E Du Guobing Yin Haojun Luo Siyang Wen Lei Lang Manran Liu Xi Tang Source Type: research
AMPK negatively regulates RANKL-induced osteoclast differentiation by controlling oxidative stress
This study aimed to clarify the mechanistic connection between AMPK and osteoclast differentiation, and the potential role of AMPK in the anti-resorptive effects of several phytochemicals. We found that receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL)-induced osteoclast differentiation, osteoclastic gene expression, and activation of mitogen-activated protein kinase (MAPK) and NF-κB were promoted in cells transfected with AMPK siRNA. AMPK knockdown led to defective synthesis of heme oxygenase-1, an antioxidant enzyme, and the upstream mediator, nuclear factor erythroid-2-related factor 2. Furthermore, ...
Source: Free Radical Biology and Medicine - June 3, 2023 Category: Biology Authors: Miori Tanaka Hirofumi Inoue Nobuyuki Takahashi Mariko Uehara Source Type: research
The role of the Nrf2/GSH antioxidant system in cisplatin resistance in malignant rhabdoid tumours
ConclusionsThese results suggest that targeting the Nrf2/GSH antioxidant system may present a novel therapeutic strategy to combat chemoresistance in rhabdoid tumours.
Source: Journal of Cancer Research and Clinical Oncology - July 28, 2023 Category: Cancer & Oncology Source Type: research
