Ghrelin inhibits IKKβ/NF-κB activation and reduces pro-inflammatory cytokine production in pancreatic acinar AR42J cells treated with cerulein
Ghrelin inhibits IKKβ/NF-κB activation and reduces pro-inflammatory cytokine production in pancreatic acinar AR42J cells treated with cerulein作者机构：Department of GastroenterologyThe First Affiliated Hospital of Guangxi Medical UniversityNanning 530021China Department of GastroenterologyThe First People’s Hospital of Nanning CityThe Fifth Affiliated Hospital of Guangxi Medical UniversityNanning 530022China Department of ChemotherapyAffiliated Tumor Hospital of Guangxi Medical UniversityNanning 530021China Department of GastroenterologySecond Affiliated Hospital of Guangxi Medical UniversityNanning 530007China Department of GastroenterologyLiuzhou General HospitalLiuzhou 545006China Department of GastroenterologyGuangxi International Zhuang Medical HospitalNanning 530001China
出 版 物：《Hepatobiliary & Pancreatic Diseases International》 (国际肝胆胰疾病杂志（英文版）)
年 卷 期：2021年第20卷第4期
页 面：366-375页
核心收录：
基 金：This study was supported by grants from the National Nat-ural Science Foundation of China(81260087 and 81560111) Guangxi Natural Science Foundation(2017GXNSFAA198068).
主 题：Acute pancreatitis Ghrelin Inflammatory cytokine Acinar cells
摘 要：Background: Previous studies have provided conflicting results regarding whether the serum ghrelin concentration can reflect the severity of acute pancreatitis(AP). The present study examined the correlation between the serum ghrelin concentration and AP severity in animal models and investigated whether altered ghrelin expression in pancreatic acinar cells influences IKK β/NF-κ B signaling and pro-inflammatory cytokine production. Methods: Mild or severe AP was induced in rats by intraperitoneal injection of cerulein or retrograde cholangiopancreatic duct injection of sodium taurocholate, respectively. After successful model induction, serum ghrelin, tumor necrosis factor-α(TNF-α), and interleukin-6(IL-6) concentrations were determined by enzyme-linked immunosorbent assay, and IKK β/NF-κ B activation was assessed by immunohistochemistry. Subsequently, stable overexpression or knockdown of ghrelin in AR42 J cells was achieved by lentiviral transfection. After transfected cells and control cells were treated with cerulein for 24 h, the TNF-αand IL-1 β levels in the supernatants were determined by enzyme-linked immunosorbent assay, and the expression levels of p-p65, IKK β, and p-IKK β were detected by Western blotting. Results: In rat AP models, AP severity was correlated with increased IKK β/NF-κ B activation, proinflammatory cytokine production, and ghrelin secretion. The levels of pro-inflammatory cytokines TNF-αand IL-1 β as well as IKK β/NF-κ B signaling activity were increased upon knockdown of ghrelin in the AP acinar cell model and decreased with ghrelin overexpression. Conclusions: Serum ghrelin is related to the severity of AP. Ghrelin may play a protective role in the pathogenesis of AP by inhibiting the pro-inflammatory cytokines and the activation of the IKK β/NF-κ B signaling pathway.
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