Epoxyeicosatrienoic acids alleviate alveolar epithelial cell senescence by inhibiting mitophagy through NOX4/Nrf2 pathway DOI Open Access

Jie‐Ru Hong,

Chen‐Yu Zhang, Wenjing Zhong

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2023, Volume and Issue: 169, P. 115937 - 115937

Published: Nov. 25, 2023

Alveolar epithelial cell (AEC) senescence is considered to be a universal pathological feature of many chronic pulmonary diseases. Our previous study found that epoxyeicosatrienoic acids (EETs), produced from arachidonic acid (ARA) through the cytochrome P450 cyclooxygenase (CYP) pathway, have significant negative regulatory effects on cellular in AECs. However, exact mechanisms by which EETs alleviate AECs still need further explored. In present study, we observed bleomycin (BLM) induced enhanced mitophagy accompanied increased mitochondrial ROS (mito-ROS) content murine alveolar line MLE12. While reduced BLM-induced and mito-ROS MLE12 cells, mechanism was related regulation NOX4/Nrf2-mediated redox imbalance. Furthermore, inhibition degradation could significantly inhibit regulate NOX4/Nrf2 balance exert anti-oxidant D-galactose-induced premature aging mice. Collectively, these findings may provide new ideas for treating age-related diseases targeting improve dysfunction reduce oxidative stress.

Language: Английский

Lactobacillus plantarum P9 ameliorates dysfunctional immune and metabolic homeostasis along the gut–liver axis in a nonalcoholic fatty liver disease with low-grade colitis mouse model DOI
Yang Zhan, Qiong Li, Tao Li

et al.

Food Bioscience, Journal Year: 2024, Volume and Issue: 61, P. 104613 - 104613

Published: July 2, 2024

Language: Английский

Citations

2

Metabolomics combined with network pharmacology reveals the protective effect of astragaloside IV on alcoholic liver disease DOI
Jinfang Hao,

Ruixian Hu,

Jianming Zhao

et al.

Phytomedicine, Journal Year: 2024, Volume and Issue: unknown, P. 156032 - 156032

Published: Sept. 1, 2024

Language: Английский

Citations

2

Autophagy and senescence of rat retinal precursor cells under high glucose DOI Creative Commons
Hanhan Peng, Wentao Han, Benteng Ma

et al.

Frontiers in Endocrinology, Journal Year: 2023, Volume and Issue: 13

Published: Jan. 4, 2023

Backgrounds Diabetic retinopathy (DR) is a common diabetic ocular disease characterized by retinal ganglion cell (RGC) changes. An abnormal environment, hyperglycemia, may progressively alter the structure and function of RGCs, which primary pathological feature neurodegeneration in DR. Accumulated studies confirmed autophagy senescence play vital role DR; however, underlying mechanisms need to be clarified. Methods This study included microarray expression profiling dataset GSE60436 from Gene Expression Omnibus (GEO) conduct bioinformatics analysis. The R software was used identify autophagy-related genes (ARGs) that were differentially expressed fibrovascular membranes (FVMs) normal retinas. Co-expression tissue-specific elicited for filtered genes. then analyzed ontology (GO) enrichment analysis, Kyoto Encyclopedia Genes Genomes (KEGG) pathway analysis Set Enrichment Analysis (GSEA). R28 cells cultured with high glucose, detected reverse transcription-quantitative (RT-qPCR) stained apoptosis kit. Results In retina, 31 ARGs (24 up-regulated genes) discovered enriched. results revealed significantly enriched autophagy, apoptosis, aging, neural function. Four hub (i.e., TP53 , CASP1 CCL2 ) up-regulated. Upregulation cellular level hyperglycemia model vitro . Conclusions Our provide evidence involved injury, protective limited. Further favour understanding progression neuroprotection

Language: Английский

Citations

6

Hepatic COX1 loss leads to impaired autophagic flux and exacerbates nonalcoholic steatohepatitis DOI Creative Commons
Qian Yu, Chang Li,

Qinghui Niu

et al.

Acta Pharmaceutica Sinica B, Journal Year: 2023, Volume and Issue: 13(6), P. 2628 - 2644

Published: March 10, 2023

The mechanisms underlying autophagic defects in nonalcoholic steatohepatitis (NASH) remain largely unknown. We aimed to elucidate the roles of hepatic cyclooxygenase 1 (COX1) autophagy and pathogenesis diet-induced mice. Human fatty liver disease (NAFLD) samples were used examine protein expression COX1 level autophagy. Cox1Δhepa mice their wildtype littermates generated fed with 3 different NASH models. found that was increased patients models accompanied by impaired required for basal hepatocytes specific deletion exacerbated inhibiting Mechanistically, directly interacted WD repeat domain, phosphoinositide interacting 2 (WIPI2), which crucial autophagosome maturation. Adeno-associated virus (AAV)-mediated rescue WIPI2 reversed flux improved phenotypes mice, indicating deletion-mediated partially dependent on WIPI2-mediated In conclusion, we demonstrated a novel role protected against WIPI2. Targeting COX1-WIPI2 axis may be therapeutic strategy NASH.

Language: Английский

Citations

6

Epoxyeicosatrienoic acids alleviate alveolar epithelial cell senescence by inhibiting mitophagy through NOX4/Nrf2 pathway DOI Open Access

Jie‐Ru Hong,

Chen‐Yu Zhang, Wenjing Zhong

et al.

Biomedicine & Pharmacotherapy, Journal Year: 2023, Volume and Issue: 169, P. 115937 - 115937

Published: Nov. 25, 2023

Alveolar epithelial cell (AEC) senescence is considered to be a universal pathological feature of many chronic pulmonary diseases. Our previous study found that epoxyeicosatrienoic acids (EETs), produced from arachidonic acid (ARA) through the cytochrome P450 cyclooxygenase (CYP) pathway, have significant negative regulatory effects on cellular in AECs. However, exact mechanisms by which EETs alleviate AECs still need further explored. In present study, we observed bleomycin (BLM) induced enhanced mitophagy accompanied increased mitochondrial ROS (mito-ROS) content murine alveolar line MLE12. While reduced BLM-induced and mito-ROS MLE12 cells, mechanism was related regulation NOX4/Nrf2-mediated redox imbalance. Furthermore, inhibition degradation could significantly inhibit regulate NOX4/Nrf2 balance exert anti-oxidant D-galactose-induced premature aging mice. Collectively, these findings may provide new ideas for treating age-related diseases targeting improve dysfunction reduce oxidative stress.

Language: Английский

Citations

5