Antigens, CD1 ; physiology ; Cicatrix, Hypertrophic ; etiology ; immunology ; HLA-DR Antigens ; physiology ; Humans ; Keloid ; etiology ; immunology ; Triamcinolone Acetonide ; pharmacology

In this study, the effect of prophylactic anti-inflammation on the development of smoke-induced emphysema was investigated. Young male guinea-pigs aged 1.5-2 months (weighing 198.3+/-26.9 g) were randomly divided into 4 groups: group A (cigarette smoke exposure only), group B (cigarette smoke exposure plus pentoxifylline-rich (PTX, 10 mg/d) forage feeding), group C (cigarette smoke exposure plus intermittent cortical steroid injection (Triamcinolone acetonide, 3 mg, i.m., every three weeks) and control group (group D: animals with sham smoke exposure, raised under the same conditions). Animals in group A, B and C were exposed to smoke of cigarettes for 1 to 1.5 h twice a day, 5 days a week. All animals were killed at the 16th week and followed by morphometrical analysis of the midsagittal sectioned lung slices. Smoke exposure of 16 weeks resulted in visible emphysematous development in Group A but not in Group B and C. It was evidenced by the indicator of air-space size, mean linear intercept (Lm): 120.6+/-16.0 microm in Group A; 89.8+/-9.2 microm in Group B and 102.4+/-17.7 microm in Group C. The average Lm in either group B or group C was shorter than that in Group A (ANOVA and Newman-Keuls test, F=8.80, P=0.0002) but comparable to that (94.8+/-13.2 microm) in group D (P>0.05). It is concluded that long-term prophylactic anti-inflammation inhibits pulmonary emphysema induced by cigarette smoking in the guinea pigs.
Animals ; Anti-Inflammatory Agents ; pharmacology ; Guinea Pigs ; Male ; Pentoxifylline ; pharmacology ; Pulmonary Emphysema ; etiology ; pathology ; prevention & control ; Random Allocation ; Smoking ; adverse effects ; Triamcinolone Acetonide ; pharmacology

In this study, the effect of prophylactic anti-inflammation on the development of smoke-induced emphysema was investigated. Young male guinea-pigs aged 1.5-2 months (weighing 198.3+/-26.9 g) were randomly divided into 4 groups: group A (cigarette smoke exposure only), group B (cigarette smoke exposure plus pentoxifylline-rich (PTX, 10 mg/d) forage feeding), group C (cigarette smoke exposure plus intermittent cortical steroid injection (Triamcinolone acetonide, 3 mg, i.m., every three weeks) and control group (group D: animals with sham smoke exposure, raised under the same conditions). Animals in group A, B and C were exposed to smoke of cigarettes for 1 to 1.5 h twice a day, 5 days a week. All animals were killed at the 16th week and followed by morphometrical analysis of the midsagittal sectioned lung slices. Smoke exposure of 16 weeks resulted in visible emphysematous development in Group A but not in Group B and C. It was evidenced by the indicator of air-space size, mean linear intercept (Lm): 120.6+/-16.0 microm in Group A; 89.8+/-9.2 microm in Group B and 102.4+/-17.7 microm in Group C. The average Lm in either group B or group C was shorter than that in Group A (ANOVA and Newman-Keuls test, F=8.80, P=0.0002) but comparable to that (94.8+/-13.2 microm) in group D (P>0.05). It is concluded that long-term prophylactic anti-inflammation inhibits pulmonary emphysema induced by cigarette smoking in the guinea pigs.
Anti-Inflammatory Agents/*pharmacology ; Pentoxifylline/pharmacology ; Pulmonary Emphysema/etiology ; Pulmonary Emphysema/pathology ; Pulmonary Emphysema/*prevention & control ; Random Allocation ; Smoking/*adverse effects ; Triamcinolone Acetonide/*pharmacology

PURPOSE: We investigated whether oxygen-induced retinopathy (OIR) results in changes in the protein expression of neuronal and inducible nitric oxide synthases (nNOS and iNOS, respectively) in rat model of OIR. In addition, we evaluated whether treatment of rats with triamcinolone acetonide (TA) prevents this response. METHODS: To promote OIR, Sprague-Dawley rats were exposed to hyperoxia from postnatal day 2 (P2) to P14. They were then returned to normoxia after P15. TA was injected into the right vitreous of P15 rats, while saline was injected into the left vitreous. At P18 the expression of nNOS and iNOS was determined using Western blotting and immunostaining techniques in retinas obtained from control rats. RESULTS: In P18 OIR rats, the abundance of nNOS and iNOS protein was significantly increased compared with controls. These increases were not observed in the retinas of rats treated with TA. The change in expression of nNOS and iNOS were specific to parvalbumin and glial fibrillary acidic protein-positive cells. Treatment with TA prevented the increased expression of nNOS and iNOS in all samples. CONCLUSIONS: Hypoxia upregulates expression of nNOS and iNOS in OIR rat retinas, which is can be prevented by treatment with TA.
Animals ; Animals, Newborn ; Anoxia/metabolism/pathology/*prevention & control ; Blotting, Western ; Disease Models, Animal ; Female ; Glucocorticoids/pharmacology ; Immunohistochemistry ; Neurons/metabolism ; Nitric Oxide Synthase Type II/*biosynthesis ; Oxygen/toxicity ; Pregnancy ; *Pregnancy, Animal ; Rats ; Rats, Sprague-Dawley ; Retina/*metabolism/pathology ; Retinal Diseases/chemically induced/pathology/*prevention & control ; Triamcinolone Acetonide/*pharmacology

BACKGROUNDRetinal degenerative diseases are the leading causes of blindness in developed world. Retinal progenitor cells (RPCs) play a key role in retina restoration. Triamcinolone acetonide (TA) is widely used for the treatment of retinal degenerative diseases. In this study, we investigated the role of TA on RPCs in hypoxia condition.

METHODSRPCs were primary cultured and identified by immunofluorescence staining. Cells were cultured under normoxia, hypoxia 6 h, and hypoxia 6 h with TA treatment conditions. For the TA treatment groups, after being cultured under hypoxia condition for 6 h, RPCs were treated with different concentrations of TA for 48-72 h. Cell viability was measured by cell counting kit-8 (CCK-8) assay. Cell cycle was detected by flow cytometry. Western blotting was employed to examine the expression of cyclin D1, Akt, p-Akt, nuclear factor (NF)-κB p65, and caspase-3.

RESULTSCCK-8 assays indicated that the viability of RPCs treated with 0.01 mg/ml TA in hypoxia group was improved after 48 h, comparing with control group (P < 0.05). After 72 h, the cell viability was enhanced in both 0.01 mg/ml and 0.02 mg/ml TA groups compared with control group (all P < 0.05). Flow cytometry revealed that there were more cells in S-phase in hypoxia 6 h group than in normoxia control group (P < 0.05). RPCs in S and G2/M phases decreased in groups given TA, comparing with other groups (all P < 0.05). There was no significant difference in the total Akt protein expression among different groups, whereas upregulation of p-Akt and NF-κB p65 protein expression and downregulation of caspase-3 and cyclin D1 protein expression were observed in 0.01 mg/ml TA group, comparing with hypoxia 6 h group and control group (all P < 0.05).

CONCLUSIONLow-dose TA has anti-apoptosis effect on RPCs while it has no stimulatory effect on cell proliferation.

Animals ; Apoptosis ; drug effects ; physiology ; Caspase 3 ; metabolism ; Cell Cycle ; drug effects ; physiology ; Cell Hypoxia ; drug effects ; physiology ; Cell Proliferation ; drug effects ; physiology ; Cell Survival ; drug effects ; physiology ; Cells, Cultured ; Cyclin D1 ; metabolism ; NF-kappa B ; metabolism ; Proto-Oncogene Proteins c-akt ; metabolism ; Rats ; Rats, Sprague-Dawley ; Retina ; cytology ; Stem Cells ; cytology ; drug effects ; Triamcinolone Acetonide ; pharmacology