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Protective effect of YHI and HHI-I against experimental acute pancreatitis in rabbits.

ABSTRACT: AIM:To observe the protective effect of combined i.v. administraction of Yuanhu injection (YHI) and Huoxuehuayu injection-I (HHI-I) against acute pancreatitis (AP) in rabbits.METHODS:Sever acute pancreatitis (SAP) was induced by retrograde infusion of artificial bile juice into biliary-pancreatic duct, and treated with YHI and HHI-I intravenously. The protective effect was judged by the survival time and rate, serum amylase, serum interleukin-6, pancreatic microcirculation and pathological alteration.RESULTS:Combined use of YHI and HHI-I could markedly increase the rabbits' 5-day survival rate after AP (83.3% in the treatment group and 33.3% in control). The serum amylase value (x-± s) decreased to 1596.6U/L± 760.50U/L in the 5th day from the high level (6320.83U/L± 2614.12U/L) in the 1st day after AP in the treatment group, while in the control group the amylase activity in the 5th day was 2095.0U/L± 1081.87U/L, being significantly different from that before AP (837.17U/L± 189.12U/L). YHI and HHI-I also obviously improved the pancreatic microcirculation and lowered the serum interleukin-6 level, one of the indices of severe pancreatitis. Pathological examination indicated all the changes typical for AP in YHI and HHI-I treatment group were milder than those in the control.CONCLUSION:YHI and HHI-I used in combination might have protective effect against acute pancreatitis in rabbits.

SUBMITTER: Zhao LG

PROVIDER: S-EPMC4723471 | biostudies-literature | 1998 Jun

REPOSITORIES: biostudies-literature

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Protective effect of YHI and HHI-I against experimental acute pancreatitis in rabbits.

Zhao Lian-Gen LG Wu Xiao-Xian XX Han En-Kun EK Chen Yu-Ling YL Chen Chi C Xu Dong-Qin DQ

World journal of gastroenterology 19980601 3

AIM:To observe the protective effect of combined i.v. administraction of Yuanhu injection (YHI) and Huoxuehuayu injection-I (HHI-I) against acute pancreatitis (AP) in rabbits.METHODS:Sever acute pancreatitis (SAP) was induced by retrograde infusion of artificial bile juice into biliary-pancreatic duct, and treated with YHI and HHI-I intravenously. The protective effect was judged by the survival time and rate, serum amylase, serum interleukin-6, pancreatic microcirculation and pathological alter ...[more]

PMID: 11819290

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Project description:BACKGROUND & AIMS:Acute pancreatitis (AP) is characterized by severe inflammation and acinar cell death. Transmembrane protein 173 (TMEM173 or STING) is a DNA sensor adaptor protein on immune cells that recognizes cytosolic nucleic acids and transmits signals that activate production of interferons and the innate immune response. We investigated whether leukocyte STING signaling mediates inflammation in mice with AP. METHODS:We induced AP in C57BL/6J mice (control) and C57BL/6J-Tmem173gt/J mice (STING-knockout mice) by injection of cerulein or placement on choline-deficient DL-ethionine supplemented diet. In some mice, STING signaling was induced by administration of a pharmacologic agonist. AP was also induced in C57BL/6J mice with bone marrow transplants from control or STING-knockout mice and in mice with disruption of the cyclic GMP-AMP synthase (Cgas) gene. Pancreata were collected, analyzed by histology, and acini were isolated and analyzed by flow cytometry, quantitative polymerase chain reaction, immunoblots, and enzyme-linked immunosorbent assay. Bone-marrow-derived macrophages were collected from mice and tested for their ability to detect DNA from dying acinar cells in the presence and absence of deoxyribonuclease (DNaseI). RESULTS:STING signaling was activated in pancreata from mice with AP but not mice without AP. STING-knockout mice developed less severe AP (less edema, inflammation, and markers of pancreatic injury) than control mice, whereas mice given a STING agonist developed more severe AP than controls. In immune cells collected from pancreata, STING was expressed predominantly in macrophages. Levels of cGAS were increased in mice with vs without AP, and cGAS-knockout mice had decreased edema, inflammation, and other markers of pancreatic injury upon induction of AP than control mice. Wild-type mice given bone marrow transplants from STING-knockout mice had less pancreatic injury and lower serum levels of lipase and pancreatic trypsin activity following induction of AP than mice given wild-type bone marrow. DNA from dying acinar cells activated STING signaling in macrophages, which was inhibited by addition of DNaseI. CONCLUSIONS:In mice with AP, STING senses acinar cell death (by detecting DNA from dying acinar cells) and activates a signaling pathway that promotes inflammation. Macrophages express STING and activate pancreatic inflammation in AP.

Project description:ObjectiveCaffeine reduces toxic Ca2+ signals in pancreatic acinar cells via inhibition of inositol 1,4,5-trisphosphate receptor (IP3R)-mediated signalling, but effects of other xanthines have not been evaluated, nor effects of xanthines on experimental acute pancreatitis (AP). We have determined effects of caffeine and its xanthine metabolites on pancreatic acinar IP3R-mediated Ca2+ signalling and experimental AP.DesignIsolated pancreatic acinar cells were exposed to secretagogues, uncaged IP3 or toxins that induce AP and effects of xanthines, non-xanthine phosphodiesterase (PDE) inhibitors and cyclic adenosine monophosphate and cyclic guanosine monophosphate (cAMP/cGMP) determined. The intracellular cytosolic calcium concentration ([Ca2+]C), mitochondrial depolarisation and necrosis were assessed by confocal microscopy. Effects of xanthines were evaluated in caerulein-induced AP (CER-AP), taurolithocholic acid 3-sulfate-induced AP (TLCS-AP) or palmitoleic acid plus ethanol-induced AP (fatty acid ethyl ester AP (FAEE-AP)). Serum xanthines were measured by liquid chromatography-mass spectrometry.ResultsCaffeine, dimethylxanthines and non-xanthine PDE inhibitors blocked IP3-mediated Ca2+ oscillations, while monomethylxanthines had little effect. Caffeine and dimethylxanthines inhibited uncaged IP3-induced Ca2+ rises, toxin-induced Ca2+ release, mitochondrial depolarisation and necrotic cell death pathway activation; cAMP/cGMP did not inhibit toxin-induced Ca2+ rises. Caffeine significantly ameliorated CER-AP with most effect at 25?mg/kg (seven injections hourly); paraxanthine or theophylline did not. Caffeine at 25?mg/kg significantly ameliorated TLCS-AP and FAEE-AP. Mean total serum levels of dimethylxanthines and trimethylxanthines peaked at >2?mM with 25?mg/kg caffeine but at <100?µM with 25?mg/kg paraxanthine or theophylline.ConclusionsCaffeine and its dimethylxanthine metabolites reduced pathological IP3R-mediated pancreatic acinar Ca2+ signals but only caffeine ameliorated experimental AP. Caffeine is a suitable starting point for medicinal chemistry.

Dataset Information

Protective effect of YHI and HHI-I against experimental acute pancreatitis in rabbits.

Publications

Protective effect of YHI and HHI-I against experimental acute pancreatitis in rabbits.

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