Biliary tract external drainage increases the expression levels of heme oxygenase-1 in rat livers

Wang, Lu; Zhao, Bing; Chen, Ying; Ma, Li; Chen, Erzhen; Mao, Enqiang

doi:10.1186/s40001-015-0152-2

Cited by 3 publications

(3 citation statements)

References 51 publications

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“…HO-1 is a stress-inducible enzyme which catalyzes the degradation of heme into CO, iron and biliverdin [ 7 ]. Under oxidative stress, such as inflammation and ischemia-reperfusion, HO-1 is induced and protects organs from damage, which in part by the anti-inflammatory effect of heme metabolites [ 31 – 35 ]. The expression of genes responsible for oxidative stress, especially HO-1 [ 16 , 36 , 37 ], are remarkably upregulated in the course of SAP, which suggests the existence of a compensatory mechanism against stress.…”

Section: Discussionmentioning

confidence: 99%

Protective effects of heme oxygenase-1 against severe acute pancreatitis via inhibition of tumor necrosis factor-α and augmentation of interleukin-10

et al. 2017

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BackgroundHeme oxygenase-1 (HO-1) is an inducible defense gene which plays a significant role in inflammation. HO-1 protects cells and tissues through the mechanism of anti-oxidation, maintaining microcirculation and anti-inflammation. The aim of the current study is to investigate the role of HO-1 on systemic inflammatory response in severe acute pancreatitis (SAP).MethodsForty male Sprague-Dawley (SD) rats were randomly assigned into four groups: control group (n = 10); SAP group (n = 10), SAP model was induced by retrograde injection of 3% sodium taurocholate through pancreatic duct; HO-1 stimulation group (n = 10), SD rats were injected 75 μg/kg hemin intraperitoneally 30 min after induction of SAP; HO-1 inhibition group (n = 10), SD rats were injected 20 μg/kg Zinc porphyrin (Zn-PP) intraperitoneally 30 min after induction of SAP. After 24 h of SAP establishment, tissues were collected for HO-1, tumor necrosis factor-α (TNF-α) and interleukin-10 (IL-10) mRNA expression, and blood samples were collected for cytokines and biochemical measurements. Meanwhile, the histopathological changes of pancreas and liver tissues were observed.ResultsThe expression of HO-1 mRNA and protein were significantly induced by SAP in rat pancreas and liver. Hemin treatment significantly decreased oxidative stress and TNF-α in plasma and tissues, while the IL-10 was significantly increased. Pancreas and liver injury induced by SAP was markedly attenuated by Hemin treatment. Moreover, inhibition of HO-1 expression by Zn-PP administration aggravated the injury caused by SAP.ConclusionsInduction of HO-1 in early SAP may modulate systemic inflammatory response and prevent pancreas and nearby organs such as liver injury through inhibition of TNF-α and augmentation of IL-10.

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Section: Discussionmentioning

confidence: 99%

Protective effects of heme oxygenase-1 against severe acute pancreatitis via inhibition of tumor necrosis factor-α and augmentation of interleukin-10

et al. 2017

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“…HO-1 is an enzyme that regulates the breakdown of heme to biliverdin, iron, and CO. 34 It was reported that HO-1 may be beneficial as it ameliorated the negative effects of oxidative stress, and hence protects organs, partly by suppressing inflammation induced by heme metabolites. 9,10,[35][36][37] In this way, HO-1 protects organs from inflammation-induced injury and oxidative stress. We previously showed that HO-1 protected the pancreas from injury during SAP by inhibiting TNFa and enhancing IL-10.…”

Section: Discussionmentioning

confidence: 99%

Shenmai Injection Upregulates Heme Oxygenase-1 to Confer Protection Against Severe Acute Pancreatitis

Zhang

Liu

Dong

et al. 2020

Journal of Surgical Research

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Background: To explore the mechanism of Shenmai injection (SMI) on severe acute pancreatitis (SAP) through heme oxygenase-1 (HO-1) signaling. Methods: A total of 40 male SpragueeDawley (SD) rats (220-260 g) were grouped into the following four categories (n ¼ 10): SAP þ SMI þ Zinc protoporphyrin (ZnPP), SAP þ SMI, SAP, and sham surgery groups. ZnPP is a specific inhibitor of HO-1. Four percent of sodium taurocholate (1 mL/kg) was retrogradely injected via the pancreatic duct to induce the SAP model. The SAP group rats received 1.6 mL/kg saline by intravenous injection 30 min after the induction of SAP. The SAP þ SMI group rats received 1.6 mL/kg SMI by intravenous injection 30 min after the induction of SAP. The SAP þ SMI þ ZnPP group rats received an intravenous injection of 1.6 mL/kg SMI and intraperitoneal administration of 30 mg/kg ZnPP 30 min after the SAP induction. Twenty-four hours after the SAP induction, blood samples were collected for the measurement of amylase, lipase, creatinine, myeloperoxidase, interleukin-10 (IL-10), tumor necrosis factor-a (TNF-a), and HO-1 level, while tissue specimens were harvested for the determination of HO-1, TNF-a, and IL-10 mRNA level. Meanwhile, histopathological changes in organs (pancreas, lung, and kidney) were stored. Results: The serum concentration of amylase, lipase, creatinine, and myeloperoxidase was higher in the SAP group than in the SAP þ SMI group. Treatment with SMI increased HO-1 and IL-10 level and reduced TNF-a level in serum and tissues compared to the SAP group (P < 0.05). Treatment with SMI abolished the organ-damaging effects of SAP (P < 0.05). Furthermore, suppression of HO-1 expression by ZnPP canceled the aforementioned effects. Conclusions: SMI confers protection against the SAP-induced systemic inflammatory response and multiple organs damage via HO-1 upregulation.

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“…As the technology becomes more minimally invasive, biliary tract external drainage (BTED) is widely applied in critically ill patients, such as severe acute pancreatitis, malignant biliary obstruction (5)(6)(7), acute cholangitis (8)(9)(10)(11). In our previous studies, BTED decreased multiorgan dysfunction in HS by affecting enterohepatic circulation of bile pigments (12)(13)(14)(15).…”

Section: Introductionmentioning

confidence: 99%

Changes of farnesoid X receptor and Takeda G‑protein coupled receptor 5 following biliary tract external drainage in hemorrhagic shock

Wang

Zhou

et al. 2021

Exp Ther Med

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Since biliary tract external drainage (BTED) is increasingly used to treat patients with shock, it is necessary to clarify pathophysiological changes following BTED in hemorrhagic shock (HS). The present study aimed to investigate the effect of BTED on farnesoid X receptor (FXR) and Takeda G-protein coupled receptor 5 (TGR-5) expression in HS. A total of 24 Sprague-Dawley rats were randomly allocated to sham, BTED, HS and HS + BTED groups. Rat models of HS were induced by drawing blood from the femoral artery until a mean arterial pressure of 40±5 mmHg was achieved and maintained for 60 min. Rat models of BTED were induced by inserting a catheter into the bile duct. The distal end of the bile duct was ligated, and the catheter was passed through the rat flank to allow external collection of bile. Reverse transcription-quantitative PCR, western blotting and immunohistochemistry were performed to detect changes in expression levels of FXR and TGR-5 in the jejunum, ileum and liver. Expression levels of FXR and TGR-5 increased significantly in jejunum and liver following HS (P<0.05). BTED significantly decreased expression levels of FXR in the liver (P<0.05) and TGR-5 in the jejunum, ileum and liver (P<0.05). In conclusion, expression levels of FXR and TGR-5 increased in HS but BTED decreased expression levels of FXR and TGR-5 in HS.

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Biliary tract external drainage increases the expression levels of heme oxygenase-1 in rat livers

Cited by 3 publications

References 51 publications

Protective effects of heme oxygenase-1 against severe acute pancreatitis via inhibition of tumor necrosis factor-α and augmentation of interleukin-10

Protective effects of heme oxygenase-1 against severe acute pancreatitis via inhibition of tumor necrosis factor-α and augmentation of interleukin-10

Shenmai Injection Upregulates Heme Oxygenase-1 to Confer Protection Against Severe Acute Pancreatitis

Changes of farnesoid X receptor and Takeda G‑protein coupled receptor 5 following biliary tract external drainage in hemorrhagic shock

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