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1.
Dig Dis Sci ; 64(5): 1390-1391, 2019 May.
Artigo em Inglês | MEDLINE | ID: mdl-30852771

RESUMO

The original version of the article unfortunately contained errors in Materials and Methods section, Figure 3 and Figure 4.

2.
Dig Dis Sci ; 64(2): 447-455, 2019 02.
Artigo em Inglês | MEDLINE | ID: mdl-30370491

RESUMO

BACKGROUND: Calcitonin gene-related peptide (CGRP) has antioxidant and anti-inflammatory activities on the pathological damage of acute pancreatitis. However, its molecular mechanism on severe acute pancreatitis (SAP) remains unknown. AIMS: To evaluate the influence of CGRP-mediated p38MAPK signaling pathway in rats with SAP. METHODS: SD rats were randomly divided into Sham group, SAP group, CGRP group (SAP rats injected with CGRP), SB203580 group (rats injected with p38MAPK pathway inhibitor SB203580), and CGRP8-37 group (SAP rats injected with CGRP8-37). Serum amylase and lipase activities were determined. Histopathological observations were evaluated, and the expression of inflammatory cytokines and oxidative stress-related indexes were measured. RESULTS: Compared with Sham group, SAP rats were increased in the activities of serum amylase and lipase, the pathologic assessment of pancreatic tissue, the levels of TNF-α, IL-1ß, IL-6, and IL-8, the content of MDA and MPO, and the expressions of CGRP, and p-p38MAPK protein, but they were decreased in SOD activity and GSH content. The above alterations were aggravated in the CGRP8-37 group when compared with SAP group. Besides, in comparison with SAP group, rats in the CGRP and SB203580 groups presented a reduction in the activities of serum amylase and lipase, the levels of inflammatory cytokines, the content of MDA and MPO, and the expressions of p-p38MAPK protein, while showed an elevation in SOD activity and GSH content. CONCLUSION: Pretreatment with CGRP alleviated oxidative stress and inflammatory response of SAP rats possibly by suppressing the activity of p38MAPK pathway, and thereby postponing the disease progression.


Assuntos
Peptídeo Relacionado com Gene de Calcitonina/farmacologia , Inibidores Enzimáticos/farmacologia , Imidazóis/farmacologia , Pâncreas/efeitos dos fármacos , Pancreatite/patologia , Fragmentos de Peptídeos/farmacologia , Piridinas/farmacologia , Proteínas Quinases p38 Ativadas por Mitógeno/antagonistas & inibidores , Doença Aguda , Amilases/sangue , Amilases/efeitos dos fármacos , Animais , Peptídeo Relacionado com Gene de Calcitonina/efeitos dos fármacos , Peptídeo Relacionado com Gene de Calcitonina/metabolismo , Citocinas/efeitos dos fármacos , Citocinas/imunologia , Progressão da Doença , Inflamação , Interleucina-1beta/efeitos dos fármacos , Interleucina-1beta/imunologia , Interleucina-6/imunologia , Interleucina-8/efeitos dos fármacos , Interleucina-8/imunologia , Lipase/sangue , Lipase/efeitos dos fármacos , Malondialdeído/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Pâncreas/imunologia , Pâncreas/patologia , Pancreatite/imunologia , Peroxidase/efeitos dos fármacos , Peroxidase/metabolismo , Distribuição Aleatória , Ratos , Ratos Sprague-Dawley , Índice de Gravidade de Doença , Transdução de Sinais , Fator de Necrose Tumoral alfa/efeitos dos fármacos , Fator de Necrose Tumoral alfa/imunologia , Proteínas Quinases p38 Ativadas por Mitógeno/efeitos dos fármacos , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo
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