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Objective:To explore the differential diagnosis of pancreatic acinar cell carcinoma (PACC) and pancreatic ductal adenocarcinoma (PDAC) based on multidetector computed tomography (MDCT) features.Methods:The clinical, pathological and MDCT imaging data of 26 patients with pathologically confirmed PACC and 145 patients with pathologically confirmed PDAC who underwent MDCT from November 2013 to April 2021 were retrospectively studied. The differences of MDCT features including tumor location, tumor size, common pancreatic duct and bile duct dilatation, pancreatitis, lymph node metastasis, cyst, pancreatic parenchyma atrophy, duodenal involvement, bile ductal and vascular involvement between the two groups were compared. Univariate analysis and multivariate analysis by logistic regression models were performed to identify the independent predictive factors for PACC.Results:The tumor size, bile duct dilatation, lymph node metastasis, pancreatic parenchyma atrophy and vascular involvement were significantly different between PACC group and PDAC group (all P value<0.05). Multivariate analysis revealed that the tumor size ( OR=1.07, 95% CI 1.028-1.15, P=0.001), lymph node metastasis ( OR=0.23, 95% CI 0.065-0.800, P=0.02), pancreatic parenchyma atrophy ( OR=0.15, 95% CI 0.048-0.490, P=0.002) were closely associated with PACC. Conclusions:The tumor size, bile duct dilatation, lymph node metastasis, pancreatic parenchyma atrophy and vascular involvement evaluated by MDCT had a certain value in differentiating PACC from PDAC, and the tumor size, lymph node metastasis and pancreatic parenchyma atrophy were independent predictors for the diagnosis of PACC.
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Objective To explore whether exendin-4 inhibits AR42J cells and its mechanism.Methods AR42J cells were treated with exendin-4 under multiple concentrations(1,5,10 pmol/L) at 24,48,72,96,120 h to assess its cell viability by MTT assay and got the IC-50 and time points.Then checking whether exendin-4 could induce the AR42Jcells apoptosis by setting normal control (NC) group,exendin-4 (Ex-4) group and Ex-4+ z-VAD-fmk (apoptosis inhibitor) group,and exploring whether 3-MA which is autophagy inhibitor could inhibit the AR42J cells apoptosis induced by exendin-4 by setting NC group,Ex-4 group and Ex-4+3-MA group.Cell viability was analyzed by MTT and the cells apoptosis was detected by flow cytometry and the protein levels of caspase-3,LC3 and p62 were studied by Western blot.Results Concentration of 10 pmol/L exendin-4 and and time point 72 h were selected for the further study.z-VAD-fmk pretreatment can significantly inhibit the cell viability of exendin-4 by (81.2±3.3)％ vs.(49.4±3.0)％ (P＜0.05).Flow cytometry showed that exendin-4 could induce the AR42J cells apoptosis by (28.2± 1.4)％ vs.(3.6±0.8)％,and increased the caspase-3 level by Western blot,which both can be reversed by (79.1 ±2.3) ％ vs.(49.8±2.5)％ (P＜0.05) when the cells were treated for 72 h,as was apoptosis ratio by (14.5±2.1)％ vs.(29.2±3.2)％.Western blot showed that exendin-4 can upregulate protein levels of LC3B-Ⅱ,p62 和 caspase-3 and 3-MA,and pretreatment can inhibit the upregulation of LC3B-Ⅱ and caspase-3 but further increased the upregulation of p62 induced by exendin-4.Conclusions Exendin-4 can induce AR42J cells apoptosis and 3-MA pretreating can inhibit exendin-4 cytotoxicity through downregulating autophagy.So auto phagy inhibitor 3-MA could potentially extenuate the cytotoxicity of exendin-4 in pancreatic acinar cells.
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Objective To investigate the effects of high-fat diet on pancreatic acinar cells' IP3 expression and CCK-induced amylase release in rats.Methods Male Wistar rats were divided into high-fat diet group and normal diet group,they were fed for 4 weeks.Blood triglycerides,cholesterol,amylase and glucose levels were determined by automatic biochemical analyzer.Pancreatic tissues were taken for histopathological observations.Pancreatic acinar cells were isolated and cultured,and intracellular inositol 1,4,5-trisphosphate (IP3) was detected using a commercial kit.Amylase release rates were measured after CCK-8 stimulation.Results The rats in high-fat diet group appeared hyperlipidemia,vacuolization of acinar cells and the lymphocytes appeared around the acinar cells can be seen on the pancreatic tissue pathology staining.The levels of IP3 in acinar cells of rats fed a high-fat diet were higher than that of normal rats [(31.807 ± 3.448) pmol/106 cells vs (24.632 ± 3.649) pmol/106 cells,t=7.479,P＜0.001];and amylase release rate in these rats'acinar cells were also higher than those of normal rats [when CCK-8=0.01 nmol/L:( 11.056 ±3.369)％ vs (7.354 ± 2.181) ％,t=3.912,P＜0.001;when CCK-8=1 nmol/L:( 13.854 ± 4.087 ) ％ vs (9.432 ±2.477) ％,t=3.939,P＜0.001 ) after CCK-8 stimulation in different concentrations.Additionally,there was a positive co-relationship between acinar cell's IP3 level and amylase release (r=0.896,P＜0.001 ).Conclusion Chronic high-fat diet induces hypersensitivity for pancreatic acinar cells' exocrine function,and IP3 as a signal molecule may play an important role in this process.
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Acinar cystic transformation of the pancreas is also known as acinar cell cystadenoma (ACC), and this is an extremely rare benign lesion that was first described in April 2002. We report here on a case of a previously asymptomatic patient with pancreatic ACC and this was diagnosed by computed tomography (CT) and magnetic resonance imaging (MRI). To the best of our knowledge, there is no previous report concerning the CT or MRI features of ACC in the medical literature. We present here the CT, MRI and pathological findings of pancreatic ACC.
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Humans , Male , Middle Aged , Cystadenoma/pathology , Pancreatic Neoplasms/pathologyABSTRACT
The relationship between intracelluar trypsinogen activation and NF-r,B activation in rat pancreatic acinar cells induced by M3 cholinergic receptor agonist (carbachoi) hyperstimulation was studied. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, the active pro- tease inhibitor (pefabloc) and NF-кB inhibitor (PDTC) in vitro. Intracelluar trypsin activity was measured by using a fluorogenie substrate. The activity of NF-кB was monitored by using electro- phoretic mobility shift assay. The results showed that after pretreatment with 2 mmol/L pefabloc, the activities of trypsin and NF-кB in pancreatic acinar cells treated with high concertrations of carbachol (10-3 mol/L) in vitro was significantly decreased as compared with control group (P＜0.01). The addi- tion of 10-2mol/L PDTC resulted in a significant decrease of NF-кB activities in pancreatic acinar cells after treated with high concertrations of carbachol (10-3 mol/L) in vitro, but the intracelluar trypsinogen activity was not obviously inhibited (P＞0.05). It was concluded that intracelluar trypsi- nogen activation is likely involved in the regulation of high concertrations of carbachol-induced NF-кB activation in pancreatic acinar cells in vitro. NF-кB activation is likely not necessary for high concertrations of carbachol-induced trypsinogen activation in pancreatic acinar cells in vitro.
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The relationship between M3 cholinergic receptor agonist (carbachol) hyperstimulationinduced pancreatic acinar cellular injury and trypsinogen activation or NF-κB activation in rats was studied in vitro. Rat pancreatic acinar cells were isolated, cultured and treated with carbachol, the active protease inhibitor (pefabloc), and NF-κB inhibitor (PDTC) in vitro. Intracellular trypsin activity was measured by using a fluorogenic substrate. The cellular injury was evaluated by measuring the leakage of LDH from pancreatic acinar cells. The results showed that as compared with control group, 10-3 mol/L carbachol induced a significant increase of the intracellular trypsin activity and the leakage of LDH from pancreatic acinar cells. Pretreatment with 2 mmol/L pefabloc could significantly decrease the activity of trypsin and the leakage of LDH from pancreatic acinar cells (P ＜0.01) following the treatment with a high concentration of carbachol (10-3 mol/L) in vitro. The addition of 10-2 mol/L PDTC didn't result in a significant decrease in the activity of trypsin and the leakage of LDH from pancreatic acinar cells treated with a high concentration of carbachol (10-3 mol/L) in vitro (P＞0.05). It was concluded that intracellular trypsinogen activation is likely involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro. NF-κB activation may not be involved in pancreatic acinar cellular injury induced by carbachol hyperstimulation in vitro.
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Reactive oxygen species (ROS), generated by infiltrating neutrophils, are considered as an important regulator in the pathogenesis and deveolpment of pancreatitis. The present study aims to investigate whether neutrophils primed by 4 beta-phorbol 12 beta-myristate 13 alpha-acetate (PMA) affect the productions H2O2 and lipid peroxide (LPO), NF-kappaB activation and cytokine production in pancreatic acinar cells, and whether these alterations were inhibited by an antioxidant, N-acetylcysteine (NAC) and superoxide dismutase (SOD). H2O2 (ferrithiocyanate method), LPO (as thiobarbiturate reactive substances), and cytokines (IL-1beta, IL-6, TNF-alpha enzyme-linked immunosorbent assay) and NF-kappaB activation (electrophoretic mobility shift assay) were analyzed in acinar cells treated with or without PMA-primed neutrophils in the absence or presence of NAC (10 mM) or SOD (300 U/ml). As a result, the productions of H2O2, LPO and TNF-alpha were increased with the ratio of PMA-primed neutrophils to acinar cells while the productions of LPO, IL-1beta, IL-6 and TNF-alpha were increased with time. PMA-primed neutrophils resulted in the activation of NF-kappaB. Both NAC and SOD inhibited neutrophil-induced alterations in acinar cells. In conclusion, ROS, generated by neutrophils, activates NF-kappaB, resulting in upregulation of inflammatary cytokines in acinar cells. Antioxidants might be clinically useful antiinflammatory agents by inhibiting oxidant-mediated activation of NF-kappaB and decreasing cytokine production.