Effects of Hydrogen Peroxide Scavenger Catalase on Villous Microcirculation in the Rat Small Intestine in a Model of Inflammatory Bowel Disease

Ruh, Joachim; Vogel, Frank; Schmidt, E.; Werner, Martin; Klar, E.; Secchi, Andreas; Gebhard, Martha Maria; Glaser, F.; Herfarth, Christian

doi:10.1006/mvre.1999.2201

Cited by 28 publications

(13 citation statements)

References 14 publications

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“…29 When the cytoplasmic extracts were examined, it could be seen that the LPS plus IFN-␥-induced CaM level was poorer in the group cotreated with catalase and LPS plus IFN-␥ as compared to the group treated with LPS plus IFN-␥ alone ( Figure 7G; P ϭ .001). The decrease in CaM in the LPS plus IFN-␥ plus catalase-treated group resulted in concomitant up-regulation in IL-12 p40 induction as compared to the LPS plus IFN-␥-treated control group ( Figure 7H; P ϭ .001).…”

Section: Nac and Catalase Down-regulate Cam Expression Leading To Up-mentioning

confidence: 94%

Hydrogen peroxide inhibits IL-12 p40 induction in macrophages by inhibiting c-rel translocation to the nucleus through activation of calmodulin protein

Khan

Rahim

Boddupalli

et al. 2006

Blood

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Although the antimicrobial activity of reactive oxygen species (ROSs) is well defined, the role of ROSs in regulating the immune response of the body is not well understood. We now provide evidence that hydrogen peroxide (H 2 O IntroductionAccumulated damage due to reactive oxygen species (ROSs) has been suggested to occur during aging 1,2 and more clearly demonstrated during the respiratory burst of phagocytes. 3,4 Hydrogen peroxide (H 2 O 2 ), is a primary component of ROSs produced in large amounts by macrophages and granulocytes and is a mediator of innate immunity against the invading pathogens. 5,6 H 2 O 2 is known to function as a second messenger 7,8 and regulates activation of many important transcription factors, such as nuclear factor-B (NF-B) and activator protein-1 (AP-1), 9,10 that control the inducible expression of genes regulating macrophage-effector functions and cytokine signaling. [11][12][13] The macrophage-induced cytokines determine the fate of the subsequent T-cell responses as type 1 14,15 or type 2. 16,17 Thus, the possibility exists that H 2 O 2 may alter the T-cell immune responses by affecting the macrophageeffector responses. The function of ROSs may not be restricted to its antimicrobial activity alone, 18 but ROSs may also play an important role in regulating the immune environment in the body. Such situations may arise during certain pathophysiologic conditions such as tuberculosis. 19,20 We earlier reported that activated macrophages from the Bruton tyrosine kinase (btk)-deficient mice (CBA/N) produced lower levels of ROSs as compared to the wild-type mice (CBA/J). 21 However, in contrast to CBA/J macrophages, the IL-12 induction was significantly higher in macrophages from CBA/N mice with T-cell responses biased toward type 1. 21,22 Although the contribution of btk enzyme in controlling the signal transduction cascades responsible for ROS production independent of IL-12 signal may not be ruled out, it is possible that btk targets the ROS pathway to influence IL-12 production. However, the exact mechanism by which ROSs down-regulate IL-12 production is not well understood. We now provide evidence that H 2 O 2 /ROSs affect the signaling events important for IL-12 production, leading to downregulation of the same in activated macrophages. Materials and methods MiceBALB/c mice were bred and maintained in the animal facility of Indian Immunologicals (IIL; Hyderabad, India). All mice were 6 to 12 weeks old and experimental protocol was approved by the Institutional Review Committee for care and usage of animals of Indian Immunologicals. Macrophage stimulation assayThe peritoneal exudate cells (PECs) were harvested by injecting 4% thioglycolate broth as described elsewhere. 23 The RAW 264.7 macrophages were obtained from NCCS (National Centre for Cell Science, Pune, India) and maintained in Dulbecco minimal essential medium (DMEM; Invitrogen, Grand Island, NY) containing 10% fetal calf serum and antibiotics (DMEM-10). The macrophages were plated at a density of 3 ϫ 10 6 cells/mL and ...

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Section: Nac and Catalase Down-regulate Cam Expression Leading To Up-mentioning

confidence: 94%

Hydrogen peroxide inhibits IL-12 p40 induction in macrophages by inhibiting c-rel translocation to the nucleus through activation of calmodulin protein

Khan

Rahim

Boddupalli

et al. 2006

Blood

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“…D-lactate, a particular final metabolic product of bacteria in gastrointestinal tract, will release into blood when intestinal mucosa barrier is damaged. Examination of D-lactate in peripheral blood can evaluate damage situation of intestinal mucosa because of lack of D-lactate dehydrogenase in mammals [4]. The other indicator is Diamine oxidase (DAO), one kind of endocellular enzyme, only exists in villus cytoplasm of intestinal stratum supravasculare in mammals.…”

Section: Introductionmentioning

confidence: 99%

Curcumin Protects Intestinal Mucosal Barrier Function of Rat Enteritis via Activation of MKP-1 and Attenuation of p38 and NF-κB Activation

et al. 2010

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BackgroundIntestinal mucosa barrier (IMB) dysfunction results in many notorious diseases for which there are currently few effective treatments. We studied curcumin's protective effect on IMB and examined its mechanism by using methotrexate (MTX) induced rat enteritis model and lipopolysaccharide (LPS) treated cell death model.Methodology/Principal FindingsCurcumin was intragastrically administrated from the first day, models were made for 7 days. Cells were treated with curcumin for 30 min before exposure to LPS. Rat intestinal mucosa was collected for evaluation of pathological changes. We detected the activities of D-lactate and diamine oxidase (DAO) according to previous research and measured the levels of myeloperoxidase (MPO) and superoxide dismutase (SOD) by colorimetric method. Intercellular adhesion molecule-1 (ICAM-1), tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) were determined by RT-PCR and IL-10 production was determined by ELISA. We found Curcumin decreased the levels of D-lactate, DAO, MPO, ICAM-1, IL-1β and TNF-α, but increased the levels of IL-10 and SOD in rat models. We further confirmed mitogen-activated protein kinase phosphatase-1 (MKP-1) was activated but phospho-p38 was inhibited by curcumin by western blot assay. Finally, NF-κB translocation was monitored by immunofluorescent staining. We showed that curcumin repressed I-κB and interfered with the translocation of NF-κB into nucleus.Conclusions/SignificanceThe effect of curcumin is mediated by the MKP-1-dependent inactivation of p38 and inhibition of NF-κB-mediated transcription. Curcumin, with anti-inflammatory and anti-oxidant activities may be used as an effective reagent for protecting intestinal mucosa barrier and other related intestinal diseases.

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“…These were shown to coincide with changes in the diameter of the main arteriole supplying this vascular bed. In fact, the scavenger was shown to attenuate the hyperemia associated with induced intestinal infl ammation (Ruh et al 2000 ). In an elegant set of experiments, Chaplin and Amberg demonstrated that the vasoconstrictor angiotensin II (Ang II) was able to generate ROS via NADPH oxidase (Chaplin and Amberg 2012 ).…”

Section: Physiological Overview Of Rosmentioning

confidence: 99%

Antioxidants and Their Effect on Stress-Induced Pathology in the Inner Ear

Shirwany¹,

Seidman

2015

Free Radicals in ENT Pathology

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Effects of Hydrogen Peroxide Scavenger Catalase on Villous Microcirculation in the Rat Small Intestine in a Model of Inflammatory Bowel Disease

Cited by 28 publications

References 14 publications

Hydrogen peroxide inhibits IL-12 p40 induction in macrophages by inhibiting c-rel translocation to the nucleus through activation of calmodulin protein

Hydrogen peroxide inhibits IL-12 p40 induction in macrophages by inhibiting c-rel translocation to the nucleus through activation of calmodulin protein

Curcumin Protects Intestinal Mucosal Barrier Function of Rat Enteritis via Activation of MKP-1 and Attenuation of p38 and NF-κB Activation

Antioxidants and Their Effect on Stress-Induced Pathology in the Inner Ear

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