scholarly journals Anti-influenza A Virus Effects and Mechanisms of Emodin and Its Analogs via Regulating PPARα/γ-AMPK-SIRT1 Pathway and Fatty Acid Metabolism

2021 ◽  
Vol 2021 ◽  
pp. 1-17
Author(s):  
Yufei Bei ◽  
Boyu Tia ◽  
Yuze Li ◽  
Yingzhu Guo ◽  
Shufei Deng ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Influenza A Virus ◽  
Fatty Acid Metabolism ◽  
Influenza A ◽  
Acid Metabolism ◽  
Fatty Acid Biosynthesis ◽  
Sirtuin 1 ◽  
Peroxisome Proliferator ◽  
In Vivo Test

The peroxisome proliferator-activated receptor (PPAR) α/γ-adenosine 5 ′ -monophosphate- (AMP-) activated protein kinase- (AMPK-) sirtuin-1 (SIRT1) pathway and fatty acid metabolism are reported to be involved in influenza A virus (IAV) replication and IAV-pneumonia. Through a cell-based peroxisome proliferator responsive element- (PPRE-) driven luciferase bioassay, we have investigated 145 examples of traditional Chinese medicines (TCMs). Several TCMs, such as Polygonum cuspidatum, Rheum officinale Baillon, and Aloe vera var. Chinensis (Haw.) Berg., were found to possess high activity. We have further detected the anti-IAV activities of emodin (EMO) and its analogs, a group of common important compounds of these TCMs. The results showed that emodin and its several analogs possess excellent anti-IAV activities. The pharmacological tests showed that emodin significantly activated PPARα/γ and AMPK, decreased fatty acid biosynthesis, and increased intracellular ATP levels. Pharmaceutical inhibitors, siRNAs for PPARα/γ and AMPKα1, and exogenous palmitate impaired the inhibition of emodin. The in vivo test also showed that emodin significantly protected mice from IAV infection and pneumonia. Pharmacological inhibitors for PPARα/γ and AMPK signal and exogenous palmitate could partially counteract the effects of emodin in vivo. In conclusion, emodin and its analogs are a group of promising anti-IAV drug precursors, and the pharmacological mechanism of emodin is linked to its ability to regulate the PPARα/γ-AMPK pathway and fatty acid metabolism.

scholarly journals Increased Excretion of C4-Carnitine Species after a Therapeutic Acetylsalicylic Acid Dose: Evidence for an Inhibitory Effect on Short-Chain Fatty Acid Metabolism

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Catharina M. C. Mels ◽  
Peet Jansen van Rensburg ◽  
Francois H. van der Westhuizen ◽  
Pieter J. Pretorius ◽  
Elardus Erasmus
Keyword(s):  
Fatty Acid ◽  
Acetylsalicylic Acid ◽  
Fatty Acid Metabolism ◽  
Short Chain Fatty Acid ◽  
Acid Metabolism ◽  
Human Subjects ◽  
Inhibitory Effect ◽  
Chain Fatty Acid ◽  
Short Chain

Acetylsalicylic acid and/or its metabolites are implicated to have various effects on metabolism and, especially, on mitochondrial function. These effects include both inhibitory and stimulatory effects. We investigated the effect of both combined and separate oral acetylsalicylic acid and acetaminophen administration at therapeutic doses on the urinary metabolite profile of human subjects. In this paper, we provided in vivo evidence, in human subjects, of a statistically significant increase in isobutyrylcarnitine after the administration of a therapeutic dose of acetylsalicylic acid. We, therefore, propose an inhibitory effect of acetylsalicylic acid on the short-chain fatty acid metabolism, possibly at the level of isobutyryl-CoA dehydrogenase.

scholarly journals Switching fatty acid metabolism by an RNA-controlled feed forward loop

2020 ◽  
Vol 117 (14) ◽  
pp. 8044-8054 ◽  
Author(s):  
Michaela Huber ◽  
Kathrin S. Fröhlich ◽  
Jessica Radmer ◽  
Kai Papenfort
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
High Throughput Sequencing ◽  
Acid Metabolism ◽  
Fatty Acid Biosynthesis ◽  
Sequencing Analysis ◽  
Rnase E ◽  
Human Pathogen ◽  
Feed Forward ◽  
Feed Forward Loop

Hfq (host factor for phage Q beta) is key for posttranscriptional gene regulation in many bacteria. Hfq’s function is to stabilize sRNAs and to facilitate base-pairing withtrans-encoded target mRNAs. Loss of Hfq typically results in pleiotropic phenotypes, and, in the major human pathogenVibrio cholerae, Hfq inactivation has been linked to reduced virulence, failure to produce biofilms, and impaired intercellular communication. However, the RNA ligands of Hfq inV. choleraeare currently unknown. Here, we used RIP-seq (RNA immunoprecipitation followed by high-throughput sequencing) analysis to identify Hfq-bound RNAs inV. cholerae. Our work revealed 603 coding and 85 noncoding transcripts associated with Hfq, including 44 sRNAs originating from the 3′ end of mRNAs. Detailed investigation of one of these latter transcripts, named FarS (fatty acid regulated sRNA), showed that this sRNA is produced by RNase E-mediated maturation of thefabB3′UTR, and, together with Hfq, inhibits the expression of two paralogousfadEmRNAs. ThefabBandfadEgenes are antagonistically regulated by the major fatty acid transcription factor, FadR, and we show that, together, FadR, FarS, and FadE constitute a mixed feed-forward loop regulating the transition between fatty acid biosynthesis and degradation inV. cholerae. Our results provide the molecular basis for studies on Hfq inV. choleraeand highlight the importance of a previously unrecognized sRNA for fatty acid metabolism in this major human pathogen.

GC/MS-based metabolomics reveals fatty acid biosynthesis and cholesterol metabolism in cell lines infected with influenza A virus

Talanta ◽  
2010 ◽  
Vol 83 (1) ◽  
pp. 262-268 ◽  
Author(s):  
Shuhai Lin ◽  
Ning Liu ◽  
Zhu Yang ◽  
Wenjun Song ◽  
Pui Wang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Influenza A Virus ◽  
Cell Lines ◽  
Influenza A ◽  
Fatty Acid Biosynthesis ◽  
Cholesterol Metabolism ◽  
Acid Biosynthesis

Free fatty acid metabolism and obesity in man: In vivo in vitro comparisons

Metabolism ◽  
1986 ◽  
Vol 35 (6) ◽  
pp. 505-514 ◽  
Author(s):  
S. Lillioja ◽  
J. Foley ◽  
C. Bogardus ◽  
D. Mott ◽  
B.V. Howard
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Free Fatty Acid Metabolism
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