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Protective Effects of Lithospermum erythrorhizon Against Cerulein-Induced Acute Pancreatitis

OBJECTIVES: We aimed to evaluate the anti-inflammatory and inhibitory effects of Lithospermum erythrorhizon (LE) on cerulein-induced acute pancreatitis (AP) in a mouse model. METHODS: Acute pancreatitis was induced via intraperitoneal injection of cerulein (50 μg/kg) every hour for 6 times. In the L...

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Detalles Bibliográficos
Autores principales: Choi, Sun Bok, Bae, Gi-Sang, Jo, Il-Joo, Seo, Seung-Hee, Kim, Dong-Goo, Shin, Joon-Yeon, Hong, Seung-Heon, Choi, Byung-Min, Park, Sang-Hyun, Song, Ho-Joon, Park, Sung-Joo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4272226/
https://www.ncbi.nlm.nih.gov/pubmed/25102438
http://dx.doi.org/10.1097/MPA.0000000000000195
Descripción
Sumario:OBJECTIVES: We aimed to evaluate the anti-inflammatory and inhibitory effects of Lithospermum erythrorhizon (LE) on cerulein-induced acute pancreatitis (AP) in a mouse model. METHODS: Acute pancreatitis was induced via intraperitoneal injection of cerulein (50 μg/kg) every hour for 6 times. In the LE, water extract (100, 250, or 500 mg/kg) was administered intraperitoneally 1 hour before the first injection of cerulein. Six hours after AP, blood, the pancreas, and the lung were harvested for further examination. In addition, pancreatic acinar cells were isolated using a collagenase method, and then, we investigated the acinar cell viability and cytokine productions. RESULTS: Treatment with LE reduced pancreatic damage and AP-associated lung injury and attenuated the severity of AP, as evidenced by the reduction in neutrophil infiltration, serum amylase and lipase levels, trypsin activity, and proinflammatory cytokine expression. In addition, treatment with LE inhibited high mobility group box 1 expression in the pancreas during AP. In accordance with in vivo data, LE inhibited the cerulein-induced acinar cell death, cytokine productions, and high-mobility group box 1 expression. Furthermore, LE also inhibited the activation of p38 mitogen-activated protein kinases. CONCLUSIONS: These results suggest that LE plays a protective role during the development of AP by inhibiting the activation of p38.