The protective effect of selenoprotein M on non-alcoholic fatty liver disease: the role of the AMPKα1–MFN2 pathway and Parkin mitophagy

Cai, Jingzeng; Huang, Jia‐Qiang; Yang, Jie; Chen, Xiaoming; Zhang, Haoran; Zhu, Yue; Liu, Qi; Zhang, Ziwei

doi:10.1007/s00018-022-04385-0

Cited by 60 publications

(32 citation statements)

References 72 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…According to the manufacturer's instructions, complementary DNA (cDNA) was synthesized from 5 μg of the total RNA using oligo dT primers and Superscript II reverse transcriptase (Bioer, Hangzhou, China). cDNA was diluted at a ratio of 1:5 with sterile water and stored at −80°C 57,58 . Expression of mitochondrial apoptosis‐related genes (caspase3, caspase9, B‐cell lymphoma 2 [Bcl‐2] Associated X‐protein [BAX], cytochrome c, BCL‐2, and p53), inflammation‐related genes (tumor necrosis factor‐alpha [TNF‐α], cyclooxygenase‐2 [COX 2], interleukin 1‐beta [IL‐1β], interleukin‐2 [IL‐2], interleukin 6 [IL‐6], and interleukin 7 [IL‐7]) and autophagy‐related genes (LC3, autophagy‐related 1 [ATG 1], autophagy‐related 2 [ATG 7], p62, mammalian target of rapamycin [mTOR], and Beclin‐1) were detected.…”

Section: Methodsmentioning

confidence: 99%

“…56 According to the manufacturer's instructions, complementary DNA (cDNA) was synthesized from 5 μg of the total RNA using oligo dT primers and Superscript II reverse transcriptase (Bioer, Hangzhou, China). cDNA was diluted at a ratio of 1:5 with sterile water and stored at À80 C. 57,58 The housekeeping gene GAPDH was used as a reference. The specific primer information is shown in Table 1.…”

Section: Real-time Quantitative Polymerase Chain Reaction Analysismentioning

confidence: 99%

See 1 more Smart Citation

Decreased thioredoxin reductase 3 expression promotes nickel‐induced damage to cardiac tissue via activating oxidative stress‐induced apoptosis and inflammation

Liu

et al. 2022

Environmental Toxicology

Self Cite

View full text Add to dashboard Cite

Thioredoxin reductase 3 (Txnrd3) plays a crucial role in antioxidant and anti-cancer activities, and sperm maturation. The damage of heavy metals, including Nickel (Ni), is the most prominent harm in social development, and hampering Txnrd3 might exacerbate Ni-induced cardiac damage. In this study, a total of 160 8-week-old C57BL/N male mice with 25-30 g weight of Txnrd3+/+ wild-type and Txnrd3À/À homozygote-type were randomly divided into eight groups. The mice in the control and Ni groups were gavaged with distilled water and a freshly prepared 10 mg/kg NiCl 2 solution. Melatonin (Mel) groups were administered at a concentration of 2 mg/kg for 21 days at the mice's 0.1 ml/10 g body weight. Ni exposure up-regulated the messenger RNA (mRNA) levels of mitochondrial apoptosis (caspase-3, caspase-9, cytochrome c, p53, and BAX), autophagy (LC3, ATG 1, ATG 7, and Beclin-1), and inflammation (TNF-α, COX 2, IL-1β, IL-2, IL-6, and IL-7)-related markers, but downregulated the mRNA levels of BCL-2, p62 and mTOR (p < .05). Ni exposure decreased the expression of BCL-2 and p62 protein but increased the expression levels of caspase-3, caspase-9, cytochrome c, p53, BAX, ATG 7, Beclin-1, TNF-α, COX 2, IL-1β and IL-2 protein (p < .05). Ni increased the contents of glutathione disulfide (GSSG) and malondialdehyde (MDA) and decreased the activities of catalase (CAT) and total superoxide dismutase (T-SOD) (p < .05). Decreased Txnrd3 expression significantly exacerbated changes compared to the Ni exposure (p < .05). Mel significantly attenuated these changes, but the effect decreased when Txnrd3 was inhibited (p < .05). In conclusion, decreased Txnrd3 expression promoted Ni-induced mitochondrial apoptosis and inflammation via oxidative stress and aggravated heart damage in mice. Decreased Txnrd3 expression significantly reduced the protective effect of Mel to Ni exposure.

show abstract

Section: Methodsmentioning

confidence: 99%

Section: Real-time Quantitative Polymerase Chain Reaction Analysismentioning

confidence: 99%

Decreased thioredoxin reductase 3 expression promotes nickel‐induced damage to cardiac tissue via activating oxidative stress‐induced apoptosis and inflammation

Liu

et al. 2022

Environmental Toxicology

Self Cite

View full text Add to dashboard Cite

show abstract

“…The phosphorylation of MLC regulates smooth muscle contractility. Motility disorders related to abnormal regulation of the Ca 2+ are observed in gastrointestinal inflammatory disorders ( 51 , 52 ). As in previous studies, our results showed that the increasing MLC phosphorylation in the DSS-induced cats was returned to normal levels by treatment with BBR, indicating that BBR benefits inflammation-related intestinal motility.…”

Section: Discussionmentioning

confidence: 99%

Berberine Depresses Inflammation and Adjusts Smooth Muscle to Ameliorate Ulcerative Colitis of Cats by Regulating Gut Microbiota

et al. 2022

Microbiol Spectr

View full text Add to dashboard Cite

show abstract

“…The cells were washed with PBS again. Then the images were observed and collected under inverted fluorescence microscope 37 …”

Section: Methodsmentioning

confidence: 99%

Curcumin alleviates ketamine‐induced oxidative stress and apoptosis via Nrf2 signaling pathway in rats' cerebral cortex and hippocampus

Zhang

Cui

Song

et al. 2022

Environmental Toxicology

View full text Add to dashboard Cite

Aims: To investigate curcumin's protective effect on nerve damage caused by ketamine anesthesia via the Nrf2 signaling pathway. Rats and PC12 cells were used in this experiment to investigate the mechanism of nerve injury caused by ketamine anesthesia. Furthermore, our findings suggest that curcumin may affect oxidative stress and apoptosis by targeting the Nrf2 pathway, thereby alleviating the nerve injury caused by ketamine. Methods:The rat cerebral cortex and hippocampus were stained with Nissl and immunohistochemistry to determine the number of neurons and the expression of Caspase-3, Bcl-2, and Bax. CCK-8 assay was used to determine the optimal concentration of ketamine, curcumin, and H 2 O 2 in PC12 cells. Flow cytometry was used to detect changes in reactive oxygen species and the rate of apoptosis in each group.To determine whether Nrf2 entered the nucleus, immunofluorescence was used.Both tissues and cells were subjected to RT-PCR and Western blotting detection at the same time. The levels of oxidative stress were determined using a malondialdehyde (MDA) and superoxide dismutase (SOD) assay kit.Results: Ketamine reduced the number of neurons in the cortex and hippocampus of rats. The proteins Bax and Caspase-3 were upregulated, while Bcl-2 was downregulated in the cortex and hippocampus. The viability of PC12 cells has decreased.MDA content increased while SOD activity decreased in cortex, hippocampus, and PC12 cells. Ketamine had an effect on the expression of some genes in the Nrf2 signaling pathway as well as apoptosis. Curcumin pretreatment may be able to prevent ketamine-induced damage. Conclusions:The oxidative stress and apoptosis caused by ketamine during growth of the cerebral cortex, hippocampus, and PC12 cells may be decreased by curcumin's activation of the Nrf2 signaling pathway. Our research provides a potential strategy for the secure administration of anesthetics in medical settings.

show abstract

The protective effect of selenoprotein M on non-alcoholic fatty liver disease: the role of the AMPKα1–MFN2 pathway and Parkin mitophagy

Cited by 60 publications

References 72 publications

Decreased thioredoxin reductase 3 expression promotes nickel‐induced damage to cardiac tissue via activating oxidative stress‐induced apoptosis and inflammation

Decreased thioredoxin reductase 3 expression promotes nickel‐induced damage to cardiac tissue via activating oxidative stress‐induced apoptosis and inflammation

Berberine Depresses Inflammation and Adjusts Smooth Muscle to Ameliorate Ulcerative Colitis of Cats by Regulating Gut Microbiota

Curcumin alleviates ketamine‐induced oxidative stress and apoptosis via Nrf2 signaling pathway in rats' cerebral cortex and hippocampus

Contact Info

Product

Resources

About