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Frontiers in Pharmacology 2023Apolipoprotein A-I (apoA-I), 90% of which is present in high-density lipoprotein (HDL), is the main constituent of HDL, has anti-inflammatory and anti-oxidant...
Apolipoprotein A-I (apoA-I), 90% of which is present in high-density lipoprotein (HDL), is the main constituent of HDL, has anti-inflammatory and anti-oxidant properties, and has received extensive attention in anti-atherosclerosis. Yet little is known about apoA-I 's role in peritoneal dialysis. In this study, by analyzing PD patients ( = 81), we found that decreased apoA/HDL-C ratio is significantly associated with rapid decline in peritoneal function. Further studies were performed in animal experiments to determine the ascendancy of apolipoprotein A-I mimetic peptide (D-4F) on peritoneum, we found that D-4F administration reduced peritoneal fibrosis and peritoneal endothelial mesenchymal transformation (EMT) induced by high glucose peritoneal dialysate, such as N-cadherin, Fibronectin, Vimentin, and α-smooth muscle actin (α-SMA) expression decreased. In mechanism, D-4F can significantly inhibit Smad2/3 phosphorylation, which is the major pathway leading to fibrosis. Furthermore, D-4F treatment inhibited NADPH oxidase and thiobarbituric acid reactive substances (TBARS) expression, increased the activity of certain enzymes, such as superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Finally, treatment with D-4F inhibits the expression of interleukins-6(IL-6), Interleukin-1β(IL-1β), and tumor necrosis factor-α(TNF-α). Taken together, based on the above research evidence, apoA-I and its peptide mimic may regulate the oxidative stress, TGF- β1/Smads signaling pathway and inflammatory response to reduce peritoneal fibrosis due to peritoneal dialysis.
PubMed: 37576813
DOI: 10.3389/fphar.2023.1106339 -
Anesthesiology Jul 2021Sepsis is one of the leading causes of mortality in intensive care units, and sedation in the intensive care unit during sepsis is usually performed intravenously. The...
BACKGROUND
Sepsis is one of the leading causes of mortality in intensive care units, and sedation in the intensive care unit during sepsis is usually performed intravenously. The inhalative anesthetic sevoflurane has been shown to elicit protective effects in various inflammatory studies, but its role in peritonitis-induced sepsis remains elusive. The hypothesis was that sevoflurane controls the neutrophil infiltration by stabilization of hypoxia-inducible factor 1α and elevated adenosine A2B receptor expression.
METHODS
In mouse models of zymosan- and fecal-induced peritonitis, male mice were anesthetized with sevoflurane (2 volume percent, 30 min) after the onset of inflammation. Control animals received the solvent saline. The neutrophil counts and adhesion molecules on neutrophils in the peritoneal lavage of wild-type, adenosine A2B receptor -/-, and chimeric animals were determined by flow cytometry 4 h after stimulation. Cytokines and protein release were determined in the lavage. Further, the adenosine A2B receptor and its transcription factor hypoxia-inducible factor 1α were evaluated by real-time polymerase chain reaction and Western blot analysis 4 h after stimulation.
RESULTS
Sevoflurane reduced the neutrophil counts in the peritoneal lavage (mean ± SD, 25 ± 17 × 105vs. 12 ± 7 × 105 neutrophils; P = 0.004; n = 19/17) by lower expression of various adhesion molecules on neutrophils of wild-type animals but not of adenosine A2B receptor -/- animals. The cytokines concentration (means ± SD, tumor necrosis factor α [pg/ml], 523 ± 227 vs. 281 ± 101; P = 0.002; n = 9/9) and protein extravasation (mean ± SD [mg/ml], 1.4 ± 0.3 vs. 0.8 ± 0.4; P = 0.002; n = 12/11) were also lower after sevoflurane only in the wild-type mice. Chimeric mice showed the required expression of the adenosine A2B receptor on the hematopoietic and nonhematopoietic compartments for the protective effects of the anesthetic. Sevoflurane induced the expression of hypoxia-inducible factor 1α and adenosine A2B receptor in the intestine, liver, and lung.
CONCLUSIONS
Sevoflurane exerts various protective effects in two murine peritonitis-induced sepsis models. These protective effects were linked with a functional adenosine A2B receptor.
Topics: Anesthetics, Inhalation; Animals; Disease Models, Animal; Hypoxia-Inducible Factor 1; Male; Mice; Mice, Inbred C57BL; Peritonitis; Receptor, Adenosine A2B; Sepsis; Sevoflurane; Signal Transduction
PubMed: 33914856
DOI: 10.1097/ALN.0000000000003788 -
Polish Journal of Radiology 2020Intra-abdominal fat is abundantly present in both the peritoneum and retroperitoneum. Fat necrosis or inflammation are common findings in abdominal imaging. The most... (Review)
Review
Intra-abdominal fat is abundantly present in both the peritoneum and retroperitoneum. Fat necrosis or inflammation are common findings in abdominal imaging. The most common pathologies that we encounter are epiploic appendagitis, omental infarction, mesenteric panniculitis, and encapsulated fat necrosis. Less common entities that can occur are pancreatic saponification, heterotopic mesenteric ossification, and pseudolipoma of the capsule of Glisson. These entities can mimic more urgent pathologies such as appendicitis, diverticulitis, or malignancies.
PubMed: 32180852
DOI: 10.5114/pjr.2020.93070 -
Pharmacology Research & Perspectives Oct 2020Acute peritonitis is an acute inflammatory response of the peritoneal cavity to physical injury and chemical stimulation. Timely resolution of this response is critical...
Acute peritonitis is an acute inflammatory response of the peritoneal cavity to physical injury and chemical stimulation. Timely resolution of this response is critical to prevent further damage to the body, which can eventually lead to more severe chronic inflammation. Arctigenin (ATG) is the main active ingredient of the Chinese medicine Arctium lappa. In recent years, there have been an increasing number of studies on the anti-inflammatory effect of ATG, but there have been few studies on the effect of ATG on acute inflammation, especially in acute peritonitis, which has not been reported. In this study, a mouse model of experimental acute peritonitis induced by thioglycolate (TG) solution was used to study the protective anti-inflammatory effect of ATG against acute peritonitis and the relevant mechanism. Our results showed that, after 12 hours of TG treatment, ATG significantly reduced inflammatory cell infiltration in mouse tissues and inhibited the secretion and expression of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-α) in mice. ATG significantly reduced the percentage of CD11b Ly6G neutrophils and F4/80 macrophages in the spleen and peritoneal exudate. In addition, ATG significantly inhibited the expression of the chemokines CCL3 and CCL4 and the adhesion molecule CD62L on the surface of CD11b-positive monocytes. ATG was observed to inhibit the phosphorylation of p65 and p38 in LPS-stimulated RAW264.7 cells. In conclusion, ATG can improve the symptoms of TG-induced acute peritonitis through immune regulation. ATG can reduce the inflammatory response in TG-induced acute peritonitis in mice.
Topics: Animals; Anti-Inflammatory Agents; Chemokines; Disease Models, Animal; Female; Furans; Gene Expression Regulation; Interleukin-6; L-Selectin; Lignans; Lipopolysaccharides; Macrophages; Mice; Neutrophils; Peritonitis; RAW 264.7 Cells; Thioglycolates; Tumor Necrosis Factor-alpha
PubMed: 32960513
DOI: 10.1002/prp2.660 -
Journal of Cellular and Molecular... May 2021Nintedanib, an Food and Drug Administration (FDA) approved multiple tyrosine kinase inhibitor, exhibits an anti-fibrotic effect in lung and kidneys. Its effect on...
Nintedanib, an Food and Drug Administration (FDA) approved multiple tyrosine kinase inhibitor, exhibits an anti-fibrotic effect in lung and kidneys. Its effect on peritoneal fibrosis remains unexplored. In this study, we found that nintedanib administration lessened chlorhexidine gluconate (CG)-induced peritoneal fibrosis and reduced collagen I and fibronectin expression. This coincided with suppressed phosphorylation of platelet-derived growth factor receptor, fibroblast growth factor receptors, vascular endothelial growth factor receptor and Src family kinase. Mechanistically, nintedanib inhibited injury-induced mesothelial-to-mesenchymal transition (MMT), as demonstrated by decreased expression of α-smooth muscle antigen and vimentin and preserved expression of E-cadherin in the CG-injured peritoneum and cultured human peritoneal mesothelial cells exposed to transforming growth factor-β1. Nintedanib also suppressed expression of Snail and Twist, two transcription factors associated with MMT in vivo and in vitro. Moreover, nintedanib treatment inhibited expression of several cytokines/chemokines, including tumour necrosis factor-α, interleukin-1β and interleukin-6, monocyte chemoattractant protein-1 and prevented infiltration of macrophages to the injured peritoneum. Finally, nintedanib reduced CG-induced peritoneal vascularization. These data suggest that nintedanib may attenuate peritoneal fibrosis by inhibiting MMT, inflammation, and angiogenesis and have therapeutic potential for the prevention and treatment of peritoneal fibrosis in patients on peritoneal dialysis.
PubMed: 33949772
DOI: 10.1111/jcmm.16518 -
Case Reports in Surgery 2021Primary omental torsion is an unusual condition, known for its rarity and for the particularity of being intraoperatively diagnosed, in nearly all cases. At the clinical...
Primary omental torsion is an unusual condition, known for its rarity and for the particularity of being intraoperatively diagnosed, in nearly all cases. At the clinical evaluation, this pathology commonly mimics other etiologies of acute abdomen. Hemoperitoneum and necrosis of the omentum are rarely associated with the omental torsion, but when the association is found, then it means that the vascular injuries are irreversible and the required surgical procedure may be far more complex than simple devolvulus. In search of the treatment of choice, laparoscopy proved its effectiveness as a diagnostic and therapeutic tool, while the open surgery approach can be described in many cases as being too invasive. A 37-year-old female patient presented with the generic symptoms of acute appendicitis. Surgical treatment was initiated. During laparoscopy, the abdomen was attentively explored, highlighting the presence of a twisted omentum with hemoperitoneum and necrosis. Omental excision and peritoneal drainage were performed. The evolution was favorable. Another check-up was done at 6 months postoperatively, displaying no signs or symptoms of relapse.
PubMed: 33708451
DOI: 10.1155/2021/5536178 -
World Journal of Clinical Cases Sep 2022Retroperitoneal sarcoma (RPS) is a rare malignancy arising from mesenchymal cells that most commonly presents as an abdominal mass and is associated with poor prognosis....
BACKGROUND
Retroperitoneal sarcoma (RPS) is a rare malignancy arising from mesenchymal cells that most commonly presents as an abdominal mass and is associated with poor prognosis. Although several studies have assessed the survival benefits of wide excision, few have reported detailed methods for achieving wide excision in patients with RPS.
AIM
To describe our experience with multidisciplinary surgical resection of RPS using intra- and extra-pelvic approaches.
METHODS
Multidisciplinary surgery is an anatomical approach that combines intra- and extra-peritoneal access within the same surgery to achieve complete RPS removal. This retrospective review of the records of patients who underwent multidisciplinary surgery for RPS analyzed surgical and survival outcomes.
RESULTS
Eight patients underwent 10 intra- and extra-pelvic surgical resections, and their median mass size was 12.75 cm (range, 6-45.5 cm). Using an intrapelvic approach, laparoscopy-assisted surgery was performed in four cases and laparotomy surgery in six. Using an extrapelvic approach, ilioinguinal and posterior approaches were used in four cases each, and the prone position and midline skin incision were shared in one. All patients' RPS masses were removed completely, and four achieved R0 resection through intra- and extra-pelvic surgery. The median estimated blood loss was 2000 mL (range, 300-20000 mL) and the median hospitalization was 12.6 d (range, 9-69 d). Reoperation was needed in two patients (one for wound necrosis and the other for bowel perforation and wound necrosis). The median overall survival rate and median progression-free survival were 64.6 and 13.7 mo, respectively.
CONCLUSION
RPS is therapeutically challenging because of its location and high risk of recurrence. Therefore, intra- and extra-pelvic surgical approaches can improve the macroscopic security of the surgical margin.
PubMed: 36186181
DOI: 10.12998/wjcc.v10.i27.9693 -
Frontiers in Physiology 2021Endometriosis is a chronic, estrogen-dependent gynecologic disorder that affects reproductive-aged women and to a lesser extent, post-menopausal women on hormone...
Endometriosis is a chronic, estrogen-dependent gynecologic disorder that affects reproductive-aged women and to a lesser extent, post-menopausal women on hormone therapy. The condition is associated with systemic and local immune dysfunctions. While its underlying mechanisms remain poorly understood, endometriosis has a genetic component and propensity for the disease is subject to environmental, nutritional, and lifestyle influences. Previously, we showed that high-fat diet (HFD) increased ectopic lesion numbers, concurrent with systemic and peritoneal changes in inflammatory and oxidative stress status, in immunocompetent recipient mice administered with endometrial fragments null for Krüppel-like factor 9 gene. Herein, we determined whether HFD modifies lesion parameters, when recipient peritoneal environment is challenged with ectopic wild-type (WT) endometrial fragments, the latter simulating retrograde menstruation common in women during the menstrual period. WT endometrium-recipient mice fed HFD (45% kcal from fat) showed reduced lesion incidence, numbers, and volumes, in the absence of changes in systemic ovarian steroid hormone and insulin levels, relative to those fed the control diet (CD, 17% kcal from fat). Lesions from HFD- and CD-fed recipients demonstrated comparable gene expression for steroid hormone receptors ( and ) and cytokines (, and ) and similar levels of DNA oxidative biomarkers. HFD moderately altered serum (3-nitrotyrosine and methionine/homocysteine) and peritoneal (reduced glutathione/oxidized glutathione) pro-oxidative status but had no effect on peritoneal inflammatory (tumor necrosis factor α and tumor necrosis factor receptor 1) mediators. Results indicate that lesion genotype modifies dietary effects on disease establishment and/or progression and if translated, could be important for provision of nutritional guidelines to women with predisposition to, or affected by endometriosis.
PubMed: 34712146
DOI: 10.3389/fphys.2021.702674 -
Microbiology Spectrum Feb 2023During the course of the infectious disease alveolar echinococcosis (AE), the larval stage of Echinococcus multilocularis develops in the liver, where an initial...
During the course of the infectious disease alveolar echinococcosis (AE), the larval stage of Echinococcus multilocularis develops in the liver, where an initial Th1/Th17 immune response may allow its elimination in resistant individuals. In patients susceptible to infection and disease, the Th2 response initiates later, inducing tolerance to the parasite. The role of interleukin 33 (IL-33), an alarmin released during necrosis and known to drive a Th2 immune response, has not yet been described during AE. Wild-type (WT) and IL-33 C57BL/6J mice were infected by peritoneal inoculation with E. multilocularis metacestodes and euthanized 4 months later, and their immune response were analyzed. Immunofluorescence staining and IL-33 enzyme-linked immunosorbent assay (ELISA) were also performed on liver samples from human patients with AE. Overall, metacestode lesions were smaller in IL-33 mice than in WT mice. IL-33 was detected in periparasitic tissues, but not in mouse or human serum. In infected mice, endogenous IL-33 modified peritoneal macrophage polarization and cytokine profiles. Th2 cytokine concentrations were positively correlated with parasite mass in WT mice, but not in IL-33 mice. In human AE patients, IL-33 concentrations were higher in parasitic tissues than in distant liver parenchyma. The main sources of IL-33 were CD31 endothelial cells of the neovasculature, present within lymphoid periparasitic infiltrates together with FOXP3 Ts. In the murine model, periparasitic IL-33 correlated with accelerated parasite growth putatively through the polarization of M2-like macrophages and release of immunosuppressive cytokines IL-10 and transforming growth factor β1 (TGF-β1). We concluded that IL-33 is a key alarmin in AE that contributes to the tolerogenic effect of systemic Th2 cytokines. Infection with the metacestode stage of Echinococcus multilocularis, known as alveolar echinococcosis, is the most severe cestodosis worldwide. However, less than 1% of exposed individuals, in which the immune system is unable to control the parasite, develop the disease. The factors responsible for this interindividual variability are not fully understood. In this study comparing wild-type and IL-33 infected mice, together with data from human clinical samples, we determined that IL-33, an alarmin released following tissue injury and involved in the pathogenesis of cancer and asthma, accelerates the progression of the disease by modulating the periparasitic microenvironment. This suggests that targeting IL-33 could be of interest for the management of patients with AE, and that IL-33 polymorphisms could be responsible for increased susceptibility to AE.
PubMed: 36786637
DOI: 10.1128/spectrum.04239-22 -
Scientific Reports Nov 2022This study aims to determine the effects of rosmarinic acid which involved the mechanisms to decrease the postoperative peritoneal adhesion formation in rats. Various...
This study aims to determine the effects of rosmarinic acid which involved the mechanisms to decrease the postoperative peritoneal adhesion formation in rats. Various incisions and removing a 1 × 1 cm piece of peritoneum was used to induce the peritoneal adhesions. Experimental groups were as follows: 1-Sham group. 2-Control group: Peritoneal adhesions were induced and no treatments were performed. 3-Treatment groups: Following inducing peritoneal adhesions, animals received rosmarinic acid with 50 and 70 mg/kg dosage, respectively. Macroscopic examination of adhesions indicated that adhesion bands were reduced in both treatment groups compared to the control group. Moreover, the adhesion score was decreased in both treatment groups on day 14. Inflammation and fibroblast proliferation were both reduced in the treatment groups on day 14. TGF-β1, TNF-α, and VEGF were all evaluated by western blot and immunohistochemistry on days 3 and 14. Treatment groups reduced inflammatory cytokines on days 3 and 14. The treatment group with a 70 mg/kg dosage decreased TGF-β1 and TNF-α levels more than the other treatment group. The administration of rosmarinic acid significantly reduced MDA and increased CAT levels. In conclusion, the rosmarinic acid was effective to reduce the adhesion bands, inflammatory cytokines, angiogenesis, and oxidative stress.
Topics: Rats; Animals; Transforming Growth Factor beta1; Tumor Necrosis Factor-alpha; Disease Models, Animal; Tissue Adhesions; Peritoneum; Cytokines; Postoperative Complications; Rosmarinic Acid
PubMed: 36329196
DOI: 10.1038/s41598-022-22000-x