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1.
Am J Respir Cell Mol Biol ; 68(2): 213-227, 2023 02.
Artigo em Inglês | MEDLINE | ID: mdl-36227848

RESUMO

Progressive fibrosing interstitial lung diseases (PF-ILDs) result in high mortality and lack effective therapies. The pathogenesis of PF-ILDs involves macrophages driving inflammation and irreversible fibrosis. Fc-γ receptors (FcγRs) regulate macrophages and inflammation, but their roles in PF-ILDs remain unclear. We characterized the expression of FcγRs and found upregulated FcγRIIB in human and mouse lungs after exposure to silica. FcγRIIB deficiency aggravated lung dysfunction, inflammation, and fibrosis in silica-exposed mice. Using single-cell transcriptomics and in vitro experiments, FcγRIIB was found in alveolar macrophages, where it regulated the expression of fibrosis-related genes Spp1 and Ctss. In mice with macrophage-specific overexpression of FcγRIIB and in mice treated with adenovirus by intratracheal instillation to upregulate FcγRIIB, silica-induced functional and histological changes were ameliorated. Our data from three genetic models and a therapeutic model suggest that FcγRIIB plays a protective role that can be enhanced by adenoviral overexpression, representing a potential therapeutic strategy for PF-ILDs.


Assuntos
Doenças Pulmonares Intersticiais , Pneumonia , Humanos , Animais , Camundongos , Adenoviridae/genética , Adenoviridae/metabolismo , Pneumonia/genética , Inflamação/genética , Inflamação/metabolismo , Receptores de IgG/genética , Receptores de IgG/metabolismo , Fibrose , Dióxido de Silício
2.
J Bone Miner Metab ; 32(6): 616-26, 2014 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-24362453

RESUMO

Osteoporosis is a chronic disease affecting millions of people worldwide. It is generally accepted that acquisition of a high peak bone mass (PBM) early in life can reduce the risk of osteoporosis later in life. The aims of this study were to investigate the effects of Fructus Ligustri Lucidi (FLL) ethanol extract on bone mineral density and its mechanical properties in growing female rats and to explore the underlying mechanisms. The rats were given different doses of FLL extract mixed with AIN-93G formula (0.40, 0.65 and 0.90 %), and a group given AIN-93G diet treatment only was used as control. The intervention lasted for 16 weeks until the animals were about 5 months old, the time when the animals almost reach their PBM. Our results showed that FLL treatment increased bone mineral density and improved bone mechanical properties in the growing female rats in a dose-dependent manner. In addition, FLL treatment significantly decreased the serum bone-resorbing marker, CTX-I, while significantly increasing serum 25(OH)D3 and thereby increasing Ca absorption and Ca retention. Intriguingly, both in vivo and in vitro results demonstrated that FLL treatment could reduce the RANKL/OPG ratio. In conclusion, FLL ethanol extract exerted beneficial effects on peak bone mass acquisition and the improvement of bone mechanical properties by favoring Ca metabolism and decreasing the RANKL/OPG ratio.


Assuntos
Densidade Óssea/efeitos dos fármacos , Reabsorção Óssea/tratamento farmacológico , Ligustrum/química , Extratos Vegetais/farmacologia , Animais , Reabsorção Óssea/sangue , Calcitriol/sangue , Cálcio/sangue , Relação Dose-Resposta a Droga , Etanol , Feminino , Osteoprotegerina/metabolismo , Extratos Vegetais/química , Ligante RANK/metabolismo , Ratos , Ratos Sprague-Dawley
3.
Acta Pharm Sin B ; 14(4): 1726-1741, 2024 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-38572107

RESUMO

Pulmonary hypertension (PH) is a fatal disorder characterized by pulmonary vascular remodeling and obstruction. The phosphodiesterase 4 (PDE4) family hydrolyzes cyclic AMP (cAMP) and is comprised of four subtypes (PDE4A-D). Previous studies have shown the beneficial effects of pan-PDE4 inhibitors in rodent PH; however, this class of drugs is associated with side effects owing to the broad inhibition of all four PDE4 isozymes. Here, we demonstrate that PDE4B is the predominant PDE isozyme in lungs and that it was upregulated in rodent and human PH lung tissues. We also confirmed that PDE4B is mainly expressed in the lung endothelial cells (ECs). Evaluation of PH in Pde4b wild type and knockout mice confirmed that Pde4b is important for the vascular remodeling associated with PH. In vivo EC lineage tracing demonstrated that Pde4b induces PH development by driving endothelial-to-mesenchymal transition (EndMT), and mechanistic studies showed that Pde4b regulates EndMT by antagonizing the cAMP-dependent PKA-CREB-BMPRII axis. Finally, treating PH rats with a PDE4B-specific inhibitor validated that PDE4B inhibition has a significant pharmacological effect in the alleviation of PH. Collectively, our findings indicate a critical role for PDE4B in EndMT and PH, prompting further studies of PDE4B-specific inhibitors as a therapeutic strategy for PH.

4.
Commun Biol ; 5(1): 81, 2022 01 20.
Artigo em Inglês | MEDLINE | ID: mdl-35058564

RESUMO

Hypertension is a common chronic disease, which leads to cardio-cerebrovascular diseases, and its prevalence is increasing. The cyclic adenosine monophosphate (cAMP)-protein kinase A (PKA) pathway participates in multiple cardiovascular diseases. Phosphodiesterase (PDE) 4 has been shown to regulate PKA activity via cAMP specific hydrolysis. However, whether PDE4-cAMP-PKA pathway influences hypertension remains unknown. Herein, we reveal that PDE4D (one of PDE4 isoforms) expression is upregulated in the aortas of experimental hypertension induced by angiotensin II (Ang II). Furthermore, knockout of Pde4d in mouse smooth muscle cells (SMCs) attenuates Ang II-induced hypertension, arterial wall media thickening, vascular fibrosis and vasocontraction. Additionally, we find that PDE4D deficiency activates PKA-AMP-activated protein kinase (AMPK) signaling pathway to inhibit myosin phosphatase targeting subunit 1 (MYPT1)-myosin light chain (MLC) phosphorylation, relieving Ang II-induced SMC contraction in vitro and in vivo. Our results also indicate that rolipram, a PDE4 inhibitor, may be a potential drug for hypertension therapy.


Assuntos
Angiotensina II/toxicidade , Nucleotídeo Cíclico Fosfodiesterase do Tipo 4/metabolismo , Hipertensão/induzido quimicamente , Miócitos de Músculo Liso/efeitos dos fármacos , Animais , Nucleotídeo Cíclico Fosfodiesterase do Tipo 4/genética , Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos , Regulação Enzimológica da Expressão Gênica/fisiologia , Masculino , Camundongos , Camundongos Knockout , Músculo Liso Vascular/citologia , Inibidores da Fosfodiesterase 4/farmacologia , Ratos , Rolipram/farmacologia
5.
Exp Mol Med ; 54(8): 1201-1213, 2022 08.
Artigo em Inglês | MEDLINE | ID: mdl-35999453

RESUMO

Abdominal aortic aneurysm (AAA) is a permanent expansion of the abdominal aorta that has a high mortality but limited treatment options. Phosphodiesterase (PDE) 4 family members are cAMP-specific hydrolyzing enzymes and have four isoforms (PDE4A-PDE4D). Several pan-PDE4 inhibitors are used clinically. However, the regulation and function of PDE4 in AAA remain largely unknown. Herein, we showed that PDE4D expression is upregulated in human and angiotensin II-induced mouse AAA tissues using RT-PCR, western blotting, and immunohistochemical staining. Furthermore, smooth muscle cell (SMC)-specific Pde4d knockout mice showed significantly reduced vascular destabilization and AAA development in an experimental AAA model. The PDE4 inhibitor rolipram also suppressed vascular pathogenesis and AAA formation in mice. In addition, PDE4D deficiency inhibited caspase 3 cleavage and SMC apoptosis in vivo and in vitro, as shown by bulk RNA-seq, western blotting, flow cytometry and TUNEL staining. Mechanistic studies revealed that PDE4D promotes apoptosis by suppressing the activation of cAMP-activated protein kinase A (PKA) instead of the exchange protein directly activated by cAMP (Epac). Additionally, the phosphorylation of BCL2-antagonist of cell death (Bad) was reversed by PDE4D siRNA in vitro, which indicates that PDE4D regulates SMC apoptosis via the cAMP-PKA-pBad axis. Overall, these findings indicate that PDE4D upregulation in SMCs plays a causative role in AAA development and suggest that pharmacological inhibition of PDE4 may represent a potential therapeutic strategy.


Assuntos
Angiotensina II , Aneurisma da Aorta Abdominal , Angiotensina II/efeitos adversos , Animais , Aneurisma da Aorta Abdominal/induzido quimicamente , Aneurisma da Aorta Abdominal/genética , Aneurisma da Aorta Abdominal/metabolismo , Apoptose , Proteínas Quinases Dependentes de AMP Cíclico , Nucleotídeo Cíclico Fosfodiesterase do Tipo 4/efeitos adversos , Nucleotídeo Cíclico Fosfodiesterase do Tipo 4/genética , Humanos , Camundongos , Camundongos Knockout , Miócitos de Músculo Liso/metabolismo
6.
Front Cardiovasc Med ; 8: 630269, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-33614752

RESUMO

Abdominal aortic aneurysm (AAA) is a cardiovascular disease with a high risk of death, seriously threatening the life and health of people. The specific pathogenesis of AAA is still not fully understood. In recent years, researchers have found that amino acid, lipid, and carbohydrate metabolism disorders play important roles in the occurrence and development of AAA. This review is aimed to summarize the latest research progress of the relationship between AAA progression and body metabolism. The body metabolism is closely related to the occurrence and development of AAA. It is necessary to further investigate the pathogenesis of AAA from the perspective of metabolism to provide theoretical basis for AAA diagnosis and drug development.

7.
Clin Chim Acta ; 515: 90-95, 2021 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-33388307

RESUMO

Abdominal aortic aneurysms (AAA) are permanent and irreversible local dilatations of the abdominal aortic wall. Recent data indicate that the transforming growth factor-beta (TGF-ß) signaling pathway exerts a protective effect on the development of AAA. Some dysregulated microRNAs (miRNA) also appear involved in the expansion of AAA and miRNA-based therapeutics have been shown to effectively inhibit this process. New evidence has revealed that TGF-ß signaling and miRNA interaction may of physiologic and pathophysiologic significance including the progression of AAA. As such, miRNA that regulate TGF-ß signaling may hold promise as potential therapeutic targets. This review explores potential crosstalk between TGF-ß signaling and miRNA in AAA in order improve our understanding of this pathology and explore development of potential therapeutic targets.


Assuntos
Aneurisma da Aorta Abdominal , MicroRNAs , Aneurisma da Aorta Abdominal/genética , Humanos , MicroRNAs/genética , Transdução de Sinais , Fator de Crescimento Transformador beta
8.
Front Cardiovasc Med ; 8: 753711, 2021.
Artigo em Inglês | MEDLINE | ID: mdl-34901214

RESUMO

Abdominal aortic aneurysm (AAA) is potentially life-threatening in aging population due to the risk of aortic rupture and a lack of optimal treatment. The roles of different vascular and immune cells in AAA formation and pathogenesis remain to be future characterized. Single-cell RNA sequencing was performed on an angiotensin (Ang) II-induced mouse model of AAA. Macrophages, B cells, T cells, fibroblasts, smooth muscle cells and endothelial cells were identified through bioinformatic analyses. The discovery of multiple subtypes of macrophages, such as the re-polarization of Trem2 + Acp5 + osteoclast-like and M2-like macrophages toward the M1 type macrophages, indicates the heterogenous nature of macrophages during AAA development. More interestingly, we defined CD45+COL1+ fibrocytes, which was further validated by flow cytometry and immunostaining in mouse and human AAA tissues. We then reconstituted these fibrocytes into mice with Ang II-induced AAA and found the recruitment of these fibrocytes in mouse AAA. More importantly, the fibrocyte treatment exhibited a protective effect against AAA development, perhaps through modulating extracellular matrix production and thus enhancing aortic stability. Our study reveals the heterogeneity of macrophages and the involvement of a novel cell type, fibrocyte, in AAA. Fibrocyte may represent a potential cell therapy target for AAA.

9.
Clin Chim Acta ; 509: 167-171, 2020 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-32505776

RESUMO

Studies have demonstrated that intestinal microbiota is associated with various metabolic diseases including obesity, nonalcoholic fatty liver, and insulin resistance. Farnesoid X receptor (FXR), also known as the bile acid receptor, belongs to the nuclear receptor superfamily, which is involved in the regulation of bile acid, glucose, and lipid metabolism. Researchers have found that intestinal microbiota can regulate FXR activity by affecting bile acid composition, and then regulate the balance of in vivo metabolism. The intestinal microbiota -FXR axis may be an ideal drug target for metabolic diseases. This review summarizes the latest research on the intestinal microbiota /FXR axis, hoping to provide a theoretical basis for further research and clinical application.


Assuntos
Microbioma Gastrointestinal , Doenças Metabólicas , Hepatopatia Gordurosa não Alcoólica , Animais , Ácidos e Sais Biliares , Humanos , Camundongos , Camundongos Endogâmicos C57BL
10.
J Clin Invest ; 130(4): 1669-1682, 2020 04 01.
Artigo em Inglês | MEDLINE | ID: mdl-31874111

RESUMO

BACKGROUNDUndifferentiated systemic autoinflammatory diseases (USAIDs) present diagnostic and therapeutic challenges. Chronic interferon (IFN) signaling and cytokine dysregulation may identify diseases with available targeted treatments.METHODSSixty-six consecutively referred USAID patients underwent underwent screening for the presence of an interferon signature using a standardized type-I IFN-response-gene score (IRG-S), cytokine profiling, and genetic evaluation by next-generation sequencing.RESULTSThirty-six USAID patients (55%) had elevated IRG-S. Neutrophilic panniculitis (40% vs. 0%), basal ganglia calcifications (46% vs. 0%), interstitial lung disease (47% vs. 5%), and myositis (60% vs. 10%) were more prevalent in patients with elevated IRG-S. Moderate IRG-S elevation and highly elevated serum IL-18 distinguished 8 patients with pulmonary alveolar proteinosis (PAP) and recurrent macrophage activation syndrome (MAS). Among patients with panniculitis and progressive cytopenias, 2 patients were compound heterozygous for potentially novel LRBA mutations, 4 patients harbored potentially novel splice variants in IKBKG (which encodes NF-κB essential modulator [NEMO]), and 6 patients had de novo frameshift mutations in SAMD9L. Of additional 12 patients with elevated IRG-S and CANDLE-, SAVI- or Aicardi-Goutières syndrome-like (AGS-like) phenotypes, 5 patients carried mutations in either SAMHD1, TREX1, PSMB8, or PSMG2. Two patients had anti-MDA5 autoantibody-positive juvenile dermatomyositis, and 7 could not be classified. Patients with LRBA, IKBKG, and SAMD9L mutations showed a pattern of IRG elevation that suggests prominent NF-κB activation different from the canonical interferonopathies CANDLE, SAVI, and AGS.CONCLUSIONSIn patients with elevated IRG-S, we identified characteristic clinical features and 3 additional autoinflammatory diseases: IL-18-mediated PAP and recurrent MAS (IL-18PAP-MAS), NEMO deleted exon 5-autoinflammatory syndrome (NEMO-NDAS), and SAMD9L-associated autoinflammatory disease (SAMD9L-SAAD). The IRG-S expands the diagnostic armamentarium in evaluating USAIDs and points to different pathways regulating IRG expression.TRIAL REGISTRATIONClinicalTrials.gov NCT02974595.FUNDINGThe Intramural Research Program of the NIH, NIAID, NIAMS, and the Clinical Center.


Assuntos
Doenças Autoimunes , Interferon Tipo I , Interleucina-18 , Síndrome de Ativação Macrofágica , Mutação , Paniculite , Proteinose Alveolar Pulmonar , Doenças Autoimunes/genética , Doenças Autoimunes/imunologia , Feminino , Humanos , Interferon Tipo I/genética , Interferon Tipo I/imunologia , Interleucina-18/genética , Interleucina-18/imunologia , Síndrome de Ativação Macrofágica/genética , Síndrome de Ativação Macrofágica/imunologia , Masculino , Paniculite/genética , Paniculite/imunologia , Proteinose Alveolar Pulmonar/genética , Proteinose Alveolar Pulmonar/imunologia
12.
Clin Chim Acta ; 495: 29-34, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-30910597

RESUMO

Farnesoid X receptor (FXR) is a transcription factor that can be activated by bile acid as well as influenced bile acid metabolism. ß-cell bile acid metabolism is mediated by FXR and closely related to the regulation of blood glucose (BG). FXR can regulate BG through multiple pathways. This review summarises recent studies on FXR regulation of BG balance via bile acid regulation, lowering glucagon-like peptide-1 (GLP-1), inhibiting gluconeogenesis, increasing insulin secretion and enhancing insulin sensitivity. In addition, the current review provides additional insight into the relationship between FXR and BG which may provide a new theoretical basis for further study on the role of FXR.


Assuntos
Glicemia/metabolismo , Receptores Citoplasmáticos e Nucleares/metabolismo , Animais , Ácidos e Sais Biliares/metabolismo , Gluconeogênese , Humanos , Insulina/metabolismo
13.
Clin Chim Acta ; 495: 109-117, 2019 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-30959044

RESUMO

Extracellular vesicles (EVs), which exist in human blood, are increased in some inflammation-related cardiovascular diseases. EVs are involved in inflammation, immunity, signal transduction, cell survival and apoptosis, angiogenesis, thrombosis, and autophagy, all of which are highly significant for maintaining homeostasis and disease progression. Therefore, EVs are also associated with key steps in atherosclerosis, including cellular lipid metabolism, endothelial dysfunction and vascular wall inflammation, ultimately resulting in vascular remodelling. In this review, we summarize recent studies on EV contents and biological function, focusing on their potential effect in atherosclerosis, including cholesterol metabolism, vascular inflammation, angiogenesis, coagulation and the development of atherosclerotic lesions. EVs may represent potential biomarkers and pharmacological targets for atherosclerotic diseases.


Assuntos
Aterosclerose/patologia , Vesículas Extracelulares/metabolismo , Animais , Aterosclerose/metabolismo , Aterosclerose/terapia , Humanos
14.
Clin Chim Acta ; 499: 118-122, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31493375

RESUMO

Vascular calcification is associated with adverse cardiovascular events that increase the risk of cardiovascular death. Unfortunately, the pathogenesis of vascular calcification is complex and incompletely understood. As important intercellular signaling molecules, the role of extracellular vesicles (EVs) in vascular calcification has attracted wide attention in recent years. This review will briefly describe the role of EVs (mainly including exosomes and microvesicles) in the process of vascular wall calcification focusing on the specific mechanisms of smooth muscle cell (SMC) differentiation and calcium-phosphorus balance to illustrate the relationship between EVs and vascular calcification. It is likely that EVs may be prognostic markers in some cardiovascular diseases and have potential therapeutic potential.


Assuntos
Vesículas Extracelulares/metabolismo , Calcificação Vascular/metabolismo , Humanos , Músculo Liso Vascular/metabolismo
15.
J Agric Food Chem ; 55(14): 5523-8, 2007 Jul 11.
Artigo em Inglês | MEDLINE | ID: mdl-17552542

RESUMO

The effects of tea water extracts (TWE), crude tea polysaccharides (CTP), and a tea polysaccharide fraction (TPF) were tested on hyperglycemic diabetic mice. Results indicated that TWE, CTP, and TPF could significantly decrease fasting blood glucose (FBG) and glucosylated serum protein (GSP) in alloxan-induced diabetic mice compared to the control group. In vitro antioxidant activities of TWE, CTP, and TPF for scavenging hydroxyl radicals and superoxide radicals decreased with the degree of purification and were lowest for TPF. High-performance gel permeation chromatography (HPGPC) and component analysis revealed the molecular mass distribution and constituents of TWE, CTP, and TPF, indicating that a 100-120 kDa fraction contained the hypoglycemic activity. This fraction was essentially composed of polysaccharides (approximately 90%) with substantial amounts of arabinogalactan proteins. The second-derivative IR spectra of TWE, CTP, and TPF with peak intensity around 1075 and 1045 cm(-1), which characterize galactopyranose in the backbone and arabinofuranose units in side branches, respectively, further substantiated the importance of the arabinogalactan proteins. Taken together, the results indicate that a soluble tea polysaccharide is the major hypoglycemic factor in tea and that this polysaccharide may be developed to a potential natural hypoglycemic functional ingredient.


Assuntos
Diabetes Mellitus Experimental/tratamento farmacológico , Hipoglicemiantes/uso terapêutico , Polissacarídeos/uso terapêutico , Chá/química , Animais , Antioxidantes/farmacologia , Glicemia/análise , Masculino , Camundongos , Polissacarídeos/farmacologia , Solubilidade
16.
Nutrients ; 8(6)2016 Jun 08.
Artigo em Inglês | MEDLINE | ID: mdl-27338459

RESUMO

Breastfed infants tend to be less prone to infections and may have improved cognitive benefits compared to formula-fed infants. Human milk oligosaccharides (HMO) are the third most abundant component of human milk, but are absent from formulae. They may be partially responsible for the benefits of breastfeeding. In this cross-sectional observational study, the HMO composition of milk from Chinese mothers was studied to determine the impact of stage of lactation, mode of delivery and geographical location. The content of 10 HMO was measured by HPLC in 446 milk samples from mothers living in three different cities in China. Around 21% of the samples contained levels of 2'-fucosyllactose (2'-FL) below the limit of quantification, which is similar to the frequency of fucosyltransferase-2 non-secretors in other populations, but 2'-FL was detected in all samples. Levels of most of the HMO studied decreased during the course of lactation, but the level of 3-fucosyllactose increased. Levels of 2'-FL and 3-fucosyllactose seem to be strongly correlated, suggesting some sort of mechanism for co-regulation. Levels of 6'-sialyllactose were higher than those of 3'-sialyllactose at early stages of lactation, but beyond 2-4 months, 3'-sialyllactose was predominant. Neither mode of delivery nor geographical location had any impact on HMO composition.


Assuntos
Lactação , Leite Humano/química , Oligossacarídeos/análise , Adulto , Aleitamento Materno , China , Cromatografia Líquida de Alta Pressão , Estudos Transversais , Parto Obstétrico/métodos , Feminino , Humanos , Lactente , Recém-Nascido , Lactose/análogos & derivados , Lactose/análise , Mães , Trissacarídeos/análise , População Urbana/estatística & dados numéricos
17.
Antioxid Redox Signal ; 16(3): 275-89, 2012 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-21905985

RESUMO

AIMS: Docosahexaenoic acid (22:6n-3; DHA) is known to play a critical role in postnatal brain development. However, no study has been performed to investigate its preventive effect on prenatal stress-induced behavioral and molecular alterations in offspring. In the present study, rats were exposed to restraint stress on days 14-20 of pregnancy, three times a day, 2 hours each time; DHA was given at the doses of 100 and 300 mg/kg/day for two weeks. RESULTS: We showed that prenatal restraint stress caused (1) learning and memory impairment, (2) BDNF mRNA level decrease, (3) oxidative damage to proteins, (4) enhanced expression of nitric oxide synthase and apoptosis, and (5) abnormalities in mitochondrial metabolism that included changes in mitochondrial complexes I-V, and enhancement of expression of proteins involved in mitochondrial fusion/fission (Mfn-1, Mfn-2, Drp-1) and autophagy (Atg3, Atg7, Beclin-1, p-Akt, and p-mTOR) in the hippocampus of offspring. INNOVATION: Besides the well-known role in child brain development, we reported the novel finding of DHA in protecting prenatal stress-induced cognitive dysfunction involving the modulation of mitochondrial function and dynamics. CONCLUSION: Maternal feeding of DHA significantly prevented prenatal stress-induced impairment of learning and memory and normalized the biomarkers of oxidative damage, apoptosis, and mitochondrial metabolism in the hippocampus of both male and female offspring. These results suggest that maternal feeding of DHA exerts preventive effects on prenatal stress-induced brain dysfunction and that modulation of mitochondrial metabolism may play critical role in DHA protection.


Assuntos
Ácidos Docosa-Hexaenoicos/farmacologia , Deficiências da Aprendizagem/prevenção & controle , Mitocôndrias/metabolismo , Neurônios/metabolismo , Estresse Oxidativo , Efeitos Tardios da Exposição Pré-Natal , Estresse Psicológico/complicações , Animais , Apoptose , Proteínas Reguladoras de Apoptose/genética , Proteínas Reguladoras de Apoptose/metabolismo , Autofagia , Fator Neurotrófico Derivado do Encéfalo/genética , Fator Neurotrófico Derivado do Encéfalo/metabolismo , Transtornos Cognitivos/etiologia , Transtornos Cognitivos/prevenção & controle , Ácidos Docosa-Hexaenoicos/metabolismo , Complexo de Proteínas da Cadeia de Transporte de Elétrons/metabolismo , Feminino , Hipocampo/efeitos dos fármacos , Hipocampo/metabolismo , Deficiências da Aprendizagem/etiologia , Masculino , Troca Materno-Fetal , Aprendizagem em Labirinto , Mitocôndrias/enzimologia , Proteínas Mitocondriais/genética , Proteínas Mitocondriais/metabolismo , Neurônios/enzimologia , Óxido Nítrico Sintase Tipo I/genética , Óxido Nítrico Sintase Tipo I/metabolismo , Óxido Nítrico Sintase Tipo II/genética , Óxido Nítrico Sintase Tipo II/metabolismo , Gravidez , Carbonilação Proteica , Ratos , Ratos Sprague-Dawley , Transcrição Gênica
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