Hypertriglyceridemia Acute Pancreatitis: Animal Experiment Research

Wang, Lu; Xu, Ting; Wang, Ruifeng; Wang, Xiaobing; Wu, Dong

doi:10.1007/s10620-021-06928-0

Cited by 22 publications

(24 citation statements)

References 138 publications

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“…All experimental procedures involving animals were carried out according to protocols approved by the Institutional Animal Ethics Committee of The First Affiliated Hospital of Harbin Medical University. For the inducible HTG model, P-407 (Poloxamer 407, Sigma-Aldrich Co., USA) was administered intraperitoneally to mice every other day (0.5 g/kg body weight (b.w)) for 7 consecutive days, the control mice were injected with PBS 50,51 . Twelve-weekold Gpihbp1 -/mice were considered with stable serum HTG level, and were used for generating HTGP model 52,53 .…”

Section: Animals and Experimental Modelmentioning

confidence: 99%

WITHDRAWN: Gut microbiota aggravates neutrophil extracellular traps-induced pancreatic injury in hypertriglyceridemic pancreatitis

Liu

Sui

et al. 2023

Preprint

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Hypertriglyceridemic pancreatitis (HTGP) is featured by higher incidence of complications and poor outcomes. Dysbiosis of gut microbiota has been established in HTGP, the impact of gut microbiota in pancreatic injury remains unclear. We observed that HTGP patients’ gut microbiota involved lower diversity and loss of beneficial bacteria, which were negatively correlated with local and systemic complications. In FMT mouse model, colonization with gut microbiota from HTGP patients exacerbated pancreatic injury through inducing neutrophil infiltration and neutrophil extracellular traps (NETs) compared to mice colonized with health volunteers’ fecal samples. Furthermore, decreased Bacteroides uniformis was demonstrated to trigger neutrophils accumulation and NETs release in HTGP, and oral administration of Bacteroides uniformis increased taurine production that alleviated pancreatic injury. In addition, taurine supplementation limited neutrophils infiltration and NETs that attenuated pancreatic injury. Notably, circulating NETs-related biomarker levels were elevated in HTGP patients and coculturing patients’ serum with neutrophils accelerated NETs release in vitro, accompanying with taurine-producing disorder. Our ﬁndings establish roles of endogenous Bacteroides uniformis-derived taurine suppressed neutrophils recruitments and NETs in HTGP, which provides potential insights of ameliorating pancreatic injury by gut microbiota modulation.

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Section: Animals and Experimental Modelmentioning

confidence: 99%

WITHDRAWN: Gut microbiota aggravates neutrophil extracellular traps-induced pancreatic injury in hypertriglyceridemic pancreatitis

Liu

Sui

et al. 2023

Preprint

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“…Pancreatic acinar cells are rich in lipase which can hydrolyze TG to produce free fatty acids (FFA). Accumulation of FFA triggers an inflammatory cascade through Ca 2+ overload, microcirculation disorders, and release of inflammatory mediators, eventually leading to HTG-AP [ 32 ]. However, these pathogenic mechanisms have not been fully elucidated in the early severe development of HTG-AP.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of TRAF6 improves hyperlipidemic acute pancreatitis by alleviating pyroptosis in vitro and in vivo rat models

et al. 2023

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Objective Hypertriglyceridemia (HTG) is one of the common causes of acute pancreatitis (AP). Hyperlipidemic acute pancreatitis (HTG-AP) is associated with higher mortality owing to its tendency for greater severity and rapid progression. The purpose of this study was to explore the mechanism of involvement of tumor necrosis factor receptor-related factor 6 (TRAF6) in pyroptosis during HTG-AP. Methods The HTG environment was simulated with palmitic acid treatment in vitro and a high-fat diet in vivo. Cerulein was used to establish the HTG-AP model, followed by genetic and pharmacological inhibition of TRAF6. Pyroptosis activation, inflammatory reaction, and the interaction between TRAF6 and pyroptosis in HTG-AP were assessed. Results HTG was found to aggravate the development of pancreatitis, accompanied by increased pyroptosis and enhanced inflammatory response in HTG-AP models. Mechanistically, TRAF6 downregulation decreased the activation of pyroptosis in cerulein-induced HTG-AP. Conclusion Collectively, inhibition of TRAF6 improved HTG-AP and the associated inflammation by alleviating pyroptosis.

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“…The authors further investigated the generator of OS in AP (Jakovljevic et al, 2018). AP is also considered to be an inflammatory response of the host to microbial insults mainly from the root canal system (Wang, Xu, et al, 2022; Wang, Yang, et al, 2022). As the disease aggravates, AP may lead to the overproduction of inflammatory cytokines (Brilhante Wolle et al, 2012; Konoplya et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Is oxidative stress involved in the hepatic inflammatory response to apical periodontitis? A comparative study in normal and hyperlipidaemic rat

Xiao

Lei

et al. 2023

Int Endodontic J

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Aim The aim of the study was to explore the involvement of oxidative stress (OS) in the hepatic inflammation induced by apical periodontitis (AP). Periapical, systemic and hepatic reaction to AP under hyperlipidaemia was also investigated. Methodology A total of 16 male Sprague–Dawley rats were fed with a hyperlipidaemic diet (HD) whereas another 16 rats with a normal diet (ND). After 9 weeks, the first molars of the right maxilla and mandible of 8 HD and 8 ND rats were exposed to induce AP (ND, ND + AP, HD and HD + AP group). After 5 weeks, rats were euthanized, the haematological tissue was collected directly from the heart, and serum levels of inflammatory cytokines were measured. Liver tissue was analysed by haematoxylin–eosin and Masson staining, and reverse transcription–polymerase chain reaction (RT‐PCR) was performed to detect mRNA expression of inflammatory cytokines. Serum, periapical, and hepatic OS parameters including total oxidant status (TOS), total antioxidant capacity (TAOC) and oxidative stress index (OSI) were measured by enzyme‐linked immunosorbent assay (ELISA). The area of AP lesion in the right maxilla or mandible was radiographically assessed. Student's t‐test was performed on the periapical data. A one‐way analysis of variance and the Kruskal–Wallis test were analysed for others. Results The HD + AP group had a larger AP lesion in the maxilla, compared with the ND + AP group (p < .05). The ND + AP group presented higher serum interleukin (IL)‐18, IL‐1β, TOS, OSI levels, lower serum TOAC levels, higher hepatic tumour necrosis factor (TNF)‐α mRNA expression and higher hepatic TOS, and OSI levels, compared with the ND group (p < .05). The HD + AP group had lower serum IL‐4 level, higher serum IL‐1β level, and higher hepatic IL‐6 and transforming growth factor (TGF) ‐β1 mRNA expression, compared with the HD group (p < .05). Conclusions Apical periodontitis could activate systemic and liver inflammation by promoting serum IL‐18, 1L‐1β, TOS and OSI expression, enhancing hepatic TOS and OSI expression and inhibiting serum TOAC expression. AP under hyperlipidaemia led to more profound periapical bone destruction in the maxilla and elicit systemic and liver inflammatory responses through elevating serum levels of IL‐1β, descending serum IL‐4 level and improving hepatic IL‐6 and TGF‐β1 expression.

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Hypertriglyceridemia Acute Pancreatitis: Animal Experiment Research

Cited by 22 publications

References 138 publications

WITHDRAWN: Gut microbiota aggravates neutrophil extracellular traps-induced pancreatic injury in hypertriglyceridemic pancreatitis

WITHDRAWN: Gut microbiota aggravates neutrophil extracellular traps-induced pancreatic injury in hypertriglyceridemic pancreatitis

Inhibition of TRAF6 improves hyperlipidemic acute pancreatitis by alleviating pyroptosis in vitro and in vivo rat models

Is oxidative stress involved in the hepatic inflammatory response to apical periodontitis? A comparative study in normal and hyperlipidaemic rat

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