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1.
World J Clin Cases ; 12(14): 2438-2444, 2024 May 16.
Artigo em Inglês | MEDLINE | ID: mdl-38765756

RESUMO

BACKGROUND: Autoimmune pancreatitis (AIP) is a rare form of autoimmune-mediated pancreatitis, which is easily misdiagnosed as pancreatic cancer and thus treated surgically. We studied the diagnosis and treatment of a patient with type 1 AIP recently admitted to our hospital, and reviewed the literature to provide a reference for clinical diagnosis of AIP. CASE SUMMARY: The chief complaint was yellowing of the body, eyes and urine for 21 d. The patient's clinical presentation was obstructive jaundice and imaging suggested pancreatic swelling. It was difficult to distinguish between inflammation and tumor. Serum immunoglobulin G4 (IgG4) was markedly elevated. IgG4 is an important serological marker for type 1 AIP. The patient was diagnosed with AIP, IgG4-related cholangitis, acute cholecystitis and hepatic impairment. After applying hormonal therapy, the patient's symptoms improved significantly. At the same time, imaging suggested that pancreatic swelling subsided, and liver function and other biochemical indicators decreased. The treatment was effective. CONCLUSION: In patients with pancreatic swelling, the possibility of AIP should be considered.

2.
Yao Xue Xue Bao ; 44(10): 1102-6, 2009 Oct.
Artigo em Chinês | MEDLINE | ID: mdl-20055131

RESUMO

In the present study, shRNA plasmid of pSi-p21 targeting p21 mRNA was constructed and the effect of p21 shRNA on curcumin-induced apoptosis of human hepatoma Huh7 cells was investigated. The effect of curcumin on the expression of p21 mRNA and protein and the silence efficiency of pSi-p21 were detected with RT-PCR and Western blotting. The effect of pSi-p21 on curcumin-induced apoptosis of Huh7 cells was evaluated with DAPI staining. The results showed that curcumin significantly upregulated p21 mRNA and protein expression, which was knocked down by pSi-p21 of Huh7 cells. DAPI staining results showed that pSi-p21 significantly decreased curcumin-induced apoptosis of Huh7 cells. The data suggested that curcumin induced apoptosis of Huh7 cells via upregulation of p21 expression.


Assuntos
Apoptose/efeitos dos fármacos , Carcinoma Hepatocelular/patologia , Curcumina/farmacologia , Inibidor de Quinase Dependente de Ciclina p21/metabolismo , Neoplasias Hepáticas/patologia , RNA Interferente Pequeno/genética , Antineoplásicos/farmacologia , Carcinoma Hepatocelular/metabolismo , Linhagem Celular Tumoral , Inibidor de Quinase Dependente de Ciclina p21/genética , Regulação Neoplásica da Expressão Gênica , Humanos , Neoplasias Hepáticas/metabolismo , Plasmídeos , RNA Mensageiro/metabolismo , Transfecção , Regulação para Cima
3.
Yao Xue Xue Bao ; 44(12): 1434-9, 2009 Dec.
Artigo em Chinês | MEDLINE | ID: mdl-21351482

RESUMO

The effect of curcumin on JAK-STAT signaling pathway was investigated in hepatoma cell lines Huh7 and Hep3B. Curcumin inhibited cell proliferation and induced apoptosis of both cell lines, but Huh7 cells were more sensitive to curcumin than Hep3B cells. Curcumin (50 micromol x L(-1)) significantly increased phosphorylations of p38 (T180/Y182) and STAT-1 (S727) in Huh7 and Hep3B cells, and caused relocalization of phosphorylated-STAT-1 (Y701) from cytoplasm to nucleus in Hep3B cells. In addition, curcumin (25 and 50 micromol x L(-1)) dramatically suppressed the phosphorylation level of STAT-1 (Y701) and resulted in a significant reduction of nuclear phosphorylated-STAT-1 (Y701) in Huh7 cells.


Assuntos
Carcinoma Hepatocelular/patologia , Curcumina/farmacologia , Janus Quinases/metabolismo , Neoplasias Hepáticas/patologia , Fator de Transcrição STAT1/metabolismo , Transdução de Sinais , Antineoplásicos Fitogênicos/isolamento & purificação , Antineoplásicos Fitogênicos/farmacologia , Apoptose , Carcinoma Hepatocelular/metabolismo , Linhagem Celular Tumoral , Proliferação de Células , Curcuma/química , Curcumina/isolamento & purificação , Humanos , Neoplasias Hepáticas/metabolismo , Fosforilação , Plantas Medicinais/química , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
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