Effects of moxibustion on behaviors and tryptophan metabolism-related products in mice with irritable bowel syndrome / 针灸推拿医学（英文版）

Objective: To observe the effect of moxibustion on behaviors and related products of tryptophan (Trp) metabolism in the colon of mice with irritable bowel syndrome (IBS), and to explore the mechanism of moxibustion in the IBS treatment.Methods: Twenty-four mice were randomly divided into a normal group, a model group, a moxibustion group, and a probiotic group, with 6 mice in each group. The visceral pain model of IBS was established by enema with 2,4,6-trinitrobenzene sulfonic acid (TNBS) solution. Mice in the moxibustion group were treated with mild moxibustion at bilateral Zusanli (ST36), and those in the probiotic group were treated with probiotics such as Bifidobacterium by gavage. Abdominal withdrawal reflex (AWR) test, elevated plus-maze (EPM) test, and forced swimming test (FST) were performed after treatment. The expression levels of 5-hydroxytryptamine (5-HT) and tryptophan hydroxylase 1 (TPH1) in the colon were detected by immunofluorescence, and the expression levels of Trp, kynurenine (Kyn), and indole-2,3-oxygenase (IDO) in the colon were detected by enzyme-linked immunosorbent assay. Results: Compared with the normal group, the AWR scores were increased significantly in the model group under different pressure values (P<0.01), the open-arm staying time and open-arm entries in the EPM test were decreased significantly (P<0.01, P<0.05), the motionless time in the FST was increased significantly (P<0.01), and the expression levels of colonic Trp, TPH1, IDO, 5-HT, and Kyn were increased significantly (P<0.01) in the models. Compared with the model group, the AWR scores were differently decreased (P<0.05 or P<0.01), the open-arm entries in the EPM test were increased (P<0.05), the motionless times in the FST were decreased (P<0.05), and the colonic expression levels of Trp, TPH1, IDO, and 5-HT were decreased (P<0.01 or P<0.05) in the moxibustion and probiotic groups; the open-arm staying time was significantly increased in the moxibustion group (P<0.01), and the colonic expression level of Kyn was significantly decreased in the probiotic group (P<0.01). Conclusion: Moxibustion at Zusanli (ST36) improves visceral pain and pain mood and down-regulates the expression levels of colonic TPH1, IDO, Trp, 5-HT, and Kyn in IBS mice.

Changes in inflammatory factors and protein expression in sulfur mustard(1LD50)-induced pulmonary in- jury in rats / 实用医学杂志

Objective To establish an animal model of SM by equal toxicity dose(1LD50)-induced acute pulmonary injury in rats and compare the differences of inflammatory factor and protein expression. Methods Rats were randomly divided into five groups. ELISA and immunohistochemical methods were measured. Results Serum INF-γ and IL-23 levels in the intraperitoneal SM group were increased compared with the tracheal SM group;there were also significant differences in serum IL-4 levels between the two groups. In the alveolar septum , the positive expression ratios of NF-Kβ1,NF-Kβp65,ERK,JNK,and p38MAPK in the intraperitoneal SM group were increased compared with the tracheal SM group. Conclusion Using SM (1LD50),There are significantly higher serum inflammatory factor levels and protein-related expression in the alveolar septum of rats intraperitoneally injected with SM compared with those administered SM by intratracheal instillation. The results suggest that pulmonary inflammatory reactions associated with SM are dependent on the route of exposure.

Mechanism underlying acute lung injury due to sulfur mustard exposure in rats.

Sulfur mustard (SM), a bifunctional alkylating agent that causes severe lung damage, is a significant threat to both military and civilian populations. The mechanisms mediating the cytotoxic effects of SM are unknown and were investigated in this study. The purpose of this study was to establish a rat model of SM-induced lung injury to observe the resulting changes in the lungs. Male rats (Sprague Dawley) were anesthetized, intratracheally intubated, and exposed to 2 mg/kg of SM by intratracheal instillation. Animals were euthanized 6, 24, 48, and 72 h post-exposure, and bronchoalveolar lavage fluid (BALF) and lung tissues were collected. Exposure of rats to SM resulted in rapid pulmonary toxicity, including partial bronchiolar epithelium cell shedding, focal ulceration, and an increased amount of inflammatory exudate and number of cells in the alveoli. There was also evidence that the protein content and cell count of BALF peaked at 48 h, and the alveolar septum was widened and filled with lymphocytes. SM exposure also resulted in partial loss of type I alveolar epithelial cell membranes, fuzzy mitochondrial cristae, detachment and dissociation of ribosomes attached to the surface of rough endoplasmic reticulum, cracked, missing, and disorganized microvilli of type II alveolar epithelial cells, and increased apoptotic cells in the alveolar septum. The propylene glycol control group, however, was the same as the normal group. These data demonstrate that the mechanism of a high concentration of SM (2 mg/kg) induced acute lung injury include histologic changes, inflammatory reactions, apoptosis, oxidative stress, and nuclear DNA damage; the degree of injury is time dependent.

Mechanisms of lung injuries exposed to sulfur mustard:recent advances / 中国药理学与毒理学杂志

Sulphur mustard (SM) is a corrosive alkylating agent that is likely to be absorbed in vivo through the lungs,eyes and skin into internal organs. SM not only can produce its peculiar cytotoxic?ity thought to be mediated by the alkylation of DNA,protein and nucleic acids,but is a strong mutagen and carcinogen. However,whatever the way SM poisoning occurs,lungs are the most vulnerable, and early death is mainly carused by both the acute respiratory distress syndrome and pulmonary infec?tion. In this review,we analyzed SM-induced lung injury mechanisms.

Morphological assessment of sulfur mustard-induced acute lung injury in rats through different routes / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To establish an animal model of sulfur mustard (SM)-induced acute lung injury in rats through different routes and compare the morphological changes in lung tissue and cells.</p><p><b>METHODS</b>One hundred and thirty-six male rats were selected and randomly divided into 5 groups, namely peritoneal cavity SM group (n=32), trachea SM group (n=32), peritoneal cavity propylene glycol group (n=32), trachea propylene glycol group (n=32), and normal control group (n=8). The rats in peritoneal cavity SM group were injected intraperitoneally with diluted SM (0.1 ml, 8 mg/kg), and the rats in trachea SM group were injected intratracheally with diluted SM (0.1 ml, 2 mg/kg). Once the rats were sacrificed at 6, 24, 48, and 72 h after SM treatment, morphological changes in lung tissue and cells were observed by light and electron microscopy.</p><p><b>RESULTS</b>In the peritoneal cavity SM group, the epithelial cells of bronchioles maintained intact with increased exudate and bleeding in alveolar cavity and large areas of pulmonary consolidation under the light microscope. In the tracheal SM group, focal ulcer formed in the epithelial cells of bronchioles with increased exudate and bleeding in alveolar cavity, partial pulmonary consolidation, and compensatory emphysema in peripheral alveolar space under the light microscope. The alveolar interval areas were widened obviously in both groups in a time-dependent manner. Under the electron microscope, we observed local loss of cellular membrane in type I alveolar epithelium, broken or lost microvilli in cells of typeⅡalveolar epithelium and fuzzy mitochondrial crista as well as the appearance of ribosome detached from rough endoplasmic reticulum in both two groups. Compared with those in the trachea SM group and the control group, the ratio of the alveolar septum average area to the visual field area in the peritoneal cavity SM group at 6, 24, 48, and 72 h was significantly higher (P<0.05).</p><p><b>CONCLUSION</b>The lung tissue injury through the intraperitoneal route is more severe than that through the tracheal route, while focal ulceration of bronchioles epithelial cells appears in the case of tracheal route. The degree of injury increases over time in both groups, and the cellular damage is approximately the same in both groups.</p>

Study on mechanism of sulfur mustard induced acute tracheal injury in rat / 重庆医学

Objective To establish the sulfur mustard (SM ) induced tracheal injury model in rat and to investigate its mecha-nism .Methods Male rats (SD) were anesthetized and intra-tracheally intubated .The SM group was intra-tracheally injected by 2 mg/kg of diluted SM ,while the propylene glycol control group only by 0 .1mL of propylene glycol and the normal control group had no any treatment .The tissue and blood samples were taken for conducting the HE and immunohistochemical staining and measuring serum enzymes and andinflammatory factors .Results In the SM group ,a large number of lymphocytes infiltration in submucosa were observed;the positive expression of caspase-3 and caspase-9 were observed in epithelium and submucosa ;serum levels of TNF-α,IL-1β,IL-6 reached the peak in 24 h;serum levels of LDH ,GP ,BARS reached the peak in 6h ,so did GGT in 24 h .In the propyl-ene glycol control group and the normal control group ,lymphocytes ,macrophages and neutrophils were rare in submucosa .Conclu-sion The mechanism of SM (2 mg/kg) induced acute tracheal injury involves the inflammatory reaction ,apoptosis and oxidative stress ,moreover the lesion degree has the correlation with time .