Autophagy protects murine macrophages from β-cypermethrin-induced mitochondrial dysfunction and cytotoxicity via the reduction of oxidation stress

He, Bingnan; Wang, Xia; Zhu, Jianbo; Kong, Baida; Wei, Lai; Jin, Yuanxiang

doi:10.1016/j.envpol.2019.04.044

Cited by 26 publications

(14 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this study, we observed that ROS levels in RAW 264.7 cells were elevated by β‐CYP. Similarly, our previous studies have also shown that exposure to β‐CYP elevated ROS levels to induce cytotoxicity and immunosuppression in RAW 264.7 cells (He et al, ; He et al, ; Wang et al, ). Notably, macrophages also regulate cell proliferation and the energy metabolism of adipocytes (Schäffler and Schölmerich, ; Sun et al, ).…”

Section: Discussionsupporting

confidence: 60%

“…After being seeded in a 12‐well plate, undifferentiated 3T3‐L1 cells were exposed to CM, RM, CRM, or CNRM for 2 days. Then, the cells were stained with reagents from apoptosis detection kits according to the manufacturer's instructions as previously described (He et al, ). Briefly, 3T3‐L1 cells were suspended in and washed with cold PBS two times.…”

Section: Methodsmentioning

confidence: 99%

“…3T3‐L1 cells were treated as described in section 2.5. After that, genomic DNA was extracted using DNA extraction kits as previously described (He et al, ), and bisulfite conversion was performed using DNA methylation detection kits according to the manufacturer's instructions. Then, methylation‐specific PCR was conducted to quantify the levels of methylated and unmethylated CEBPA promoter under the following cycling conditions: 95 °C for 3 min, followed by 40 cycles of 95 °C for 15 s, 56 °C for 30 s and 72 °C for 1 min and a final step of 72 °C for 10 min.…”

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

β‐Cypermethrin Alleviated the Inhibitory Effect of Medium from RAW 264.7 Cells on 3T3‐L1 Cell Maturation into Adipocytes

Wang

Jin

et al. 2020

Lipids

Self Cite

View full text Add to dashboard Cite

Studies have elucidated that pyrethroids induce adipogenesis. It is also known that macrophages can affect the homeostasis of adipose tissue. However, whether and how the β-cypermethrin (β-CYP)-mediated inhibition of the macrophages affects adipogenesis remain unknown. To explore the effects of β-CYP on adipogenesis through modulating the function of macrophages, 3T3-L1 cells, a preadipocyte cell line, were exposed to culture medium from either RAW 264.7 cells, a macrophage cell line (RM), or β-CYP-treated RAW 264.7 cells (CRM). CRM decreased the inhibitory effects of RM treatment on cell proliferation and adipogenesis, as lipid accumulation, the CEBPA content, and Fasn and Acaca expression in 3T3-L1 cells were higher following CRM treatment than following RM treatment through the higher levels of the demethylated CEBPA promoter in 3T3-L1 cells. However, the medium from β-CYPand Nacetyl-L-cysteine-cotreated RAW 264.7 cells (CNRM) partially restored the inhibitory effects of RAW 264.7 cells on 3T3-L1 cells that had been reduced by CRM, indicating that β-CYP might reduce the cytotoxicity and inhibitory effects of RAW 264.7 cells on the adipogenesis of 3T3-L1 cells through elevating ROS levels in RAW 264.7 cells. Moreover, exposure to β-CYP downregulated the TNF-α secretion in RAW 264.7 cells. In conclusion, these data demonstrated that β-CYP affected the function of RAW 264.7 cells, alleviating their inhibitory effects on adipogenesis and CEBPA demethylation in 3T3-L1 cells. β-CYP might achieve these effects through downregulating the secretion of TNF-α via elevating ROS levels in RAW 264.7 cells. Our experiments provide a new perspective on the obesogenic effect of pyrethroids.

show abstract

Section: Discussionsupporting

confidence: 60%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

β‐Cypermethrin Alleviated the Inhibitory Effect of Medium from RAW 264.7 Cells on 3T3‐L1 Cell Maturation into Adipocytes

Wang

Jin

et al. 2020

Lipids

Self Cite

View full text Add to dashboard Cite

show abstract

“…Macrophages are immune cells that play important role in pathogen removal from the cells. It was observed that β-cypermethrin and cyhalothrin treatment decreased phagocytic activity and nitric oxide production in macrophage cells (He et al, 2019). No activity was detected at low concentration of cyhalothrin whereas macrophage activity was blocked at higher concentration.…”

Section: Hazardous Effects Of Pyrethroidsmentioning

confidence: 99%

Insight Into Microbial Applications for the Biodegradation of Pyrethroid Insecticides

et al. 2019

View full text Add to dashboard Cite

Pyrethroids are broad-spectrum insecticides and presence of chiral carbon differentiates among various forms of pyrethroids. Microbial approaches have emerged as a popular solution to counter pyrethroid toxicity to marine life and mammals. Bacterial and fungal strains can effectively degrade pyrethroids into non-toxic compounds. Different strains of bacteria and fungi such as Bacillus spp., Raoultella ornithinolytica, Psudomonas flourescens , Brevibacterium sp., Acinetobactor sp., Aspergillus sp., Candida sp., Trichoderma sp., and Candia spp., are used for the biodegradation of pyrethroids. Hydrolysis of ester bond by enzyme esterase/carboxyl esterase is the initial step in pyrethroid biodegradation. Esterase is found in bacteria, fungi, insect and mammalian liver microsome cells that indicates its hydrolysis ability in living cells. Biodegradation pattern and detected metabolites reveal microbial consumption of pyrethroids as carbon and nitrogen source. In this review, we aim to explore pyrethroid degrading strains, enzymes and metabolites produced by microbial strains. This review paper covers in-depth knowledge of pyrethroids and recommends possible solutions to minimize their environmental toxicity.

show abstract

“…Autophagy can directly remove inflammasomes. In addition, autophagy can also reduce inflammation by eliminating inflammatory stimuli, such as ROS, mitochondrial deoxyribonucleic acid or damaged organelles, to maintain homeostasis 17,18 . Previous observations found that autophagic activity can attenuate cerebral and intestinal I/RI by eliminating mitochondrial deoxyribonucleic acid and mitochondrial ROS, and inhibiting the activation of NLRP3 inflammasome 19,20 .…”

Section: Introductionmentioning

confidence: 99%

Activation of autophagy inhibits nucleotide‐binding oligomerization domain‐like receptor protein 3 inflammasome activation and attenuates myocardial ischemia‐reperfusion injury in diabetic rats

Zhang

et al. 2020

J of Diabetes Invest

View full text Add to dashboard Cite

Aims/Introduction Diabetic hearts are more vulnerable to ischemia‐reperfusion injury (I/RI). The activation of nucleotide‐binding oligomerization domain‐like receptor protein 3 (NLRP3) inflammasome can mediate the inflammatory process, and hence might contribute to myocardial I/RI. Activation of autophagy can eliminate excess reactive oxygen species and alleviate myocardial I/RI in diabetes. The present study aimed to investigate whether the activation of autophagy can alleviate diabetic myocardial I/RI through inhibition of NLRP3 inflammasome activation. Materials and Methods A dose of 65 mg/kg streptozotocin was given by tail vein injection to establish a type 1 diabetes model in the rats. The left anterior descending coronary artery was ligated for 30 min followed by reperfusion for 2 h to establish a myocardial I/RI model. H9C2 cardiomyocytes were exposed to high glucose (33 mmol/L) and subjected to hypoxia–reoxygenation (6 h hypoxia followed by 4 h reoxygenation). Results The diabetic rats showed significant inhibition of cardiac autophagy (decreased LC3‐II/I and increased p62) that was concomitant with increased activation of NLRP3 inflammasome (increased NLRP3, apoptosis‐related spots protein cleaved caspase‐1, interleukin‐18, interleukin‐1β) and more severe myocardial I/RI (elevated creatine kinase myocardial band, lactate dehydrogenase and larger infarct size). However, administration of rapamycin, an inhibitor of the autophagy, to activate autophagy resulted in the inhibition of NLRP3 inflammasome, and finally alleviated myocardial I/RI. In vitro, high glucose inhibited autophagy, while activating NLRP3 inflammasome in H9C2 cardiomyocytes and aggravating hypoxia–reoxygenation injury, but rapamycin reversed these adverse effects of high glucose. Conclusion Activation of autophagy can suppress the formation of NLRP3 inflammasome, which in turn attenuates myocardial ischemia‐reperfusion injury in diabetic rats.

show abstract

Autophagy protects murine macrophages from β-cypermethrin-induced mitochondrial dysfunction and cytotoxicity via the reduction of oxidation stress

Cited by 26 publications

References 67 publications

β‐Cypermethrin Alleviated the Inhibitory Effect of Medium from RAW 264.7 Cells on 3T3‐L1 Cell Maturation into Adipocytes

β‐Cypermethrin Alleviated the Inhibitory Effect of Medium from RAW 264.7 Cells on 3T3‐L1 Cell Maturation into Adipocytes

Insight Into Microbial Applications for the Biodegradation of Pyrethroid Insecticides

Activation of autophagy inhibits nucleotide‐binding oligomerization domain‐like receptor protein 3 inflammasome activation and attenuates myocardial ischemia‐reperfusion injury in diabetic rats

Contact Info

Product

Resources

About