Shimada A.,Azabu UniversityKanagawa |
Kohara Y.,Tottori University |
Naota M.,Tottori University |
Kobayashi Y.,Tottori University |
And 3 more authors.
Folia Histochemica et Cytobiologica | Year: 2015
Introduction. Exposure to Asian sand dust (ASD) is associated with enhanced pulmonary morbidity and mortality, and the reporting of such cases has rapidly increased in East Asia since 2000. The purpose of the study was to assess chronic lung toxicity induced by ASD. Material and methods. A total of 174 ICR mice were randomly divided into 5 control and 17 exposure groups. Suspensions of low dose (0.2, 0.4 mg) and high dose (3.0 mg) of ASD particles in saline were intratracheally instilled into ICR mice, followed by sacrifice at 24 hours, 1 week, and 1, 2, 3 and 4 months after instillation. Paraffin sections of lung tissues were stained with hematoxylin and eosin and by immunohistochemistry to detect a-smooth muscle actin, collagen III, matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinases-1 (TIMP-1), CD3, CD20, immunoglobulin G, interleukin-1β and inducible nitric oxide synthase. Results. A lung histological examination revealed similar patterns in the lesions of the groups treated with high (3.0 mg) or low dose (0.4 mg) of ASD. Acute inflammation was observed 24 h after treatment and subsided after 1 week; persistent granulomatous changes were observed at 2 months, focal lymphocytic infiltration at 3 months, and granuloma formation at 4 months. An increase in the size of granulomatous lesions was observed over time and was accompanied by collagen deposition in the lesions. The cytoplasm of macrophages in inflammatory lesions showed positive immunolabeling for MMP-9 at 24 h, 1 and 2 months after instillation of 3.0 mg of ASD. Positive immunolabeling for TIMP-1 was demonstrated in the cytoplasm of macrophages at 2 and 4 months after instillation of 3.0 mg of ASD. These findings suggest association between the expression of MMP-9 and TIMP-1 with the development of lung granulomatous lesions. Conclusions. These findings suggest that collagen deposition resulting from the altered regulation of extracellular matrix is associated with granuloma formation in the lungs of mice treated with ASD. © Polish Society for Histochemistry and Cytochemistry Folia Histochem Cytobiol. 2015. Source
Tamano H.,University of ShizuokaShizuoka |
Shakushi Y.,University of ShizuokaShizuoka |
Watanabe M.,Watanabe Oyster Laboratory Company Ltd |
Ohashi K.,University of ShizuokaShizuoka |
And 4 more authors.
Biological Bulletin | Year: 2015
The effects of 3,5-dihydroxy-4-methoxybenzyl alcohol (DHMBA), and zinc-both components of the Pacific oyster Crassostrea gigas-were examined by glutamatergic neuron activity in rats in an in vivo microdialysis experiment and an in vitro brain slice experiment. The basal concentration of extracellular glutamate in the hippocampus was decreased under hippocampal perfusion with DHMBA (1 mmol l−1) or ZnCl2 (μmol l−1), indicating that DHMBA and Zn2+suppress glutamatergic neuron activity under basal (static) conditions. To assess the preventive effect of DHMBA and Zn2+ on glutamate release from neuron terminals, brain slices were pretreated with DHMBA (1 mmol l−1) or ZnCl2 (100nmol l−1) for 1 h, then stimulated with high K+. A high, K+-induced increase in extracellular Zn2+ level, an index of glutamate release, was suppressed with pretreatment with DHMBA or zinc. A high, K+-induced increase in intracellular Ca2+ level was also suppressed with pretreatment with DHMBA or Zn2+. These results suggest that DHMBA and Zn2+, previously taken up in the hippocampal cells, suppress high, K+-induced glutamate release in the hippocampus, probably via presynaptic suppression of intracellular Ca2+ signaling. It is likely that Zn2+ and DHMBA play a preventive role in suppressing excess glutamatergic neuron activity in rats and mice. © 2015 Marine Biological Laboratory. Source