胰腺炎
急性胰腺炎
促炎细胞因子
肝细胞生长因子
内科学
氧化应激
医学
内分泌学
水肿
谷胱甘肽
炎症
胰腺
蓝绿藻
细胞因子
受体
化学
胆囊收缩素
酶
生物化学
作者
Mayrel Palestino Domínguez,Mario Peláez-Luna,Roberto Lazzarini‐Lechuga,Ignacio Rodríguez-Ochoa,Verónica Souza,Roxana U. Miranda,Benjamín Pérez-Aguilar,Leticia Bucio,Jens U. Marquardt,Luis E. Gómez–Quiroz,María Concepción Gutiérrez‐Ruiz
摘要
Acute pancreatitis is a multifactorial disease associated with profound changes of the pancreas induced by release of digestive enzymes that lead to increase in proinflammatory cytokine production, excessive tissue necrosis, edema, and bleeding. Elevated levels of hepatocyte growth factor (HGF) and its receptor c‐Met have been observed in different chronic and acute pancreatic diseases including experimental models of acute pancreatitis. In the present study, we investigated the protective effects induced by the recombinant human HGF in a mouse model of cerulein‐induced acute pancreatitis. Pancreatitis was induced by 8 hourly administrations of supramaximal cerulein injections (50 µg/kg, ip). HGF treatment (20 µg/kg, iv), significantly attenuated lipase content and amylase activity in serum as well as the degree inflammation and edema overall leading to less severe histologic changes such as necrosis, induced by cerulein. Protective effects of HGF were associated with activation of pro‐survival pathways such as Akt, Erk1/2, and Nrf2 and increase in executor survival‐related proteins and decrease in pro‐apoptotic proteins. In addition, ROS content and lipid peroxidation were diminished, and glutathione synthesis increased in pancreas. Systemic protection was observed by lung histology. In conclusion, our data indicate that HGF exerts an Nrf2 and glutathione‐mediated protective effect on acute pancreatitis reflected by a reduction in inflammation, edema, and oxidative stress.
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