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1.
Front Neurosci ; 17: 1074327, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-37360175

RESUMO

Introduction: Erectile dysfunction (ED), especially psychological ED (pED), is usually accompanied with psychological factors, which are related to abnormal activity in brain regions involved in sexual behavior. However, the mechanisms underlying functional changes in the brain of pED are still unclear. The present study aimed to explore the abnormalities of brain function, as well as their relationships with sexual behavior and emotion in pED patients. Materials and methods: Resting state functional magnetic resonance imaging (rs-fMRI) data were collected from 31 pED patients to 31 healthy controls (HCs). The values of amplitude of fractional amplitude of low-frequency fluctuation (fALFF) and functional connectivity (FC) were calculated and compared between groups. In addition, the associations between abnormal brain regions and clinical features were evaluated by Pearson correlation analyses. Results: Compared to HCs, pED patients demonstrated decreased fALFF values in the left medial superior frontal gyrus (had decreased FC values with the left dorsolateral superior frontal gyrus), the left lingual gyrus (had decreased FC values with the left parahippocamal gyrus and insula), the left putamen (had decreased FC values with the right caudate) and the right putamen (had decreased FC values with the left putamen and the right caudate). The fALFF values of the left medial superior frontal gyrus were negatively correlated with the fifth item scores of International Index of Erectile Function (IIEF-5). Negative relationships were found between fALFF values of the left putamen and the second item scores of Arizona Sexual Scale (ASEX). FC values between the right putamen and caudate were negatively related to the state scores of State-Trait Anxiety Inventory (STAI-S). Conclusion: Altered brain function were found in the medial superior frontal gyrus and caudate-putamen of pED patients, which were associated with sexual function and psychological condition. These findings provided new insights into the central pathological mechanisms of pED.

2.
Toxicology ; 467: 153088, 2022 02 15.
Artigo em Inglês | MEDLINE | ID: mdl-34979169

RESUMO

Elemicin (Ele) is a constituent of natural alkenylbenzene present in many foods and herbs. Ele exposure could induce hepatomegaly and hepatosteatosis. However, the role of gut microbiota in Ele-induced hepatotoxicity remains unclear. Here, the mice were treated with 200 mg/kg/day of Ele for 4 weeks with or without depletion of gut microbiota by antibiotics cocktail treatment. The mice treated with Ele showed enlargement of liver and slight hepatosteatosis, accompanied by higher levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), triglyceride (TG). Ele could also shift the structure of fecal microbiota and increase the richness. Functional prediction of the microbiota revealed the enrichment of non-alcoholic fatty liver disease pathway upon Ele exposure. Compared with control group, Patescibacteria and Epsilonbacteraeota were significantly enriched at the phylum level upon Ele treatment. A total of 20 genera were significant with respect specifically to Ele exposure, including decreased Alistipes and elevated Ruminiclostridium_9 and Gordonibacter. Among them, 13 retained significant associations with ALT and TG by Spearman correlation test, 4 were correlated with AST. Further MaAsLin analysis revealed that ALT was associated with 4 differentially abundant genera, such as Alistipes and Ruminiclostridium_9 and Gordonibacter. In addition, only Alistipes was significantly correlated with serum TG. Intriguingly, depletion of the microbiota significantly attenuated hepatosteatosis, restore increased ALT, AST and TG and inhibit the expression of genes involved in de novo lipogenesis and adipocyte differentiation, such as Fasn, ADIPOQ and leptin. Collectively, depletion of gut microbiota protected against Ele induced aberrant lipid metabolism in mice.


Assuntos
Bactérias/efeitos dos fármacos , Doença Hepática Induzida por Substâncias e Drogas/etiologia , Fígado Gorduroso/induzido quimicamente , Microbioma Gastrointestinal/efeitos dos fármacos , Hepatomegalia/induzido quimicamente , Metabolismo dos Lipídeos/efeitos dos fármacos , Fígado/efeitos dos fármacos , Pirogalol/análogos & derivados , Alanina Transaminase/sangue , Animais , Aspartato Aminotransferases/sangue , Bactérias/crescimento & desenvolvimento , Bactérias/metabolismo , Biomarcadores/sangue , Doença Hepática Induzida por Substâncias e Drogas/metabolismo , Doença Hepática Induzida por Substâncias e Drogas/microbiologia , Doença Hepática Induzida por Substâncias e Drogas/patologia , Disbiose , Fígado Gorduroso/metabolismo , Fígado Gorduroso/microbiologia , Fígado Gorduroso/patologia , Hepatomegalia/metabolismo , Hepatomegalia/microbiologia , Hepatomegalia/patologia , Fígado/metabolismo , Fígado/patologia , Camundongos Endogâmicos C57BL , Pirogalol/toxicidade , Triglicerídeos/sangue
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