RESUMO
Artemisia ordosica is one of the main shrubby perennials belonging to Artemisia species of Asteraceae and could be used in folk Chinese/Mongolian medicine to treat symptoms of various inflammatory ailments. The present study was conducted to investigate the protective effects of dietary Artemisia ordosica polysaccharide (AOP) against lipopolysaccharide (LPS) induced oxidative stress in broilers via Nrf2/Keap1 and TLR4/NF-κB pathway. A total of 192 1-day-old Arbor Acres male broilers were randomly allotted to four treatments with 6 replicates (n = 8): (1) CON group, non-challenged broilers fed basal diet; (2) LPS group, LPS-challenged broilers fed basal diet; (3) AOP group, non-challenged broilers fed basal diet supplemented with 750 mg/kg AOP; (4) LPS+AOP group, LPS-challenged broilers fed basal diet supplemented with 750 mg/kg AOP. The trial included starter phase (d 1-14), stress period â (d 15-21), convalescence â (d 22-28), stress period â ¡ (d 29-35) and convalescence â ¡ (d 36-42). During stress period â (on d 15, 17, 19 and 21) and stress period â ¡ (on d 29, 31, 33 and 35), broilers were injected intra-abdominally either with LPS solution or with an equal amount of sterile saline. The results showed that dietary AOP supplementation alleviated LPS-induced reduction in antioxidant enzyme activity and excessive production of ROS, 8-OHdG and PC in serum of broilers challenged with LPS. Moreover, dietary AOP supplementation alleviated the decrease of T-AOC and activities of SOD, CAT and GPx in liver of broilers challenged with LPS by increasing expression of Nrf2, and inhibiting over-expression of Keap1 both at gene and protein level. Additionally, dietary AOP supplementation decreased the over-production of IL-1ß and IL-6 in liver of broilers challenged by LPS through decreasing mRNA expression of TLR4, MyD88, NF-κB P65, IL-1ß and IL-6, and alleviating the increase of protein expression of TLR4, IKKß, NF-κB P65, IL-1ß, IL-6, and the decrease of protein expression of IkBα. In conclusion, dietary AOP supplementation could alleviate LPS-induced oxidative stress through Nrf2/Keap1 and TLR4/NF-κB pathway.
Assuntos
Artemisia , Lipopolissacarídeos , Ração Animal/análise , Animais , Artemisia/metabolismo , Galinhas/metabolismo , Dieta , Suplementos Nutricionais , Proteína 1 Associada a ECH Semelhante a Kelch/genética , Lipopolissacarídeos/toxicidade , Masculino , Fator 2 Relacionado a NF-E2/genética , NF-kappa B/genética , NF-kappa B/metabolismo , Estresse Oxidativo , Polissacarídeos , Receptor 4 Toll-Like/genéticaRESUMO
To increase awareness of IgG4-related retroperitoneal fibrosis (IgG4-RRPF) and reduce clinical misdiagnosis. We report a 79-year-old man with multiple organs involvement of IgG4-RRPF, who developed right lower extremity edema, hemoptysis and fever. The abdomen computed tomography (CT) scan image showed lymph nodes enlargement. The positron emission tomography/CT scan image showed pancreatic malignancy with multiple nodal lymph node metastasis, lung fibroblast proliferation, and right lung apex bullae. The chest CT scan image showed pulmonary multiple lymph nodes with calcification in the mediastinum. Posterior peritoneum magnetic resonance imaging showed the body and tail of the pancreas parenchymatous mass. The serum IgG4 concentration was high. The fibrous connective tissue with IgG4-positive plasma cells infiltration in the left supraclavicular lymph node biopsy was found. Fiberoptic bronchoscopy showed diffuse alveolar hemorrhage, and the transbronchial lung biopsy found no cancer cells. The patient was treated with glucocorticoids and immunosuppressive agents. After 2 months treatment, the patient showed rapid improvement. This is a case of IgG4-RRPF with multiple organs involvement. Glucocorticoid is the first-line treatment.
Assuntos
Edema/diagnóstico , Febre/diagnóstico , Glucocorticoides/uso terapêutico , Hemoptise/diagnóstico , Imunoglobulina G/sangue , Neoplasias Pancreáticas/diagnóstico , Fibrose Retroperitoneal/diagnóstico , Idoso , Edema/complicações , Edema/tratamento farmacológico , Edema/imunologia , Febre/complicações , Febre/tratamento farmacológico , Febre/imunologia , Hemoptise/complicações , Hemoptise/tratamento farmacológico , Hemoptise/imunologia , Humanos , Imunossupressores/uso terapêutico , Perna (Membro)/irrigação sanguínea , Perna (Membro)/patologia , Pulmão , Masculino , Neoplasias Pancreáticas/complicações , Neoplasias Pancreáticas/tratamento farmacológico , Neoplasias Pancreáticas/imunologia , Plasmócitos/imunologia , Plasmócitos/patologia , Fibrose Retroperitoneal/complicações , Fibrose Retroperitoneal/tratamento farmacológico , Fibrose Retroperitoneal/imunologia , Tomografia Computadorizada por Raios X , Resultado do TratamentoRESUMO
OBJECTIVE: The aim of this study was to explore whether miR-650 could inhibit the proliferation of glioma by regulating FAM83F and to investigate the specific role of miR-650 in glioma occurrence. PATIENTS AND METHODS: The expression of FAM83F in tumor or para-cancerous tissues of 24 glioma patients was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Meanwhile, FAM83F expression in 6 glioma cell lines (LN229, U87, U251, LN308, SNB19 and H4) was also detected. Subsequently, the proliferation of glioma cells transfected with miR-650 mimics was evaluated by cell counting kit-8 (CCK-8) and EDU (5-ethynyl-2'-deoxyuridine) assay, respectively. In addition, Luciferase reporter gene assay and rescue experiment were applied to verify the relationship between miR-650 and FAM83F. RESULTS: MiR-650 expression in glioma tissues was significantly decreased, while the expression of FAM83F was remarkably upregulated. This indicated that the level of miR-650 was negatively correlated with that of FAM83F. Similar results were obtained in glioma cells. We then transfected miR-650 mimics into LN229 and U251 cells, and found that the expression of miR-650 was significantly upregulated. Meanwhile, the viability of cells significantly decreased. In addition, the interaction between miR-650 and FAM83F was verified by Luciferase reporter gene assay. Rescue experiments showed that miR-650 could inhibit cell proliferation by targeting FAM83F. CONCLUSIONS: MiR-650 was lowly expressed in glioma tissues, which could promote cell proliferation through up-regulating the expression of FAM83F.