Cadmium induced skeletal underdevelopment, liver cell apoptosis and hepatic energy metabolism disorder in Bufo gargarizans larvae by disrupting thyroid hormone signaling

Abstract BackgroundAmmonia (NH3) is a well-known environmental pollution gas, threatening human health. NH3 is also the most harmful gas to poultry for many years. Some studies have found NH3 can damage eyes, respiratory system, and digestive system. However, molecular mechanism of NH3 toxicity on chicken livers remains unclear. MethodsIn this study, we selected chicken liver as research object and successfully duplicated NH3 poisoning model of chickens. The ultrastructure of chicken livers was observed. The activities of ATPases (Na+K+-ATPase, Mg++-ATPase, Ca++-ATPase, and Ca++Mg++-ATPase) and the expression of energy metabolism-related genes (HK1, HK2, PK, PFK, PDHX, CS, LDHA, LDHB, AMPK, SDHA, SDHB, and avUCP) and autophagy-related genes (PI3K, LC3I, LC3II, Beclin1, SQSTM1, mTOR, ULK1, ATG5, ATG12, and ATG13) were measured to explore the effect of NH3 on energy metabolism and autophagy in chicken livers.ResultsOur results showed that excess NH3 caused liver tissue damage. Meanwhile, ATPases activities were inhibited during NH3 treatment. Moreover, we found that NH3 exposure altered the expression of energy metabolism-related and autophagy-related genes. NH3-induced compensatory increase of AMPK activated autophagy process through inhibiting mTOR and promoting ULK1. In addition. there was dose-dependent and time-dependent effects on all detected indexes in NH3-caused chicken liver damage. ConclusionExcess NH3 induced energy metabolism disorder and autophagy via AMPK/mTOR/ULK1 pathway in chicken livers.

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Extraction of breviscapine from Erigeron breviscapus and its effect on oxidative stress, inflammation, energy metabolism disorder and apoptosis in rats with uterine ischemia-reperfusion injury

Food Science and Technology ◽

10.1590/fst.31421 ◽

2021 ◽

Author(s):

Yunxiu ZHAO ◽

Yongzhen ZHANG ◽

Yanyan ZHANG ◽

Bing HAN ◽

Huan CHANG ◽

...

Keyword(s):

Oxidative Stress ◽

Energy Metabolism ◽

Reperfusion Injury ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Metabolism Disorder ◽

Erigeron Breviscapus ◽

Energy Metabolism Disorder

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LncRNA FENDRR Inhibits ox-LDL Induced Mitochondrial Energy Metabolism Disorder in Aortic Endothelial Cells via miR-18a-5p/PGC-1α Signaling Pathway

Frontiers in Endocrinology ◽

10.3389/fendo.2021.622665 ◽

2021 ◽

Vol 12 ◽

Author(s):

Guiming Wang ◽

Yudong Yang ◽

Honggang Ma ◽

Liuming Shi ◽

Wenbin Jia ◽

...

Keyword(s):

Energy Metabolism ◽

Mitochondrial Dysfunction ◽

Signaling Pathway ◽

Antioxidant Defense ◽

Signal Pathway ◽

Transcription Activator ◽

Mitochondrial Energy Metabolism ◽

Aortic Endothelial Cells ◽

Metabolism Disorder ◽

Energy Metabolism Disorder

Atherosclerosis (AS) is the main cause of morbidity and mortality in the world. Mitochondrial dysfunction is closely related to AS. At present, several signaling pathways related to mitochondrial dysfunction have been found, one of which is around PGC-1α. PGC-1α is a transcription activator, which is related to mitochondrial biogenesis and antioxidant defense. In this study, we explored the effect of miR-18a-5p/PGC-1α signaling pathway on mitochondrial energy metabolism in HAECs with ox-LDL treatment. The results showed that the mitochondrial energy metabolism disorder in HAECs treated by ox-LDL was related to the downregulation of LncRNA FENDRR and PGC-1α. FENDRR could reverse ox-LDL induced mitochondrial energy metabolism disorder and upregulate the PGC-1α expression. FENDRR could be used as ceRNA to inhibit the miR-18a-5p expression and reduce the negative regulation of miR-18a-5p on PGC-1α. Downregulation of miR-18a-5p expression or upregulation of PGC-1α in ox-LDL treated HAECs could reverse mitochondrial energy metabolism disorder. In conclusion, these findings suggested that FENDRR/miR-18a-5p/PGC-1α signaling pathway regulated mitochondrial energy metabolism in HAECs; ox-LDL downregulated the expression of PGC-1α and cause mitochondrial energy metabolism disorder by inhibiting this signal pathway.

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