Animals ; Female ; Male ; Rabbits ; Tumor Necrosis Factor-alpha ; analysis ; Vibration ; adverse effects

OBJECTIVE: To observe the effect of long-term moxa smoke exposure of different concentrations on olfactory function in rats, and provide experimental basis of safety study of moxa smoke produced by moxibustion. METHODS: Forty SD rats were randomly divided into a normal control group, a low-concentration moxa smoke group, a moderate-concentration moxa smoke group and a high-concentration moxa smoke group, 10 rats in each one. The rats in the moxa smoke groups were put into three plexiglass moxibustion boxes with different moxa smoke concentrations, 4 hours per times, twice a day for 90 days. The general state of rats was evaluated before and during the experiment. After the intervention, the olfactory function was evaluated by two-bottle experiment (TBE); the morphology of nasal mucosa was observed by HE staining; the apoptosis of olfactory epithelial cells in nasal mucosa was detected by TUNEL method; the serum levels of interleukin-1 (IL-1), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were detected by ELISA method. RESULTS: In the late stage of moxa smoke exposure (45-90 days into intervention), the behavioral activity of rats in the moderate-concentration moxa smoke group and the high-concentration moxa smoke group was weaker than that in the normal control group, and their response to stimulation was strong, and their mental state was worse. After intervention, the drinking rate of vinegar-water mixture in the moderate-concentration moxa smoke group and the high-concentration moxa smoke group was higher than that in the normal control group and the low-concentration moxa smoke group ( CONCLUSION The long-term exposure to low, moderate and high concentrations of moxa smoke could cause pathological changes in nasal mucosa and increase the serum levels of IL-1, IL-6 and TNF-α; the moderate and high concentrations of moxa smoke exposure could cause a series of damage to olfactory function and reduce olfactory sensitivity in rats.
Animals ; Interleukin-1 ; Interleukin-6 ; Rats ; Rats, Sprague-Dawley ; Smoke/adverse effects* ; Tumor Necrosis Factor-alpha

OBJECTIVETo study the possible induction effect of exposure to 50 Hz magnetic field (MF) on clustering of cell membrane surface receptors for epidermal growth factor (EGF) and tumor necrosis factor (TNF), the starting site of signals of biological effects, and its possible intervention effect.

METHODSLung fibroblasts of Chinese hamster (CHL) were exposed to EGF, TNF, 0.4 mT 50 Hz MF, 0.4 mT noise MF, and 0.4 mT 50 Hz MF combined with 0.4 mT noise MF. Respectively, for different durations, following the treatment, EGF and TNF receptors on the cell membrane were marked by corresponding antibodies with immunohistochemical method, then observed under a confocal microscope.

RESULTSClustering of cell membrane receptors could be induced 5 min after treatment with EGF and TNF, as well as with 50 Hz MF at 0.4 mT, which reached the peak in 15 min. While noise MF with the same intensity did not induce clustering of cell membrane receptors. Superposition of noise MF with the same intensity could inhibit clustering of cell membrane receptors induced by 50 Hz MF.

CONCLUSIONClustering of EGF and TNF receptors on the cell membrane could be induced by 50 Hz MF, suggesting that membrane receptors would be one of the sites where MF signals coupled, and noise MF with the same intensity could inhibit these effects.

Animals ; Cell Line ; Cricetinae ; Electromagnetic Fields ; adverse effects ; Epidermal Growth Factor ; pharmacology ; Fibroblasts ; drug effects ; metabolism ; radiation effects ; Noise ; adverse effects ; Receptor, Epidermal Growth Factor ; metabolism ; Receptors, Cell Surface ; metabolism ; Receptors, Tumor Necrosis Factor ; metabolism ; Tumor Necrosis Factor-alpha ; pharmacology

OBJECTIVETo explore the influence of exogenous putrescine and cadaverine on pro-inflammatory factors in the peripheral blood of rabbits.

METHODSForty ordinary adult New Zealand rabbits were divided into saline, necrotic tissue homogenate (NTH), putrescine, and cadaverine groups according to the random number table, with 10 rabbits in each group. Saline, NTH, 10 g/L putrescine, and 10 g/L cadaverine were respectively peritoneally injected into rabbits of corresponding group in the amount of 1 mL/kg. The blood sample in the volume of 2 mL was collected from the central artery of rabbit ears before injection and at 2, 6, 12, 24, 30, 36, 48, 60 hours post injection (PIH). Contents of TNF-α, IL-1, and IL-6 in the serum were determined with enzyme-linked immunosorbent assay. Data were processed with repeated measurement data analysis of variance and Spearman correlation analysis, and cubic model curve was applied in curve fitting for the contents of inflammatory factors.

RESULTS(1) The serum contents of TNF-&alpha;, IL-1, and IL-6 were increased in NTH, putrescine, and cadaverine groups in different degrees at most post injection time points. There was no significant change in the concentrations of the three pro-inflammatory factors in saline group, and they were significantly lower than those of the other three groups at most post injection time points (with F values from 3.49 to 13.58, P values all below 0.05). The serum contents of TNF-&alpha;, IL-1, and IL-6 in putrescine group began to increase at PIH 2, 6, and 6, which was similar to the trend of NTH group, but the changes were delayed compared with those of cadaverine group(all at PIH 2). The peak values of TNF-&alpha;, IL-1, and IL-6 in putrescine group were respectively (339 ± 36), (518 ± 44), and (265.9 ± 33.5) pg/mL, which were significantly lower than those of cadaverine group [ (476 ± 86), (539 ± 22), and (309.4 ± 27.1) pg/mL], with F values respectively 5.11, 1.90, and 5.56, P values all below 0.05. (2) The period of time in which contents of TNF-&alpha;, IL-1, and IL-6 began to increase (PIH 3-4) and the peaking time of the three pro-inflammatory cytokines (PIH 18-30) in putrescine group appeared later than those of cadaverine group (PIH 2 and 12-30). The duration of peaking time of the three pro-inflammatory cytokines in putrescine group was shorter than that of cadaverine group (PIH 18-30 vs. PIH 12-30). The increasing period and the duration of peaking time of TNF-&alpha;, IL-1, and IL-6 in putrescine group were close to those of NTH group (PIH 3-5 and 18-30). The correlation coefficient test analysis showed that the trends of changes in contents of three pro-inflammatory cytokines in putrescine group were significantly correlated with those of NTH group (r(TNF-&alpha;) = 0.933, P < 0.01; r(IL-1) = 0.967, P < 0.01; r(IL-6) = 0.950, P < 0.01). The obvious correlation between cadaverine group and NTH group was only found in the contents of IL-1 and IL-6 (r(IL-1) = 0.913, P < 0.01; r(IL-6) = 0.883, P < 0.05).

CONCLUSIONSBoth exogenous putrescine and cadaverine can cause inflammatory reaction in rabbits. The trend of the inflammatory reaction induced by putrescine was similar with that by NTH, suggesting that putrescine may play a leading role in the inflammatory reaction induced by necrotic tissue decomposition.

Animals ; Cadaverine ; adverse effects ; Inflammation ; blood ; Interleukin-1 ; blood ; Interleukin-6 ; blood ; Necrosis ; blood ; Putrescine ; adverse effects ; Rabbits ; Tumor Necrosis Factor-alpha ; blood

No abstract available.
Female ; Humans ; *Immunocompromised Host ; Immunosuppressive Agents/*adverse effects ; Male ; Tuberculosis/*immunology ; Tumor Necrosis Factor-alpha/*antagonists & inhibitors

Long-term poor dietary habits can cause changes in the intestinal flora, resulting in the production of a large number of lipopolysaccharide, increase intestinal mucosal permeability, and activate the entrance of a large number of inflammatory factors into the portal vein. In addition, a high carbohydrate diet can increase liver metabolic burden, increase mitochondrial oxidative phosphorylation, leading to oxidative stress, generate new fat during adenosine triphosphate synthesis, and thus resulting in ectopic fat accumulation, which further activate nuclear factor-κB signaling pathway and release inflam- matory factors such as tumor necrosis factor-α, interleukin-1β (IL-1β), IL-6, and so on. This leads to obesity and insulin resis- tance, ultimately triggering systemic low-grade inflammation. This article reviews the mechanism of poor dietary habits leading to systemic low-grade inflammation, the clinical and experimental research progress of keloids and systemic low-grade inflammation, the association between dietary habits and keloid constitution, and puts forward the hypothesis that poor dietary habits may lead to the occurrence and development of keloids.
Diet/adverse effects* ; Feeding Behavior ; Humans ; Inflammation/metabolism* ; Keloid/physiopathology* ; NF-kappa B/metabolism* ; Tumor Necrosis Factor-alpha/metabolism*

Etanercept is a tumor necrosis factor (TNF) inhibitor that has been used for the treatment of chronic inflammatory diseases including rheumatoid arthritis, ankylosing spondylitis and psoriatic arthritis. Because of its immunosuppressive activity, opportunistic infections have been noted in treated patients, most notably caused by Mycobacterium tuberculosis. Tuberculosis may present in an extrapulmonary or disseminated form. Since TNF-alpha inhibitors have been used in Korea, a few cases of TNF-alpha inhibitor associated tuberculosis have been described. However, tuberculous arthritis has not been previously reported. We describe a case of tuberculous arthritis in a 57-year-old woman with rheumatoid arthritis who was treated with etanercept.
Antirheumatic Agents/*adverse effects ; Arthritis, Rheumatoid/drug therapy ; Female ; Humans ; Immunoglobulin G/*adverse effects ; Middle Aged ; Receptors, Tumor Necrosis Factor ; Tuberculosis, Osteoarticular/*chemically induced ; Tumor Necrosis Factor-alpha/*antagonists & inhibitors

OBJECTIVETo observe the effect of the decomposition products of necrotic tissues from wounds on the serum levels of inflammation factors in comparison with endotoxin.

METHODSThirty adult New Zealand rabbits were randomly divided into 3 groups and received injections of saline, necrotic tissue homogenate or endotoxin. From each rabbit, blood samples (2 ml) were collected from the central artery of the ears at 0, 2, 6, 12, 24, 30, 36, 48, and 60 h after the injection for measurement of serum levels of tumor necrosis factor-alpha (TNF-&alpha;), interleukin-1 (IL-1) and IL-6.

RESULTSThe serum level of TNF-&alpha;, IL-1 and IL-6 in the rabbits increased 2-4 h after injection of the necrotic tissue homogenate and reached the peak level at 12 h, followed by a gradual reduction since 36 h. No obvious changes in the levels of the inflammatory factors were found in saline group (P<0.01). Compared with endotoxin, necrotic tissue homogenate resulted in an early increment (2-4 h vs 5-6 h) and significantly higher peak levels (at 30 h) of the inflammation factors (P<0.05). Curve fitting showed a distinct difference between necrotic tissue homogenate and endotoxin in their effect on the inflammatory factors.

CONCLUSIONThe necrotic tissue decomposition products contain toxic substances that possess a different toxicity profile from endotoxin, and their toxicity can be even stronger.

Animals ; Endotoxins ; adverse effects ; Inflammation ; Interleukin-1 ; blood ; Interleukin-6 ; blood ; Necrosis ; Rabbits ; Tumor Necrosis Factor-alpha ; blood ; Wounds and Injuries ; blood ; pathology

OBJECTIVETo investigate the effects of simulated nitrogen-oxygen saturation exposure at a water depth of 50 m on the expression of inflammatory mediators including interleukin-6 (IL-6), interleukin-10 (IL-10), and tumor necrosis factor-alpha (TNF-&alpha;) in the external auditory canal (EAC) of rabbits.

METHODSTwo batches of New Zealand rabbits were exposed to nitrogen-oxygen saturated at a water depth of 50 m. After exposure, the epithelial tissue in the EAC was analyzed using hematoxylin-eosin (HE) staining, and the changes in expression of inflammatory mediators including IL-6, IL-10, and TNF-&alpha; in the EAC of rabbits were determined by real-time polymerase chain reaction (PCR).

RESULTSAccording to the result of HE staining, more inflammatory cell infiltration, small vascular congestion, and mucosal edema in the EAC of rabbits were observed in the exposure group than in the control group. Additionally, compared with the control group, the exposure group had increased expression of IL-6 and TNF-&alpha; and reduced expression of IL-10 in the EAC of rabbits according to the result of real-time PCR.

CONCLUSIONThe nitrogen-oxygen saturation exposure at a water depth of 50 m can cause inflammatory injuries in the EAC of rabbits. The mechanism may be associated with increased expression of IL-6 and TNF-&alpha; and reduced expression of IL-10.

Animals ; Disease Models, Animal ; Ear Canal ; physiopathology ; Environmental Exposure ; adverse effects ; Inflammation Mediators ; metabolism ; Interleukin-10 ; metabolism ; Interleukin-6 ; metabolism ; Nitrogen ; adverse effects ; Oxygen ; adverse effects ; Rabbits ; Tumor Necrosis Factor-alpha ; metabolism ; Water ; adverse effects

OBJECTIVETo investigate the effect of formaldehyde exposure on the expression of inflammatory cytokines in human bronchial epithelial cells (16HBE cells).

METHODS16HBE cells were treated with formaldehyde with a concentration of 0, 0.04, 0.08, 0.16, 0.32, or 0.64 mmol/L for 24 hours, and MTT assay was applied to measure proliferative activity and calculate median lethal dose; 16HBE cells were exposed to formaldehyde with a concentration of 0, 0.04, 0.16, 0.64, or 1.20 mmol/L for 4 hours, MTT assay was applied to measure proliferative activity, and enzyme-linked immunosorbent assay was applied to measure the levels of Th1, Th2, and Th17 cytokines and tumor necrosis factor &alpha;(TNF-&alpha;) in cell supernatant.

RESULTSCompared with the control group, the 0.32-and 0.64-mmol/L exposure groups had significant decreases in cell viability (P<0.05); all exposure groups had reductions in interleukin(IL)-2 and IL-12, but no significant changes in interferon-γ and IL-10. In the 1.20-mmol/L exposure group, there was an increase in IL-4, with the increasing exposure dose, IL-5 and IL-6 tended to increase first and then decrease, and there was no significant change in IL-13; with the increasing exposure dose, IL-8 tended to increase first and then decrease, and there was no significant change in IL-17. In all the exposure groups, TNF-&alpha; increased and tended to increase significantly with the increasing exposure dose(P<0.05).

CONCLUSIONFormaldehyde exposure can cause imbalance between Th1 and Th2 cytokines secreted by 16HBE cells, as well as increased expression of IL-8 and TNF-&alpha;.

Cells, Cultured ; Cytokines ; metabolism ; Epithelial Cells ; drug effects ; metabolism ; Formaldehyde ; adverse effects ; Humans ; Interferon-gamma ; metabolism ; Interleukins ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism