scholarly journals The Effect of Pneumonic Pasteurellosis on Apoptosis and Nitric Oxide Synthase in the Lungs in Calves

2020 ◽  
Vol 8 (5) ◽  
pp. 1166-1170
Author(s):  
Orhan Yavuz ◽  
Güngör Çağdaş Dinçel
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Caspase 3 ◽  
Neuronal Nitric Oxide Synthase ◽  
Inflammatory Cells ◽  
Caspase 9 ◽  
Pneumonic Pasteurellosis ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Pneumonic Pasteurellosis (PP) is an infectious disease caused by Pasteurella multocida and Mannheimia haemolytica, mostly observed in cattle, sheep and calves. PP is characterized by fibrinous bronchopneumonia and pleuritis in the lungs. In this study, it was aimed to determine Caspase-3, Caspase-9, inducible nitric oxide synthase and neuronal nitric oxide synthase expressions by immunohistochemical methods in the lungs suffered from PP. For this purpose, twenty lung tissues were collected from calves with PP. For the Control Group, ten lungs of calves were collected from Aksaray Slaughterhouse. After necropsies of calves were confirmed to be PP by bacteriological examinations. Then the routine histological process was performed to tissues, and stained by Hematoxylin & Eosin for histopathology, and Caspase-3, Caspase-9, inducible nitric oxide synthase and neuronal nitric oxide synthase antibody staining for immunohistochemistry. The immunohistochemical findings indicated that Caspase-3, Caspase-9, inducible nitric oxide synthase and neuronal nitric oxide synthase positive reactions were seen in alveolar, bronchial and bronchiolar epithelia, and desquamated inflammatory cells in the lumens. In addition, the peripheral neural extensions were immunopositive for neuronal nitric oxide synthase and vascular endothelial cell were positive for inducible nitric oxide synthase. The findings can contribute to a better understanding of expressions of molecules such as Caspase and nitric oxide synthase. These results show that apoptosis and nitric oxide synthase expressions have triggered by airway epithelia and inflammatory cells in the lungs with Pneumonic Pasteurellosis in calves.

Geldanamycin inhibits hemorrhage-induced increases in caspase-3 activity: role of inducible nitric oxide synthase

2007 ◽  
Vol 103 (3) ◽  
pp. 1045-1055 ◽  
Author(s):  
Juliann G. Kiang ◽  
Phillip D. Bowman ◽  
Xinyue Lu ◽  
Yansong Li ◽  
Brian W. Wu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Caspase 3 ◽  
Gene Transfection ◽  
Organ Injury ◽  
Molecular Events ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Hemorrhage has been shown to increase inducible nitric oxide synthase (iNOS) and deplete ATP levels in tissues and geldanamycin limits both processes. Moreover, it is evident that inhibition of iNOS reduces caspase-3 and increases survival. Thus we sought to identify the molecular events responsible for the beneficial effect of geldanamycin. Hemorrhage in mice significantly increased caspase-3 activity and protein while treatment with geldanamycin significantly limited these increases. Similarly, geldanamycin inhibited increases in proteins forming the apoptosome (a complex of caspase-9, cytochrome c, and Apaf-1). Modulation of the expression of iNOS by iNOS gene transfection or siRNA treatment demonstrated that the level of iNOS correlates with caspase-3 activity. Our data indicate that geldanamycin limits caspase-3 expression and protects from organ injury by suppressing iNOS expression and apoptosome formation. Geldanamycin, therefore, may prove useful as an adjuvant in fluids used to treat patients suffering blood loss.

Increased Apoptosis in Infiltrating Mononuclear Cells of Colorectal Cancer

2002 ◽  
Vol 126 (6) ◽  
pp. 686-691
Author(s):  
George G. Chen ◽  
Janet F. Y. Lee ◽  
Ursula P. F. Chan ◽  
Hu Xu ◽  
Ping C. Ip ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Colorectal Cancer ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Caspase 3 ◽  
Mononuclear Cells ◽  
Colorectal Cancer Cells ◽  
Cancer Tissues ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Abstract Context.—Disturbance in apoptosis has been proposed as one of the mechanisms involved in the immune response targeting tumor outgrowth. How colorectal cancer cells escape from attack by the immune system is not yet fully understood. Objective.—To investigate apoptotic molecules associated with colorectal cancer counterattack. Design and Setting.—Tissue samples of colon from 12 patients with colorectal cancer were collected and analyzed by immunostaining. In addition to tumorous tissues, corresponding nontumorous specimens of colon were obtained as controls. Main Outcome Measures.—We examined the expression of Bcl-2, Bcl-xl, Bax, caspase-3, and inducible nitric oxide synthase in infiltrating mononuclear cells of colorectal cancer tissues and also in colorectal cancer tissues. The TUNEL assay was used to detect in situ apoptosis. Results.—Apoptosis was barely detectable in specimens of colorectal cancer, which was consistent with an increase in Bcl-2 level and a decrease in caspase-3 level. In contrast, infiltrating mononuclear cells of tumorous tissues showed a marked increase in apoptosis compared with those of nontumorous tissues. The increased apoptosis might have resulted from an imbalance of antiapoptotic and proapoptotic molecules, as reflected by reduction of Bcl-2 level and elevation of Bax level. The elevated caspase-3 levels found in this study could be a downstream effector of the Bcl-2 and Bax apoptotic pathways. A significant increase in inducible nitric oxide synthase observed in the infiltrating mononuclear cells might contribute to immunosuppression seen in colorectal cancer. Conclusion.—It is tempting to speculate that aberrant expression of apoptotic molecules and inducible nitric oxide synthase in infiltrating mononuclear cells provides the underlying mechanism through which colorectal cancer cells escape attack by the immune system and subsequently grow without control.

Androstenediol inhibits the trauma-hemorrhage-induced increase in caspase-3 by downregulating the inducible nitric oxide synthase pathway

2007 ◽  
Vol 102 (3) ◽  
pp. 933-941 ◽  
Author(s):  
Juliann G. Kiang ◽  
Russell M. Peckham ◽  
Leah E. Duke ◽  
Tomoharu Shimizu ◽  
Irshad H. Chaudry ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Transcription Factors ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Caspase 3 ◽  
Molecular Events ◽  
Tissue Trauma ◽  
Oxide Synthase ◽  
Interfering Rna ◽  
Inducible Nitric Oxide

Soft tissue trauma and hemorrhage (T-H) diminishes various aspects of liver function, while it increases hepatic nitrate/nitrite, inducible nitric oxide synthase (iNOS), and endothelin-1 levels. Treatment with androstenediol (AED) inhibits the T-H-induced alterations of the above parameters. We sought to identify the molecular events underlying the beneficial effect of AED. Exposure of rats to T-H significantly increased the caspase-3 activity and protein, whereas treatment with AED significantly limited these increases. AED treatment also suppressed the T-H-induced increase in iNOS by effectively altering the levels of key transcription factors involved in the regulation of iNOS expression. Immunoprecipitation and immunoblotting analyses indicate that T-H increased apoptosome formation, and AED treatment significantly decreased it. Modulating the iNOS protein by transfecting cells with iNOS gene or small interfering RNA further confirmed the correlation between iNOS and caspase-3. Our data indicate that AED limits caspase-3 expression by suppressing the expression of transcription factors involved in the production of iNOS, resulting in decreased apoptosome. AED can potentially be a useful adjuvant for limiting liver apoptosis following T-H shock.

scholarly journals A Comparison of the Effects of Neuronal Nitric Oxide Synthase and Inducible Nitric Oxide Synthase Inhibition on Cartilage Damage

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Nevzat Selim Gokay ◽  
Ibrahim Yilmaz ◽  
Baran Komur ◽  
Ahu Senem Demiroz ◽  
Alper Gokce ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Cartilage Damage ◽  
Neuronal Nitric Oxide Synthase ◽  
Cartilage Regeneration ◽  
Nitric Oxide Synthase Inhibitor ◽  
Synthase Inhibitor ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The objective of this study was to investigate the effects of selective inducible nitric oxide synthase and neuronal nitric oxide synthase inhibitors on cartilage regeneration. The study involved 27 Wistar rats that were divided into five groups. On Day 1, both knees of 3 rats were resected and placed in a formalin solution as a control group. The remaining 24 rats were separated into 4 groups, and their right knees were surgically damaged. Depending on the groups, the rats were injected with intra-articular normal saline solution, neuronal nitric oxide synthase inhibitor 7-nitroindazole (50 mg/kg), inducible nitric oxide synthase inhibitor amino-guanidine (30 mg/kg), or nitric oxide precursor L-arginine (200 mg/kg). After 21 days, the right and left knees of the rats were resected and placed in formalin solution. The samples were histopathologically examined by a blinded evaluator and scored on 8 parameters. Although selective neuronal nitric oxide synthase inhibition exhibited significant (P=0.044) positive effects on cartilage regeneration following cartilage damage, it was determined that inducible nitric oxide synthase inhibition had no statistically significant effect on cartilage regeneration. It was observed that the nitric oxide synthase activation triggered advanced arthrosis symptoms, such as osteophyte formation. The fact that selective neuronal nitric oxide synthase inhibitors were observed to have mitigating effects on the severity of the damage may, in the future, influence the development of new agents to be used in the treatment of cartilage disorders.

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