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Article ; Online: Effect of a probiotic fermented milk supplementation on behavior and sleep.

Freitas, Samara M / Franco, Beatriz / Saragiotto, Giulio / Morais, Milca A / Simabuco, Fernando M / Cunha, Diogo T / Esteves, Andrea M / Antunes, Adriane E C

Nutritional neuroscience

2023 , Page(s) 1–13

Abstract: This study attempted to analyze the effect of supplementing Wistar-Kyoto rats with fermented milk containing the ... ...

Abstract	This study attempted to analyze the effect of supplementing Wistar-Kyoto rats with fermented milk containing the probiotic
Language	English
Publishing date	2023-07-26
Publishing country	England
Document type	Journal Article
ZDB-ID	1447449-9
ISSN	1476-8305 ; 1028-415X
ISSN (online)	1476-8305
ISSN	1028-415X
DOI	10.1080/1028415X.2023.2240990
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Article ; Online: Hypothalamic α7 nicotinic acetylcholine receptor (α7nAChR) is downregulated by TNFα-induced Let-7 overexpression driven by fatty acids.

Simino, Laís A P / Baqueiro, Mayara N / Panzarin, Carolina / Lopes, Priscilla K F / Góis, Mariana M / Simabuco, Fernando M / Ignácio-Souza, Letícia M / Milanski, Marciane / Ross, Michael G / Desai, Mina / Torsoni, Adriana S / Torsoni, Marcio A

FASEB journal : official publication of the Federation of American Societies for Experimental Biology

2023 Volume 37, Issue 9, Page(s) e23120

Abstract: The α7nAChR is crucial to the anti-inflammatory reflex, and to the expression of neuropeptides that control food intake, but its expression can be decreased by environmental factors. We aimed to investigate whether microRNA modulation could be an ... ...

Abstract	The α7nAChR is crucial to the anti-inflammatory reflex, and to the expression of neuropeptides that control food intake, but its expression can be decreased by environmental factors. We aimed to investigate whether microRNA modulation could be an underlying mechanism in the α7nAchR downregulation in mouse hypothalamus following a short-term exposure to an obesogenic diet. Bioinformatic analysis revealed Let-7 microRNAs as candidates to regulate Chrna7, which was confirmed by the luciferase assay. Mice exposed to an obesogenic diet for 3 days had increased Let-7a and decreased α7nAChR levels, accompanied by hypothalamic fatty acids and TNFα content. Hypothalamic neuronal cells exposed to fatty acids presented higher Let-7a and TNFα levels and lower Chrna7 expression, but when the cells were pre-treated with TLR4 inhibitor, Let-7a, TNFα, and Chrna7 were rescued to normal levels. Thus, the fatty acids overload trigger TNFα-induced Let-7 overexpression in hypothalamic neuronal cells, which negatively regulates α7nAChR, an event that can be related to hyperphagia and obesity predisposition in mice.
MeSH term(s)	Animals ; Mice ; alpha7 Nicotinic Acetylcholine Receptor/genetics ; alpha7 Nicotinic Acetylcholine Receptor/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Fatty Acids ; Down-Regulation ; Hypothalamus/metabolism
Chemical Substances	alpha7 Nicotinic Acetylcholine Receptor ; Tumor Necrosis Factor-alpha ; Fatty Acids
Language	English
Publishing date	2023-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639186-2
ISSN	1530-6860 ; 0892-6638
ISSN (online)	1530-6860
ISSN	0892-6638
DOI	10.1096/fj.202300439RR
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Zs.A 2266: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (1.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 296: Show issues

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Article ; Online: Acute exercise modulates Trim63 and Bmal1 in the skeletal muscle of IL-10 knockout mice.

da Mata, Gustavo Eduardo / Bricola, Rafael / Ribeiro, Danielle Naves / Simabuco, Fernando M / Pauli, José R / de Freitas, Ellen C / Ropelle, Eduardo R / da Silva, Adelino S R / Pinto, Ana P

Cytokine

2023 Volume 175, Page(s) 156484

Abstract: ... started at 6 m/min, followed by 3 m/min increments every 3 min until animal exhaustion. Two hours after ...

Abstract	The anti-inflammatory role of physical exercise is mediated by interleukin 10 (IL-10), and their release is possibly upregulated in response to IL-6. Previous studies demonstrated that mice lacking IL-6 (IL-6 KO mice) exhibited diminished exercise tolerance, and reduced strength. Rev-erbα, a transcriptional suppressor involved in circadian rhythm, has been discovered to inhibit the expression of genes linked to bodily functions, encompassing inflammation and metabolism. It also plays a significant role in skeletal muscle and exercise performance capacity. Given the potential association between Rev-erbα and the immune system and the fact that both pathways are modulated following acute aerobic exercise, we examined the physical performance of IL-10 KO mice and analyzed the modulation of the atrophy and Rev-erbα pathways in the muscle of wild type (WT) and IL-10 KO mice following one session of acute exercise. For each phenotype, WT and IL-10 KO were divided into two subgroups (Control and Exercise). The acute exercise session started at 6 m/min, followed by 3 m/min increments every 3 min until animal exhaustion. Two hours after the end of the exercise protocol, the gastrocnemius muscle was removed and prepared for the reverse transcription-quantitative polymerase chain reaction (RT-q-PCR) and immunoblotting technique. In summary, compared to WT, the IL-10 KO animals showed lower body weight and grip strength in the baseline. The IL-10 control group presented a lower protein content of BMAL1. After the exercise protocol, the IL-10 KO group had higher mRNA levels of Trim63 (atrophy signaling pathway) and lower mRNA levels of Clock and Bmal1 (Rev-erbα signaling pathway). This is the first study showing the relationship between Rev-erbα and atrophy in IL-10 KO mice. Also, we accessed a public database that analyzed the gastrocnemius of MuRF KO mice submitted to two processes of muscle atrophy, a denervation surgery and dexamethasone (Dexa) injections. Independently of knockout, the denervation demonstrated lower Nr1d1 levels. In conclusion, IL-10 seems to be a determinant in the Rev-erbα pathway and atrophy after acute exercise, with no modulation in the baseline state.
MeSH term(s)	Animals ; Mice ; ARNTL Transcription Factors/genetics ; ARNTL Transcription Factors/metabolism ; Atrophy ; Interleukin-10/genetics ; Interleukin-6/genetics ; Mice, Knockout ; Muscle Proteins/genetics ; Muscle, Skeletal/metabolism ; RNA, Messenger/metabolism ; Tripartite Motif Proteins ; Ubiquitin-Protein Ligases
Chemical Substances	ARNTL Transcription Factors ; Interleukin-10 (130068-27-8) ; Interleukin-6 ; Muscle Proteins ; RNA, Messenger ; Trim63 protein, mouse (EC 2.3.2.27) ; Tripartite Motif Proteins ; Ubiquitin-Protein Ligases (EC 2.3.2.27) ; IL10 protein, mouse ; Bmal1 protein, mouse
Language	English
Publishing date	2023-12-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1018055-2
ISSN	1096-0023 ; 1043-4666
ISSN (online)	1096-0023
ISSN	1043-4666
DOI	10.1016/j.cyto.2023.156484
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Article ; Online: Regular swimming exercise prevented the acute and persistent mechanical muscle hyperalgesia by modulation of macrophages phenotypes and inflammatory cytokines via PPARγ receptors.

de Azambuja, Graciana / Jorge, Carolina O / Gomes, Beatriz B / Lourenço, Hayla R / Simabuco, Fernando M / Oliveira-Fusaro, Maria Claudia G

Brain, behavior, and immunity

2021 Volume 95, Page(s) 462–476

Abstract: Physically active individuals are less likely to develop chronic pain, and physical exercise is an established strategy to control inflammatory diseases. Here, we hypothesized that 1) peripheral pro-inflammatory macrophages phenotype contribute to ... ...

Abstract	Physically active individuals are less likely to develop chronic pain, and physical exercise is an established strategy to control inflammatory diseases. Here, we hypothesized that 1) peripheral pro-inflammatory macrophages phenotype contribute to predisposition of the musculoskeletal to chronic pain, and that 2) activation of PPARγ receptors, modulation of macrophage phenotypes and cytokines through physical exercise would prevent persistent muscle pain. We tested these hypotheses using swimming exercise, pharmacological and immunochemical techniques in a rodent model of persistent muscle hyperalgesia. Swimming prevented the persistent mechanical muscle hyperalgesia most likely through activation of PPARγ receptors, as well as activation of PPARγ receptors by 15d-PGJ
MeSH term(s)	Animals ; Cytokines ; Hyperalgesia ; Macrophages ; Male ; Mice ; Muscles/metabolism ; PPAR gamma ; Phenotype ; Physical Conditioning, Animal ; Prostaglandin D2/analogs & derivatives
Chemical Substances	15-deoxyprostaglandin J2 ; Cytokines ; PPAR gamma ; Prostaglandin D2 (RXY07S6CZ2)
Language	English
Publishing date	2021-05-06
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639219-2
ISSN	1090-2139 ; 0889-1591
ISSN (online)	1090-2139
ISSN	0889-1591
DOI	10.1016/j.bbi.2021.05.002
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Zs.A 2276: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 327: Show issues

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Article ; Online: TLR4-interactor with leucine-rich repeats (TRIL) is involved in diet-induced hypothalamic inflammation.

Moura-Assis, Alexandre / Nogueira, Pedro A S / de-Lima-Junior, Jose C / Simabuco, Fernando M / Gaspar, Joana M / Donato, Jose / Velloso, Licio A

Scientific reports

2021 Volume 11, Issue 1, Page(s) 18015

Abstract: Obesity and high-fat diet (HFD) consumption result in hypothalamic inflammation and metabolic dysfunction. While the TLR4 activation by dietary fats is a well-characterized pathway involved in the neuronal and glial inflammation, the role of its ... ...

Abstract	Obesity and high-fat diet (HFD) consumption result in hypothalamic inflammation and metabolic dysfunction. While the TLR4 activation by dietary fats is a well-characterized pathway involved in the neuronal and glial inflammation, the role of its accessory proteins in diet-induced hypothalamic inflammation remains unknown. Here, we demonstrate that the knockdown of TLR4-interactor with leucine-rich repeats (Tril), a functional component of TLR4, resulted in reduced hypothalamic inflammation, increased whole-body energy expenditure, improved the systemic glucose tolerance and protection from diet-induced obesity. The POMC-specific knockdown of Tril resulted in decreased body fat, decreased white adipose tissue inflammation and a trend toward increased leptin signaling in POMC neurons. Thus, Tril was identified as a new component of the complex mechanisms that promote hypothalamic dysfunction in experimental obesity and its inhibition in the hypothalamus may represent a novel target for obesity treatment.
MeSH term(s)	Adipose Tissue/metabolism ; Adipose Tissue/pathology ; Animals ; Diet, High-Fat/adverse effects ; Energy Metabolism/genetics ; Gene Expression Regulation ; Glucose Tolerance Test ; Hypothalamus/pathology ; Inflammation ; Intercellular Signaling Peptides and Proteins/deficiency ; Intercellular Signaling Peptides and Proteins/genetics ; Male ; Membrane Proteins/deficiency ; Membrane Proteins/genetics ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Neurons/metabolism ; Neurons/pathology ; Obesity/etiology ; Obesity/metabolism ; Obesity/pathology ; Pro-Opiomelanocortin/genetics ; Pro-Opiomelanocortin/metabolism ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Signal Transduction ; Toll-Like Receptor 4/genetics ; Toll-Like Receptor 4/metabolism
Chemical Substances	Intercellular Signaling Peptides and Proteins ; Membrane Proteins ; RNA, Messenger ; Tlr4 protein, mouse ; Toll-Like Receptor 4 ; Tril protein, mouse ; Pro-Opiomelanocortin (66796-54-1)
Language	English
Publishing date	2021-09-09
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-97291-7
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Article ; Online: Exercise training restores weight gain and attenuates hepatic inflammation in a rat model of non-celiac gluten sensitivity.

Pauli, José R / Muñoz, Vitor R / Vieira, Renan Fudoli Lins / Nakandakari, Susana C B R / Macêdo, Ana Paula Azevêdo / de Lima, Robson Damasceno / Antunes, Gabriel Calheiros / Simabuco, Fernando M / da Silva, Adelino Sanchez Ramos / de Moura, Leandro P / Ropelle, Eduardo R / Cintra, Dennys E / Mekary, Rania A / Zaghloul, Iman

Journal of cellular biochemistry

2023 Volume 124, Issue 4, Page(s) 520–532

Abstract: Gluten intolerance is associated with several disorders in the body. Although research has grown in recent years, the understanding of its impact on different tissues and the effects of physical exercise in mitigating health problems in the condition of ... ...

Abstract	Gluten intolerance is associated with several disorders in the body. Although research has grown in recent years, the understanding of its impact on different tissues and the effects of physical exercise in mitigating health problems in the condition of gluten intolerance are still limited. Therefore, our objective was to test whether gliadin would affect metabolism and inflammation in liver tissue and whether aerobic physical exercise would mitigate the negative impacts of gliadin administration in rodents. Wistar rats were divided into exercised gliadin, gliadin, and control groups. Gliadin was administered by gavage from birth to 60 days of age. The rats in the exercised gliadin group performed an aerobic running exercise training protocol for 15 days. At the end of the experiments, physiological, histological, and molecular analyzes were performed in the study. Compared to the control group, the gliadin group had impaired weight gain and increased gluconeogenesis, lipogenesis, and inflammatory biomarkers in the liver. On the other hand, compared to the gliadin group, animals in the exercise-gliadin group had a recovery in body weight, improved insulin sensitivity, and a reduction in some gluconeogenesis, lipogenesis, and inflammatory biomarkers in the liver. In conclusion, our results revealed that the administration of gliadin from birth impaired weight gain and induced an increase in hepatic inflammatory cytokines, which was associated with an impairment of glycemic homeostasis in the liver, all of which were attenuated by adding aerobic exercise training in the gliadin group.
MeSH term(s)	Rats ; Animals ; Gliadin ; Rats, Wistar ; Celiac Disease/metabolism ; Weight Gain ; Inflammation/chemically induced ; Inflammation/therapy ; Biomarkers
Chemical Substances	Gliadin (9007-90-3) ; Biomarkers
Language	English
Publishing date	2023-02-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.30387
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Article ; Online: Correction: p53 and metabolism: from mechanism to therapeutics.

Simabuco, Fernando M / Morale, Mirian G / Pavan, Isadora C B / Morelli, Ana P / Silva, Fernando R / Tamura, Rodrigo E

Oncotarget

2018 Volume 9, Issue 74, Page(s) 34030

Abstract: This corrects the article DOI: 10.18632/oncotarget.25267.]. ...

Abstract	[This corrects the article DOI: 10.18632/oncotarget.25267.].
Language	English
Publishing date	2018-09-21
Publishing country	United States
Document type	Journal Article ; Published Erratum
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.26181
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Article ; Online: Genetic ablation of Toll-like Receptor 4 seems to activate the apoptosis pathway in the skeletal muscle of mice after acute physical exercise.

Marafon, Bruno B / Pinto, Ana P / de Vicente, Larissa G / da Rocha, Alisson L / Simabuco, Fernando M / Ropelle, Eduardo R / de Moura, Leandro P / Cintra, Dennys E / Pauli, José R / Silva, Adelino S R da

Cell biochemistry and function

2022

Abstract: Many conditions, such as inflammation and physical exercise, can induce endoplasmic reticulum (ER) stress. Toll-like Receptor 4 (TLR4) can trigger inflammation and ER stress events. However, there are still no data in the literature regarding the role of ...

Abstract	Many conditions, such as inflammation and physical exercise, can induce endoplasmic reticulum (ER) stress. Toll-like Receptor 4 (TLR4) can trigger inflammation and ER stress events. However, there are still no data in the literature regarding the role of TLR4 in ER stress during exercise in skeletal muscle. Therefore, the current investigation aimed to verify the responses of ER stress markers in wild-type (WT) and Tlr4 global knockout (KO) mice after acute and chronic physical exercise protocols. Eight-week-old male WT and KO mice were submitted to acute (moderate or high intensity) and chronic (4-week protocol) treadmill exercises. Under basal conditions, KO mice showed lower performance in the rotarod test. Acute high-intensity exercise increased eIF2α protein in the WT group. After the acute high-intensity exercise, there was an increase in Casp3 and Ddit3 mRNA for the KO mice. Acute moderate exercise increased the cleaved Caspase-3/Caspase-3 in the KO group. In response to chronic exercise, the KO group showed no improvement in any performance evaluation. The 4-week chronic protocol did not generate changes in ATF6, CHOP, p-IRE1α, p-eIF2α/eIF2α, and cleaved Caspase-3/Caspase-3 ratio but reduced BiP protein compared with the KO-Sedentary group. These results demonstrate the global deletion of Tlr4 seems to have the same effects on UPR markers of WT animals after acute and chronic exercise protocols but decreased performance. The cleaved Caspase-3/Caspase-3 ratio may be activated by another pathway other than ER stress in Tlr4 KO animals.
Language	English
Publishing date	2022-11-22
Publishing country	England
Document type	Journal Article
ZDB-ID	283643-9
ISSN	1099-0844 ; 0263-6484
ISSN (online)	1099-0844
ISSN	0263-6484
DOI	10.1002/cbf.3765
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Article ; Online: Knockout of NRF2 triggers prostate cancer cells death through ROS modulation and sensitizes to cisplatin.

Mancini, Mariana C S / Morelli, Ana P / Severino, Matheus B / Pavan, Isadora C B / Zambalde, Érika P / Góis, Mariana M / Silva, Luiz G S da / Quintero-Ruiz, Nathalia / Romeiro, Caio F / Dos Santos, Daniel F G / Bezerra, Rosângela M N / Simabuco, Fernando M

Journal of cellular biochemistry

2022

Abstract: Prostate cancer (PCa) represents the second most common cancer in men and affects millions worldwide. Chemotherapy is a common treatment for PCa but the development of resistance is often a problem during therapy. NRF2 (nuclear factor erythroid 2-related ...

Abstract	Prostate cancer (PCa) represents the second most common cancer in men and affects millions worldwide. Chemotherapy is a common treatment for PCa but the development of resistance is often a problem during therapy. NRF2 (nuclear factor erythroid 2-related factor 2) is one of the major transcription factors regulating antioxidant enzymes and is also involved with drug efflux and detoxification. Cancer cells submitted to chemotherapy often promote NRF2 activation to benefit themselves with the cytoprotective response. Here, we found that DU145 and PC3 PCa cell lines have different responses regarding NRF2 activation, when subjected to arsenite-induced stress, even in the presence of MG132, a proteasome inhibitor. We also observed that only in PC3 cells treated with arsenite, NRF2 was able to translocate to the nucleus. To better understand the role of NRF2 in promoting chemoresistance, we performed CRISPR knockout of NRF2 (NKO) in DU145 and PC3 cells. The effectiveness of the knockout was confirmed through the downregulation of NRF2 targets (p < 0.0001). PC3 NKO cells exhibited higher levels of reactive oxygen species (ROS) compared to wild-type cells (p < 0.0001), while this alteration was not observed in DU145 NKO cells. Despite no modulation in ROS content, a lower IC50 value (p < 0.05) for cisplatin was observed in DU145 NKO cells, suggesting that the knockout sensitized the cells to the treatment. Besides, the treatment of DU145 NKO with cisplatin led cells to apoptosis as observed by the increased levels of PARP1 cleavage (p < 0.05), possibly triggered by increased DNA damage. Reduced levels of KU70 and phospho-CHK2 (p < 0.05) were also detected. The data presented here support that NRF2 is a mediator of oncogenesis and could be a potential target to sensitize PCa cells to chemotherapy, reinforcing the importance of knowing the specific genetic and biochemical characteristics of the cancer cells for a more effective approach against cancer.
Language	English
Publishing date	2022-10-03
Publishing country	United States
Document type	Journal Article
ZDB-ID	392402-6
ISSN	1097-4644 ; 0730-2312
ISSN (online)	1097-4644
ISSN	0730-2312
DOI	10.1002/jcb.30333
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Article ; Online: IL-6 deletion decreased REV-ERBα protein and influenced autophagy and mitochondrial markers in the skeletal muscle after acute exercise.

Pinto, Ana P / Muñoz, Vitor R / da Rocha, Alisson L / Rovina, Rafael L / Ferrari, Gustavo D / Alberici, Luciane C / Simabuco, Fernando M / Teixeira, Giovana R / Pauli, José R / de Moura, Leandro P / Cintra, Dennys E / Ropelle, Eduardo R / Freitas, Ellen C / Rivas, Donato A / da Silva, Adelino S R

Frontiers in immunology

2022 Volume 13, Page(s) 953272

Abstract: Interleukin 6 (IL-6) acts as a pro and anti-inflammatory cytokine, has an intense correlation with exercise intensity, and activates various pathways such as autophagy and mitochondrial unfolded protein response. Also, IL-6 is interconnected to circadian ...

Abstract	Interleukin 6 (IL-6) acts as a pro and anti-inflammatory cytokine, has an intense correlation with exercise intensity, and activates various pathways such as autophagy and mitochondrial unfolded protein response. Also, IL-6 is interconnected to circadian clock-related inflammation and can be suppressed by the nuclear receptor subfamily 1, group D, member 1 (
MeSH term(s)	Animals ; Mice ; Autophagy/genetics ; Biomarkers ; Gene Products, rev ; Interleukin-6/genetics ; Interleukin-6/metabolism ; Muscle, Skeletal/metabolism ; Nuclear Receptor Subfamily 1, Group D, Member 1/genetics ; Nuclear Receptor Subfamily 1, Group D, Member 1/metabolism
Chemical Substances	Biomarkers ; Gene Products, rev ; Interleukin-6 ; Nuclear Receptor Subfamily 1, Group D, Member 1 ; SR9009 ; interleukin-6, mouse ; Nr1d1 protein, mouse
Language	English
Publishing date	2022-10-13
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.953272
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