Pathophysiology of chronic pancreatitis induced by dibutyltin dichloride joint ethanol in mice

Zhang, Hong; Liu, Bin; Xu, Xichen; Jiang, Tingting; Zhang, Xiaoqin; Shi, Yunfan; Chen, Yu; Liu, Fang; Gu, Jun; Zhu, Lijun; Wu, Nan

doi:10.3748/wjg.v22.i10.2960

Cited by 21 publications

(14 citation statements)

References 32 publications

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“…The handicap of the model is the collateral cytotoxic damage to the liver and biliary duct. The model-associated lethality is quite high at 30% (58).…”

Section: Dibutyltin Dichloride-induced Cpmentioning

confidence: 99%

“…Another model based on the sentinel acute pancreatitis episode hypothesis is the dibutyltin dichloride (DBTC) model, which was established in rats (57) and was thought not to be applicable in mice because of the bile duct anatomy of mice (8). However, Zhang et al (58) recently created a protocol for DBTC-induced CP in mice by combining it with ethanol. DBTC is an organotin compound that causes cytotoxic damage on the surface epithelium of the bile duct and leads directly to pancreatic injury (59).…”

Section: Dibutyltin Dichloride-induced Cpmentioning

confidence: 99%

“…Depending on timing and dose, DBTC leads to acute, edematous pancreatitis, which progresses to pancreatic fibrosis and chronic inflammation but also induces bile duct and liver lesions (59). Ethanol intake enhances the toxic damage on the pancreas, leading to more-intense pancreatitis (57 (58). The application of DBTC, together with continuous ethanol intake, resulted in a model that showed progression from AP to CP and also mimicked the 2 main etiologies of the human CP: alcohol intake and duct obstruction.…”

Section: Dibutyltin Dichloride-induced Cpmentioning

confidence: 99%

“…Furthermore, alterations in the spinal cord of the neuropeptides and calcitonin gene-related peptide were detected, suggesting central nociceptive changes (12) as well as an increased expression of bradykinin-receptors in thoracic dorsal root ganglia (60). This model requires technical proficiency in the injection technique because subcutaneous injection, instead of intravenous injection, can lead to necrosis, and the speed of the injection must not be too fast because, otherwise, pulmonary embolism can occur (58). Once learned, this model is simple to perform.…”

Section: Dibutyltin Dichloride-induced Cpmentioning

confidence: 99%

“…). Zhang et al(58) combined 1 single intravenous injection of DBTC with mice fed daily ethanol (10% ethanol in drinking water) in mice. After 1 wk, the mice developed acute pancreatitis with increased serum enzyme levels; after 2 wk, duct dilation, fibrosis, and inflammatory infiltrates, predominantly macrophages and T cells, were observed, progressing over 2 mo…”

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confidence: 99%

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Genetically inducedvs.classical animal models of chronic pancreatitis: a critical comparison

et al. 2018

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Chronic pancreatitis (CP) is an utmost complex disease that is pathogenetically linked to pancreas-intrinsic ( e.g., duct obstruction), environmental-toxic ( e.g., alcohol, smoking), and genetic factors. Studying such a complex disease naturally requires validated experimental models. In the past 2 decades, the various animal models of CP usually addressed either the pancreas-intrinsic ( e.g., the caerulein model), the environmental-toxic ( e.g., diet-induced models), or the genetic component of CP. As such, these models were far from mirroring CP in its full spectrum, and the correct choice of models was vital for valid scientific conclusions on CP. The quest for mechanistic, genetic models gave rise to models based on gene modification and transgene insertion, such as the PRSS1 and the IL-1β/IL-1β models. Recently, we witnessed the development of highly exciting models that rely on the importance of autophagy in CP, that is, the murine pancreas-specific Atg5 and LAMP2 knockout models. Today, critical comparison of these several models is more important than ever for guiding research on CP in an efficient direction. The present review outlines the characteristics of the new genetic models in comparison with the well-known classic models for CP, notes the caveats in the choice of models, and also indicates novel directions for model development.-Klauss, S., Schorn, S., Teller, S., Steenfadt, H., Friess, H., Ceyhan, G. O., Demir, I. K. Genetically induced vs. classical animal models of chronic pancreatitis: a critical comparison.

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“…The handicap of the model is the collateral cytotoxic damage to the liver and biliary duct. The model-associated lethality is quite high at 30% (58).…”

Section: Dibutyltin Dichloride-induced Cpmentioning

confidence: 99%

Section: Dibutyltin Dichloride-induced Cpmentioning

confidence: 99%

Section: Dibutyltin Dichloride-induced Cpmentioning

confidence: 99%

Section: Dibutyltin Dichloride-induced Cpmentioning

confidence: 99%

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confidence: 99%

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Genetically inducedvs.classical animal models of chronic pancreatitis: a critical comparison

et al. 2018

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Diffusion Metrics for Staging Pancreatic Fibrosis and Correlating With Epithelial‐Mesenchymal Transition Markers in a Chronic Pancreatitis Rat Model at 11.7T MRI

Zhang

Yang

et al. 2019

Magnetic Resonance Imaging

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BackgroundChronic pancreatitis (CP) is characterized by pancreatic fibrosis, in which a epithelial‐mesenchymal transition (EMT)‐like process is observed. However, few noninvasive approaches have been reported to evaluate pancreatic fibrosis and EMT in an animal model based on diffusion imaging.PurposeTo evaluate pancreatic fibrosis in CP by conventional diffusion‐weighted imaging (DWI), intravoxel incoherent motion (IVIM), and diffusion kurtosis imaging (DKI) and then explore the correlation between diffusion parameters and the EMT markers in an animal model.Study TypeProspective controlled imaging histological correlation.PopulationForty‐five rats with CP induced by injecting dibutyltin dichloride solution and 10 normal rats comprised the control group.Field Strength/Sequence11.7T MR, diffusion imaging with 10 b‐values.AssessmentApparent diffusion coefficient (ADC), IVIM‐associated perfusion fraction (f), pseudodiffusion coefficient (D*), diffusion coefficient (D), DKI‐associated mean kurtosis (MK), and mean corrected diffusion coefficient (MD) were quantitatively measured and correlated with pancreatic fibrosis stages as well as the EMT markers E‐cadherin and α‐smooth muscle actin (α‐SMA) expression. The discriminative performance of diffusion parameters for staging fibrosis was compared.Statistical TestsSpearman's correlation, Student's t‐test, and a receiver operating characteristic curve was conducted for statistical analysis.ResultsADC, D, and MD (r = –0.637, –0.688, and –0.535; P < 0.001) were negatively correlated with pancreatic fibrosis staging, but MK (r = 0.740, P < 0.001) had a positive correlation. ADC, D, MD, and MK were significantly correlated with α‐SMA (r = –0.684, –0.728, –0.627, and 0.721, all P < 0.001), while MK was significantly correlated with E‐cadherin (r = –0.606, P < 0.001). The area under the curve (AUC) was not significantly different (P > 0.05) among ADC (0.797, 0.816, 0.873), D (0.862, 0.810, 0.895), MD (0.767, 0.772, 0.801), and MK (0.836, 0.893, 0.951) for F1 or greater, F2 or greater, and F3 pancreatic fibrosis separately.Data ConclusionADC, D, MD, and MK were helpful for assessing pancreatic fibrosis staging, and these diffusion parameters were also significantly correlated with the expression of EMT markers in pancreatic fibrosis.Level of Evidence: 2Technical Efficacy Stage: 2J. Magn. Reson. Imaging 2020;52:197–206.

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The Application of Urinary Proteomics in Early Detection of Digestive Diseases

Zhang

Qin

2019

Urine

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Pathophysiology of chronic pancreatitis induced by dibutyltin dichloride joint ethanol in mice

Cited by 21 publications

References 32 publications

Genetically inducedvs.classical animal models of chronic pancreatitis: a critical comparison

Genetically inducedvs.classical animal models of chronic pancreatitis: a critical comparison

Diffusion Metrics for Staging Pancreatic Fibrosis and Correlating With Epithelial‐Mesenchymal Transition Markers in a Chronic Pancreatitis Rat Model at 11.7T MRI

The Application of Urinary Proteomics in Early Detection of Digestive Diseases

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