Demethoxycurcumin (DMC), one of the components of curcuminoids, has antitumor activities in many human cancer cells and is known to induce apoptosis in human leukemia cells. However, there are no reports showing the effects of DMC on the immune response in leukemia mice in vivo. Herein, we evaluated the impact of DMC on immune responses in WEHI-3-generated leukemia mice in vivo.Fifty male BALB/c mice were separated randomly into five groups. Group I is normal mice, and groups II-V mice of generated leukemia by WEHI-3 cells. Group II-V mice were intraperitoneally injected with dimethyl sulfoxide (DMSO, as the positive control), 15, 30, and 60 mg/kg of DMC, respectively, every two days for 14 days. The body weight, blood, peritoneal fluid, liver, and spleen were individually analyzed.DMC did not significantly affect animal appearance and body weight. It decreased liver and spleen weight at a high dose. DMC did not affect the cluster of differentiation 3 (CD3) and CD19 cell populations but induced decrease of CD11b at 30 mg/kg treatment. However, DMC at low dose significantly increased the cluster of macrophage (Mac-3) cell populations, but at high dose it decreased them. DMC increased macrophage phagocytosis from peripheral blood mononuclear cells at 15 mg/kg treatment and peritoneal cavity at 15, 30 and 60 mg/kg of DMC treatments. DMC did not significantly affect the cytotoxic activity of natural killer (NK) cells. Furthermore, DMC decreased B and T cell proliferation at high doses.DMC elevated macrophage phagocytosis in leukemia mice in vivo.
Introduction:
The treatment of peritoneal dialysis in end-stage renal disease is increasing in clinical practice. The main purpose of this study was to evaluate the effect of far-infrared radiation therapy on inflammation and the cellular immunity of patients undergoing peritoneal dialysis.
Materials and Methods:
We recruited 56 patients undergoing peritoneal dialysis, and we included 32 patients from the experimental group and 24 patients from the control group in the final analysis. The experimental evaluation in our study was as follows:
(1) We used abdominal computed tomography to measure the diameter and degree of hardening of the abdominal veins and large blood vessels to explore the changes in abdominal blood vessels. (2) The study compared the effects of peritoneal dialysis using albumin, blood urea nitrogen, creatinine, white blood cell, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, erythrocyte sedimentation rate, Hs-CRP clearance rate, and HBAlC. (3) We compared the cytokine concentration of blood between the two groups while controlling for GM-CSF, IL-2, IFN-γ, IL-6, IL-18, IL-4, IL-5, IL-13, IL-12p70, TNF-α, and IL-1β.
Results and Discussion:
(1) There was no significant difference in the abdominal blood vessels of the experimental group relative to the control group according to abdominal CT measured over 6 months. (2) Our study demonstrates the statistically significant effect of FIR therapy on the following parameters: albumin (p = 0.048*), creatinine (p = 0.039*), and Hs-CRP (p < 0.001**) decreased significantly, and glomerular filtration rate (eGFR, p = 0.043*) and glucose (p < 0.001**) increased significantly. Our study found that, in the experimental group, albumin and creatinine decreased significantly due to FIR therapy for 6 months. However, our study also found that, in the experimental group, glucose (p < 0.001**) increased significantly due to FIR therapy for 6 months. Peritoneal dialysis combined with FIR can reduce the side effects of glucose in dialysis buffer, which interferes with peritoneal inflammation and peritoneal mesothelial cell fibrosis. In addition, we also found that, in the experimental group, Hs-CRP (p < 0.001**) decreased significantly due to FIR therapy for 6 months. (3) No statistical significance in the inflammatory cytokines related to FIR therapy differences was observed in our study. IFN-γ (p = 0.124), IL-12p70 (p = 0.093), IL-18 (p = 0.213), and TNF-α (p = 0.254) did not exhibit significant improvements in peritoneal dialysis with FIR treatment over 6 months. IFN-γ and IL-18 in the plasma of patients in the experimental group and the control group were higher in the third month than in the first month.
Conclusion:
We found that the effect of peritoneal dialysis improved significantly with FIR therapy, and significant improvements in the peritoneal permeability and inflammatory response were observed.
end-stage renal disease; peritoneal dialysis; far-infrared therapy (FIR)
Background/Aim: Laminarin, a typical component of fungal cell walls, has been shown to induce immune responses in both adult and larval locusts. We investigated the effects of laminarin on immune response and glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT) and lactate dehydrogenase (LDH) levels in normal mice. Materials and Methods: Thirty-six normal BALB/c mice were randomly divided into four groups and treatments were provided by gavage. Group I mice acted as normal control; mice of groups II-IV received laminarin at different doses (100 μl at 1, 2.5 and 5.0 mg/mouse in double-distilled water, respectively). All animals were treated for 14 days and were weighed, blood was collected for determination of cell markers, liver and spleen samples were weighed. Spleens were used for phagocytosis and determination of natural killer (NK) cell activity and cell proliferation by flow cytometric assay. Results: Laminarin reduced the body weights and weights of liver and spleen. Laminarin increased CD3, CD19 and Mac-3 cell populations at 2.5 and 5 mg/mouse, however, these did not affect CD11b marker levels. Laminarin (1 and 5 mg/mouse) reduced macrophage phagocytosis from peripheral blood mononuclear cells, but did not affect phagocytosis by macrophages from the peritoneal cavity. At an effector:target ratio of 50:1, laminarin reduced NK cell cytotoxic activity at all levels, but at a ratio of 25:1, only at 1 mg treatment. Laminarin did not affect T-cell and B-cell proliferation. Laminarin increased the level of GPT and reduced that of LDH at all doses, indicating laminarin can protect against liver injury. Laminarin is worthy of investigation in future experiments on improving immune responses.
Sulforaphane (SFN) is an isothiocyanate, inducing cytotoxic effects in various human cancer cells, including leukemia cells through cell cycle arrest and apoptosis. However, the effect of SFN on the immune responses in a leukemia mouse model remains to be investigated. The present study investigated whether SFN has an effect on the immune responses in a WEHI‑3‑induced leukemia mouse model in vivo. Normal BALB/c mice were injected with WEHI‑3 cells to generate the leukemia mouse model, and were subsequently treated with placebo or SFN (0, 285, 570 and 1,140 mg/kg) for 3 weeks. Following treatment, all mice were weighted and blood samples were collected. In addition, liver and spleen samples were isolated to determine cell markers, phagocytosis and natural killer (NK) cell activities, and cell proliferation was examined using flow cytometry. The results indicated that SFN treatment had no significant effect on the spleen weight, however it decreased liver and body weight. Furthermore, SFN treatment increased the percentage levels of CD3 (T cells) and CD19 (B cell maker), however had no effect on the levels of CD11b (monocytes) or Mac‑3 (macrophages), compared with the WEHI‑3 control groups. The administration of SFN increased the phagocytosis of macrophages from peripheral blood mononuclear cells and peritoneal cavity, and increased the activity of NK cells from splenocytes. Administration of SFN promoted T and B cell proliferation following stimulation with concanavalin A and lipopolysaccharide, respectively.
Abstract Treatment of GMM‐1 (a goldfish melanocytoma cell line) cells with epinephrine induced a rapid cell expansion (flattening of cells, extension and broadening of cellular processes) similar to the effect of dexamethasone reported previously (Shih et al., 1990). Studies on the possible involvement of secondary messengers in cell expansion indicated that (i) both 8‐bromo‐CAMP and forskolin caused cell shrinking (the opposite of cell expansion); (ii) TPA also caused cell shrinking; (iii) phospholipid derivatives, such as 1,2‐dioctanoyl‐sn‐glycerol, lysophosphatidic acid, and arachidonic acid caused cell expansion; and (iv) EGTA (calcium chelator) and nifedipine (calcium channel blocker) inhibited the effect of epinephrine. Together with the previous findings, these observations indicate that epinephrine and dexamethasone may share a common pathway in triggering an external calcium influx to cause cell expansion. The results of the effects of epinephrine agonists and antagonists, together with those of other workers, also show that there are multiple isoforms of adrenoceptor in the goldfish.
The total bilirubin value of a male infant was 385 μmol/l on day 5. Liver function test results were normal and there was no evidence of sepsis and no hemolysis reaction. Phototherapy was administered and on day 8 the patient's total bilirubin level was 255 μmol/l. Intermittent episodes of hyperbilirubinemia occurred without phototherapy, with the total bilirubin level reaching 335 μmol/l on day 19. A 3-day regimen of phenobarbital was administered and on day 24 his total bilirubin level was 180 μmol/l. The patient was discharged. At the age of 2 months, the total bilirubin value was 27 μmol/l. His direct bilirubin value was <15% of total bilirubin in every determination. A family study of the <i>UDP-glucuronosyltransferase</i><i>(UGT)</i><i>1A1 </i>gene showed that the infant carries a homozygous mutation at nucleotide -3279 plus compound heterozygous mutations at nucleotides 782 and 1091. The mutation at nucleotide 782 is a novel finding. Gilbert's syndrome was diagnosed.
The cover image is based on the Original Article Ouabain induces Apoptotic Cell Death in human prostate DU 145 cancer cells through DNA damage and TRAIL pathways by Jing-Gung Chung et al., https://doi.org/10.1002/tox.22834
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