Propofol Attenuates Hypoxia/Reoxygenation-Induced Apoptosis and Autophagy in HK-2 Cells by Inhibiting JNK Activation

Wang, Huaxin; Peng, Xuan; Huang, Yayi; Xiao, Yong; Wang, Zhuo; Li, Zhan

doi:10.3349/ymj.2019.60.12.1195

Cited by 6 publications

(6 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Subsequently, it was confirmed that the apoptotic events in NRK-52E cells cultivated under high UA levels were dependent on ROS generation. Inhibition of ROS has been demonstrated as protective in several experimental cell models, such as hypoxia reoxygenation, unilateral ureteral obstruction (UUO), chronic renal failure and diabetic nephropathy ( 45 – 48 ). The findings of the present study offered an explanation for the renal cell protective effects of ROS scavengers.…”

Section: Discussionmentioning

confidence: 99%

Reactive oxygen species induced by uric acid promote NRK‑52E cell apoptosis through the NEK7‑NLRP3 signaling pathway

Wang

et al. 2021

Mol Med Rep

View full text Add to dashboard Cite

increasing uric acid (ua) could induce renal tubular epithelial cell (NRK-52E) injury. However, the specific mechanism by which UA induces renal tubular epithelial cell injury remains unknown. It was hypothesized that UA induces renal tubular epithelial cell injury through reactive oxygen species (ROS) and the Never in mitosis gene A (NIMA)-related kinase 7 (NEK7)/NLR family pyrin domain containing 3 (NLRP3) signaling pathway. TUNEL assay and flow cytometry were applied to measure apoptosis, and the results of the present study showed that UA treatment induced apoptosis of NRK-52E cells in a concentration-dependent manner. Western blotting was performed to determine the expression levels of cleaved caspase-3, Bax and Bcl-xl, it was found that levels were significantly increased after UA treatment in NRK-52E cells. ROS and apoptosis were predominantly induced in NRK-52E cells and there was an association between roS and apoptosis. Enhanced expression of NEK7, NLRP3, apoptosis-associated speck-like and caspase-1 were observed in NRK-52E cells treated with ua. The roS inhibitor, n-acetyl-l-cysteine, exerted a protective effect on the UA-induced apoptosis of tubular epithelial cells by reducing excess roS production, which significantly inhibited NEK7 and NLRP3 inflammasome activation. These results indicated that UA activates ROS and induces apoptosis of NRK-52E cells. The mechanism might be related to the regulation of the NEK7/NLRP3 signaling pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Reactive oxygen species induced by uric acid promote NRK‑52E cell apoptosis through the NEK7‑NLRP3 signaling pathway

Wang

et al. 2021

Mol Med Rep

View full text Add to dashboard Cite

show abstract

“…The association between propofol and autophagy is complex. For example, propofol attenuates hypoxia/reoxygenation-induced autophagy in HK-2 cells, but induces autophagy in C2C12 cells (16). The present study aimed to elucidate the antitumor molecular mechanism of propofol on human lung adenocarcinoma cells and its potential application on lung cancer therapy.…”

Section: Introductionmentioning

confidence: 94%

“…Autophagy is a conserved complex process which maintains the normal function and structure of cells (15,16). Autophagy is involved in the occurrence and progression of lung cancer.…”

Section: Introductionmentioning

confidence: 99%

Demethylation of HACE1 gene promoter by propofol promotes autophagy of human A549 cells

Yang

Zhao

et al. 2020

Oncol Lett

View full text Add to dashboard Cite

Propofol (2,6-diisopropylphenol) is one of the most commonly used intravenous anesthetics and possesses a number of non-anesthetic effects, including antitumor function. The aim of the present study was to elucidate the antitumor molecular mechanism of propofol on A549 and H1299 cells. A549 and H1299 cells were treated in the presence or absence of different concentrations (0, 60 or 120 µmol) of propofol for different durations (0, 24, 48 or 72 h), and proliferation was detected by MTT and colony formation assays; the protein levels of optineurin (OPTN) ubiquitination, HECT domain and ankyrin repeat containing E3 ubiquitin protein ligase 1 (HACE1), methyl-CpG binding domain protein 3 (MBD3) and Microtubule-associated protein 1A/1B-light chain 3 were detected by immunoblotting or quantitative (q)PCR; the methylation state of the HACE1 gene promoter was detected by bisulfite DNA sequencing; and binding of MBD3 on HACE1 gene promoter was detected by chromatin immunoprecipitation-qPCR. Propofol inhibited proliferation of A549 and H1299 cells and promoted HACE1-OPTN axis-mediated selective autophagy activity by increasing the protein expression levels of HACE1 via demethylating its promoter region. Furthermore, propofol promoted expression levels of MBD3 and binding to the-1,000 to-1 bp (transcription start site) region of HACE1 gene promoter. MBD3-knockdown experiments indicated that propofol inhibited proliferation of A549 cells in a MBD3-dependent manner. Thus, the findings of the present study provided a potential antitumor molecular mechanism mediated by propofol.

show abstract

“…The activity of caspase-3 in RAW264.7 cells was detected using Caspase-3 Activity Assay Kit (Beyotime Institute of Biotechnology, China) following the manufacturers' instructions. In short, 100 μL lysate was added into the RAW264.7 cells for 15 min on dry ice and centrifuged (20,000 g, 4°C) 15 min, then 50 μL supernatant, 40 μL detection buffer, and 10 μL caspase-3 substrate acetyl-Asp -Glu-Val-Asp p-nitroanilide (2 mM) 16 were added into 96well plates for 60 min. The absorbance of p-nitroanilide was determined at 405 nm using a microtiter plate reader (Bio-Rad, USA).…”

Section: Caspase-3 Activity Assaymentioning

confidence: 99%

“…14,15 Controlling the pathological changes and protecting the tissue from damage is a usual strategy. ID13 remarkably alleviated pathological status, inhibited the production of pro-inflammatory cytokines, 16 and suppressed the TLR2-NF-κB signal pathway. 17 Daphnetin conferred protection against S. aureus-induced pneumonia by anti-inflammation and enhanced mTOR-dependent autophagy.…”

Section: Introductionmentioning

confidence: 97%

Mangiferin Inhibits Apoptosis and Autophagy Induced by Staphylococcus aureus in RAW264.7 Cells

Xu¹,

Yao²,

Wang³

et al. 2020

JIR

View full text Add to dashboard Cite

Purpose Staphylococcus aureus ( S. aureus ) is an important bacterial pathogen, which creates infective inflammation to human being and animals. Mangiferin (MG) is one of the natural flavonoids with anti-inflammatory, anti-bacterial, and anti-oxidative properties. However, the anti-apoptosis and anti-autophagy of MG are unknown. Hence, this study was aimed to research the inhibition of MG on S. aureus -induced apoptosis and autophagy in RAW264.7 cells. Methods The RAW264.7 cells were pretreated with MG, or pretreated with SP600125 or anisomycin synchronously, and then infected with S. aureus (MOI=100:1). The viability and proliferation status of RAW264.7 cells were detected by MTT and EdU assay. The relative expression of TNF-α, IL-6 and IL-10 protein was tested with ELISA. The levels of Bax, Bcl-2, caspase-3, c-Jun N-terminal kinase (JNK), extracellular-regulated protein kinase (ERK), p38, LC3, Beclin-1, p62, phosphorylated JNK, phosphorylated p38 and phosphorylated ERK in cells were detected by Western blotting. The apoptosis rate of RAW264.7 cells was analyzed by flow cytometric assay. Results The study showed that MG significantly attenuated RAW264.7 cells apoptosis and autophagy caused by S. aureus . MG alleviated S. aureus -induced apoptosis by down-regulating the protein level of active caspase-3 and Bax and up-regulating the level of Bcl-2. MG also inhibited S. aureus -induced autophagy via decreasing the protein level of LC3-II/LC3-I and Beclin-1 or increasing the protein expression of p62. This protective role was dependent on the up-regulation of JNK signal pathway, which was confirmed by using JNK agonist and inhibitor. Conclusion Our results demonstrated that MG might protect RAW264.7 cells from S. aureus -induced apoptosis and autophagy via inhibiting JNK/Bax-dependent signal pathway. Therefore, MG may be a potential agent against pathological cell damage induced by S. aureus infection.

show abstract

Propofol Attenuates Hypoxia/Reoxygenation-Induced Apoptosis and Autophagy in HK-2 Cells by Inhibiting JNK Activation

Cited by 6 publications

References 26 publications

Reactive oxygen species induced by uric acid promote NRK‑52E cell apoptosis through the NEK7‑NLRP3 signaling pathway

Reactive oxygen species induced by uric acid promote NRK‑52E cell apoptosis through the NEK7‑NLRP3 signaling pathway

Demethylation of <em>HACE1</em> gene promoter by propofol promotes autophagy of human A549 cells

<p>Mangiferin Inhibits Apoptosis and Autophagy Induced by <em>Staphylococcus aureus</em> in RAW264.7 Cells</p>

Contact Info

Product

Resources

About

Propofol Attenuates Hypoxia/Reoxygenation-Induced Apoptosis and Autophagy in HK-2 Cells by Inhibiting JNK Activation

Cited by 6 publications

References 26 publications

Reactive oxygen species induced by uric acid promote NRK‑52E cell apoptosis through the NEK7‑NLRP3 signaling pathway

Reactive oxygen species induced by uric acid promote NRK‑52E cell apoptosis through the NEK7‑NLRP3 signaling pathway

Demethylation of <em>HACE1</em> gene promoter by propofol promotes autophagy of human A549&nbsp;cells

<p>Mangiferin Inhibits Apoptosis and Autophagy Induced by <em>Staphylococcus aureus</em> in RAW264.7 Cells</p>

Contact Info

Product

Resources

About

Demethylation of <em>HACE1</em> gene promoter by propofol promotes autophagy of human A549 cells