Taurochenodeoxycholic acid mediates cAMP-PKA-CREB signaling pathway

Qi, Youchao; Duan, Guozhen; Mao, Wei; Liu, Qian; Zhang, Yongliang; Li, Peifeng

doi:10.1016/s1875-5364(20)60033-4

Cited by 18 publications

(17 citation statements)

References 18 publications

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“…Therefore, further metabolomic profiling analysis of quadriceps muscles between Swimming and Tumor groups identified a variety of DEMs, including taurochenodeoxycholic acid, taurocholic acid, ascorbic acid and eicosapentaenoic acid, which are closely related to inflammation and immune regulation. Among them, taurfodeoxycholic acid plays an important role in anti-inflammatory effects through the TGR5 receptor-induced cAMP-PKA-CREB signaling pathway, specifically by activating kappa light chain enhancer in B cells, reducing the activities of TNF-α, IL-1β and IL-6 ( Qi et al, 2020 ). Taurocholic acid not only exhibits the effects of anti-inflammation, lowering blood pressure, and reducing the amplitude and frequency of cardiac contraction ( Taranto et al, 2001 ), it is also involved in immune response by directly inhibiting the apoptosis of immune cells at different stages ( Schwarz et al, 1975 ; Rodriguez-Garay et al, 1999 ).…”

Section: Discussionmentioning

confidence: 99%

Swimming Attenuates Muscle Wasting and Mediates Multiple Signaling Pathways and Metabolites in CT-26 Bearing Mice

Xie²,

Liu³

et al. 2022

Front. Mol. Biosci.

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Objectives: To investigate the effects of swimming on cancer induced muscle wasting and explore its underlying mechanism in CT-26 bearing mice.Methods: BALB/c mice (n = 16) injected with CT-26 cells were divided into two groups, including Tumor group (n = 8) and Swimming group (n = 8). Another 8 un-injected mice were set as Control group. Mice in Swimming group were subjected to physical training for swimming twice per day for 30 min intervals and 6 days per week for a total of 4 weeks. The tumor volume was monitored every 3 days and tumor weight was measured at the end of experiment. The changes of muscle function, pathological and cell apoptosis of quadriceps muscles were further assessed, and its underlying mechanisms were further explored using multiple biological technologies.Results: Swimming obviously alleviated tumor volume and weight in CT-26 bearing mice. Moreover, swimming attenuated the decrease of muscle tension, autonomic activities, and increase of muscle atrophy, pathological ultrastructure, as well as cell apoptosis of quadriceps muscles in CT-26 bearing mice. Furthermore, swimming significantly down-regulated the protein expression of NF-κB, p-NF-κB, TNF-α, IL-1β, IL-6 and Bax, while up-regulated the expression of Bcl-2. Further differential expressed metabolites (DEMs) analysis identified a total of 76 (in anion mode) and 330 (in cationic mode) DEMs in quadriceps muscles of CT-26 bearing mice after swimming, including taurochenodeoxycholic acid, taurocholic acid, ascorbic acid and eicosapentaenoic acid.Conclusion: Swimming attenuates tumor growth and muscle wasting, and by suppressing the activation of NF-κB signaling pathway mediated inflammation, reducing the level of Bax medicated cell apoptosis, as well as modulating multiple metabolites might be the importantly underlying mechanisms.

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Section: Discussionmentioning

confidence: 99%

Swimming Attenuates Muscle Wasting and Mediates Multiple Signaling Pathways and Metabolites in CT-26 Bearing Mice

Xie²,

Liu³

et al. 2022

Front. Mol. Biosci.

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“…Thus, the anti-inflammatory functions of vitamin E may indirectly result from its suppressive effects on oxidative stress. Furthermore, vitamin E was found to directly stimulate the production of cyclic adenosine monophosphate (cAMP) in human peripheral mononuclear cells via the EP2/EP4 receptors and adenylyl cyclase [ 42 ], which in turn activated its downstream proteins (protein kinase A and cAMP response element binding) and then suppressed the release of pro-inflammatory cytokines (such as TNF-α and IL-6) from monocytes [ 43 ]. Importantly, there was evidence to demonstrate that up-regulation of TNF-α triggered the production of IL-6 [ 44 ], while IL-6 stimulated the transcription and synthesis of CRP [ 45 ] and IgE [ 46 ].…”

Section: Discussionmentioning

confidence: 99%

Vitamin Supplementation Protects against Nanomaterial-Induced Oxidative Stress and Inflammation Damages: A Meta-Analysis of In Vitro and In Vivo Studies

Xie

Yang

et al. 2022

Nutrients

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The extensive applications of nanomaterials have increased their toxicities to human health. As a commonly recommended health care product, vitamins have been reported to exert protective roles against nanomaterial-induced oxidative stress and inflammatory responses. However, there have been some controversial conclusions in regards to this field of research. This meta-analysis aimed to comprehensively evaluate the roles and mechanisms of vitamins for cells and animals exposed to nanomaterials. Nineteen studies (seven in vitro, eleven in vivo and one in both) were enrolled by searching PubMed, EMBASE, and Cochrane Library databases. STATA 15.0 software analysis showed vitamin E treatment could significantly decrease the levels of oxidants [reactive oxygen species (ROS), total oxidant status (TOS), malondialdehyde (MDA)], increase anti-oxidant glutathione peroxidase (GPx), suppress inflammatory mediators (tumor necrosis factor-α, interleukin-6, C-reactive protein, IgE), improve cytotoxicity (manifested by an increase in cell viability and a decrease in pro-apoptotic caspase-3 activity), and genotoxicity (represented by a reduction in the tail length). These results were less changed after subgroup analyses. Pooled analysis of in vitro studies indicated vitamin C increased cell viability and decreased ROS levels, but its anti-oxidant potential was not observed in the meta-analysis of in vivo studies. Vitamin A could decrease MDA, TOS and increase GPx, but its effects on these indicators were weaker than vitamin E. Also, the combination of vitamin A with vitamin E did not provide greater anti-oxidant effects than vitamin E alone. In summary, we suggest vitamin E alone supplementation may be a cost-effective option to prevent nanomaterial-induced injuries.

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“…Since any intense acute physical stress is a pro-inflammatory stimulus with an anti-inflammatory counter-regulation, this could explain the downregulation of this bile acid in athletes [ 26 ]. The regulation of cAMP is also linked to this bile acid, so that regular energetic stress could also influence the release of TCDCA [ 27 ]. CA and CDCA represent primary bile acids, which are synthesized from cholesterol in the liver, and they are converted to secondary bile acids (DCA and TCA) in the intestine [ 28 ].…”

Section: Discussionmentioning

confidence: 99%

Sustained Endurance Training Leads to Metabolomic Adaptation

et al. 2022

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Endurance training induces several adaptations in substrate metabolism, especially in relation to glycogen conservation. The study aimed to investigate differences in the metabolism of lipids, lipid-like substances, and amino acids between highly trained and untrained subjects using targeted metabolomics. Depending on their maximum relative oxygen uptake (VO2max), subjects were categorized as either endurance-trained (ET) or untrained (UT). Resting blood was taken and plasma isolated. It was screened for changes of 345 metabolites, including amino acids and biogenic amines, acylcarnitines, glycerophosphocholines (GPCs), sphingolipids, hexoses, bile acids, and polyunsaturated fatty acids (PUFAs) by using liquid chromatography coupled to tandem mass spectrometry. Acylcarnitine (C14:1, down in ET) and five GPCs (lysoPC a C18:2, up in ET; PC aa C42:0, up in ET; PC ae C38:2, up in ET; PC aa C38:5, down in ET; lysoPC a C26:0, down in ET) were differently regulated in ET compared to UT. TCDCA was down-regulated in athletes, while for three ratios of bile acids CA/CDCA, CA/(GCA+TCA), and DCA/(GDCA+TDCA) an up-regulation was found. TXB2 and 5,6-EET were down-regulated in the ET group and 18S-HEPE, a PUFA, showed higher levels in 18S-HEPE in endurance-trained subjects. For PC ae C38:2, TCDCA, and the ratio of cholic acid to chenodeoxycholic acid, an association with VO2max was found. Numerous phospholipids, acylcarnitines, glycerophosphocholines, bile acids, and PUFAs are present in varying concentrations at rest in ET. These results might represent an adaptation of lipid metabolism and account for the lowered cardiovascular risk profile of endurance athletes.

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Taurochenodeoxycholic acid mediates cAMP-PKA-CREB signaling pathway

Cited by 18 publications

References 18 publications

Swimming Attenuates Muscle Wasting and Mediates Multiple Signaling Pathways and Metabolites in CT-26 Bearing Mice

Swimming Attenuates Muscle Wasting and Mediates Multiple Signaling Pathways and Metabolites in CT-26 Bearing Mice

Vitamin Supplementation Protects against Nanomaterial-Induced Oxidative Stress and Inflammation Damages: A Meta-Analysis of In Vitro and In Vivo Studies

Sustained Endurance Training Leads to Metabolomic Adaptation

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