scholarly journals Effects of cigarette smoke on Haemophilus influenzae-induced otitis media in a rat model

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sung-Won Choi ◽  
Sunmi Choi ◽  
Eun-Jin Kang ◽  
Hyun Min Lee ◽  
Se-Joon Oh ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Haemophilus Influenzae ◽  
Cigarette Smoke ◽  
Otitis Media ◽  
Inflammatory Reaction ◽  
Rat Model ◽  
The Other ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Group Control

AbstractExposure to cigarette smoke (CS) is a factor that could delay or worsen the recovery of otitis media (OM) by causing inflammatory swelling of the Eustachian tube (ET). However, despite the suggested relationship, little is known about the association between OM and CS. Therefore, we aimed to evaluate the effects of CS on the development, progression, and recovery of OM, as well as the histological and molecular changes caused by CS exposure, by using a rat model of OM infected with non-typeable Haemophilus influenzae (NTHi). Eighty Sprague–Dawley rats with normal middle ears (MEs) were divided into four groups (n = 20 rats/group): control, CS, OM, and CS + OM. The CS and CS + OM groups were exposed to CS for 2 weeks. The inflammatory reaction to NTHi was more intense and lasted longer in the CS + OM group than in the other groups. Goblet cell proliferation and mucus secretion in the ET were more significant in the CS and CS + OM groups than in the other groups. These findings suggested that because CS directly affects the ET and ME mucosa, bacterial OM can become more severe and may resolve more slowly in the presence of CS exposure rather than in its absence.

Endothelin-A receptor antagonist BQ-610 blocks cigarette smoke-induced mitogenesis in rat airways and vessels

1997 ◽  
Vol 272 (4) ◽  
pp. L614-L618 ◽  
Author(s):  
F. Dadmanesh ◽  
J. L. Wright
Keyword(s):  
Cell Proliferation ◽  
Cigarette Smoke ◽  
Airway Epithelial ◽  
Sprague Dawley ◽  
Cell Nuclei ◽  
Sprague Dawley Rats ◽  
Endothelin A ◽  
Bq 610 ◽  
Air Control ◽  
Wall Components

To ascertain whether endothelin may play a role in cigarette smoke-induced cell proliferation in the airways and arterial vasculature of the lung, we exposed groups of seven Sprague-Dawley rats to either room air (control) plus saline infusion, an intravenous infusion of the selective endothelin A antagonist BQ-610 (control BQ-610), the smoke of 10 cigarettes (smoke only), or the smoke of 10 cigarettes after intravenous BQ-610 infusion (smoke + BQ-610). Cell proliferation was quantified by determining the percentage of cell nuclei labeled by 5-bromo-2'-deoxyuridine. We separately evaluated the cells in the epithelium and wall components of the bronchioles, and endothelium and wall components of the peribronchiolar and perialveolar ductular arteries. We found that cigarette smoke produced significant cell proliferation in the airway epithelium and wall, in the peribronchiolar arterial endothelial compartment, and in both the endothelial and wall compartments of the perialveolar ductular arteries. Pretreatment with BQ-610 reduced the peribronchiolar arterial endothelial and the perialveolar ductular arterial wall proliferation to control lev- els and reduced but did not totally abrogate the smoke-in- duced proliferation of the airway epithelial, airway wall, and perialveolar ductular arterial endothelial compartments. We conclude that cigarette smoke-induced cell proliferation of the airways and pulmonary arterial vessels is at least partially mediated through stimulation of the endothelin-A receptors.

scholarly journals THERAPEUTIC PROFILING OF NANO ENCAPSULATED DIOSGENIN VIA ATTENUATING HORMONAL STATUS, CELL PROLIFERATION, INFLAMMATORY RESPONSES, AND APOPTOSIS IN AN ANIMAL MODEL OF MAMMARY ONCOGENESIS

2021 ◽  
pp. 126-132
Author(s):  
MANOBHARATHI VENGAIMARAN ◽  
KALAIYARASI DHAMODHARAN ◽  
MIRUNALINI SANKARAN
Keyword(s):  
Cell Proliferation ◽  
Molecular Docking ◽  
Cyclin D1 ◽  
Inflammatory Responses ◽  
Chitosan Nanoparticles ◽  
Hormonal Status ◽  
Sprague Dawley ◽  
Therapeutic Impact ◽  
Sprague Dawley Rats ◽  
Tnf Α

Objective: The central motive of this study is to explore the therapeutic impact of Diosgenin encapsulated Chitosan nanoparticles (DG@CS-NP) on mammary carcinogenesis in female Sprague Dawley rats via modulating hormonal status, cell proliferation, inflammatory responses, and Apoptosis. Methods: 7,12-dimethylbenz(a)anthracene (DMBA) was administered subcutaneously near the mammary gland (25 mg/kg b. wt) to provoke mammary tumor in female Sprague Dawley rats. Following the progress of a tumor, DMBA-induced tumor-bearing rats were medicated orally with 5 mg/kg b. wt of DG@CS-NP. Consequently, the expression of ER, PR, PCNA, Cyclin D1, NF-κB, TNF-α, Bcl-2, Caspases-3, and p53 in experimental rats were revealed via architectural immunohistochemistry. Further, Diosgenin interactions with these proteins were evidently confirmed by molecular docking analysis. Results: As a result, we noticed diminished levels of ER, PR, PCNA, Cyclin D1, NF-κB, TNF-α, and Bcl-2 expressions in DG@CS-NP medicated rats as well as with elevated levels of Caspases-3 and p53 expressions. In DMBA rats, the expressions were vice versa. Additionally, molecular docking analyses support these outcomes by highlighting the strong interaction between Diosgenin and breast cancer targets. Conclusion: These reports prove that DG@CS-NP imposes its therapeutic impact by hormonal adjustments, downregulating proteins involved in inflammation and cellular proliferation, and thereby promotes apoptosis by impeding apoptotic inhibitors.

scholarly journals Effect of GuiXiong Xiaoyi Wan in Treatment of Endometriosis on Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Zhixing Jin ◽  
Li Wang ◽  
Zhiling Zhu
Keyword(s):  
Cell Proliferation ◽  
Rat Model ◽  
Flow Cytometric Analysis ◽  
Lesion Size ◽  
Negative Control ◽  
Terminal Deoxynucleotidyl Transferase ◽  
High Dose ◽  
Sprague Dawley ◽  
Induced Apoptosis ◽  
Cd4 Lymphocytes

Objective. To evaluate the effect of GuiXiong Xiaoyi Wan (GXXYW) on the development of endometriosis in a rat model.Methods. Sprague-Dawley rats with surgically induced endometriosis were randomly treated with low-dose GXXYW, high-dose GXXYW, or vehicle (negative control) for 28 days. Immunohistochemistry was used to assess cell proliferation in the lesions. The terminal deoxynucleotidyl transferase- (TdT-) mediated dUTP biotin nick end labelling (TUNEL) method was performed to analyse the apoptosis induced by GuiXiong Xiaoyi Wan. The percentages of CD3+ lymphocytes, CD4+ lymphocytes, and CD8+ lymphocytes in the spleens of the rats were evaluated using flow cytometric analysis.Results. Treatment with GXXYW significantly decreased the lesion size, inhibited cell proliferation, and induced apoptosis in endometriotic tissue. The spleens of GXXYW-treated rats also demonstrated a significant increase in the percentage of CD4+ lymphocytes and a significant decrease in the percentage of CD8+ lymphocytes.Conclusions. These results suggest that, in a rat model, GXXYW may be effective in the suppression of the growth of endometriosis, possibly through the inhibition of cell proliferation, the induction of apoptosis of endometriotic cells, and the regulation of the immune system.

Regional effect of naltrexone in the nucleus of the solitary tract in blockade of NPY-induced feeding

2000 ◽  
Vol 278 (2) ◽  
pp. R499-R503 ◽  
Author(s):  
C. M. Kotz ◽  
M. J. Glass ◽  
A. S. Levine ◽  
C. J. Billington
Keyword(s):  
Cerebrospinal Fluid ◽  
Food Intake ◽  
Paraventricular Nucleus ◽  
Opioid Receptors ◽  
The Other ◽  
Solitary Tract ◽  
Sprague Dawley ◽  
Regional Effect ◽  
Sprague Dawley Rats ◽  
Artificial Cerebrospinal Fluid

Naltrexone (NLTX) in the nucleus of the solitary tract (NTS) decreases feeding induced by neuropeptide Y (NPY) in the paraventricular nucleus (PVN). We sought to determine the NTS region most sensitive to NLTX blockade of PVN NPY-induced feeding. Male Sprague-Dawley rats were fitted with two cannulas; one in the PVN and one in a hindbrain region: caudal, medial, or rostral NTS or 1 mm outside the NTS. Animals received NLTX (0, 1, 3, 10, and 30 μg in 0.3 μl) into the hindbrain region just prior to PVN NPY (0.5 μg, 0.3 μl) or artificial cerebrospinal fluid (0.3 μl). Food intake was measured at 2 h following injection. PVN NPY stimulated feeding, and NLTX in the medial NTS significantly decreased NPY-induced feeding at 2 h, whereas administration of NLTX in the other hindbrain regions did not significantly influence PVN NPY induced feeding. These data suggest that opioid receptors in the medial NTS are most responsive to feeding signals originating in the PVN after NPY stimulation.

Buprenorphine alleviation of pain does not compromise the rat monoarthritic pain model

2017 ◽  
Vol 16 (1) ◽  
pp. 167-167
Author(s):  
M.S. Berke ◽  
Klas S.P. Abelson
Keyword(s):  
Rat Model ◽  
Joint Stiffness ◽  
Positive Control ◽  
Negative Control ◽  
Pain Tolerance ◽  
Control Group ◽  
Mechanical Stimuli ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
A Minor

Abstract Aims This study investigated the effects of buprenorphine treatment on pain and welfare parameters and model specific parameters in a rat model of monoarthritis to eliminate unnecessary pain from this model. Methods 32 male Sprague Dawley rats were divided into four groups: (1) A negative control without arthritis receiving no analgesia. (2) A positive monoarthritic control group receiving no analgesia, but subcutaneous saline injections twice a day. (3) A positive control with monoarthritis receiving subcutaneous carprofen once a day and saline once a day. (4) A group with monoarthritis receiving subcutaneous buprenorphine twice a day. Monoarthritis was induced with an injection of 0.02 ml Complete Freund’s Adjuvant intra-articularly in the left tibiotarsal joint. Treatment with analgesia was initiated at day 15 and the rats were euthanized at day 23. Results The induced monoarthritis elicited a pronounced acute inflammation. Several parameters such as bodyweight, mobility, stance, joint-stiffness and lameness scores were affected. A marked mechanical hyperalgesia in the tarsal area was observed by Electronic Von Frey testing, but no severe compromise of the animal welfare was seen at any time. Signs of chronic development began to appear from day 10 after the monoarthritic induction. No significant change in serum cytokines and faecal corticosterone measurements was found after administration of buprenorphine. A minor decrease in body weight was seen, and a higher pain tolerance to mechanical stimuli was observed, indicating pain alleviation. The histological examination confirmed monoarthritic development in all monoarthritic rats and revealed periarticular lesions suggesting diffusion of adjuvant from intra-articular injection site to the periphery. Conclusions The study demonstrated that buprenorphine has an analgesic effect in the adjuvant induced monoarthritic rat model, without obvious interference with the development of arthritis.

Measurement of Cell Proliferation in the Kidneys of Fischer 344 and Sprague-Dawley Rats after Gavage Administration of Hydroquinone

1994 ◽  
Vol 23 (3) ◽  
pp. 397-406 ◽  
Author(s):  
J. C. ENGLISH ◽  
LOUISE G. PERRY ◽  
MILAN VLAOVIC ◽  
CAROLYN MOYER ◽  
JOHN L. O'DONOGHUE
Keyword(s):  
Cell Proliferation ◽  
Sprague Dawley ◽  
Fischer 344 ◽  
Sprague Dawley Rats

EXCRETION OF CATECHOL AMINES BY WHITE RATS IN THE COLD

1964 ◽  
Vol 42 (4) ◽  
pp. 567-577 ◽  
Author(s):  
Lorraine C. Smith ◽  
L.-P. Dugal
Keyword(s):  
The Other ◽  
Sprague Dawley ◽  
White Rats ◽  
Sprague Dawley Rats ◽  
Old Rats ◽  
Catechol Amines ◽  
Sustained Increase

Exposure of white rats to 2 °C for 20 weeks caused an immediate and sustained increase in the excretion of catechol amines as compared to controls kept at 23 °C. Adrenaline excretion increased approximately three to four times while noradrenaline excretion increased about eight times. There were no marked differences between Wistar and Sprague–Dawley rats in the amounts of adrenaline and noradrenaline excreted at 23 °C or 2 °C. 'Old' rats kept in activity cages excreted much more of the catechol amines both at 23 °C and 2 °C than did the other rats and they showed a peak for adrenaline excretion after 1 week and for noradrenaline excretion after 3 to 4 weeks in the cold.

scholarly journals Effect of Cigarette Smoke on Bronchial Reactivity

1995 ◽  
Vol 2 (4) ◽  
pp. 231-235
Author(s):  
JL Wright ◽  
J-P Sun ◽  
S Vedal ◽  
A Churg
Keyword(s):  
Pulmonary Function ◽  
Cigarette Smoke ◽  
Pulmonary Function Tests ◽  
Lung Compliance ◽  
Forced Expiratory Volume ◽  
Smoke Exposure ◽  
Cigarette Smoke Exposure ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Different Strains

OBJECTIVE: To compare the effects of a brief low level exposure to cigarette smoke in rats with known low (Sprague-Dawley) and high (Fisher) airway responsiveness, to test the hypothesis that airways reactivity influences the severity or duration of pulmonary function alterations after cigarette smoke exposure.METHODS: Baseline pulmonary function tests and methacholine dose response tests were conducted in 10 Sprague-Dawley and 10 Fisher rats. On the following day, the animals were reanaesthetized, and breathed for 1 min from a 2 L chamber into which 25 mL of fresh cigarette smoke had been injected, followed by a second set of pulmonary function and methacholine response tests; a final set was performed two weeks later.RESULTS: Sprague-Dawley rats were larger, with larger lung volumes, compliance and flow rates, but Fisher rats showed a fourfold higher airway reactivity. Although neither resistance nor response to methacholine changed in either strain of animal, Sprague-Dawley rats showed an increase in residual volume post smoke, which was not sustained over two weeks, and sustained small increases in vital capacity, total lung capacity and static lung compliance, with a sustained decrease in forced expiratory volume in 0.1 s, while Fisher rats showed only a small sustained increase in functional residual capacity.CONCLUSIONS: Although there are marked differences in pulmonary function between the two different strains of rats, increased airways responsiveness per se does not make the animal more sensitive to the acute effects of cigarette smoke, and the effects of cigarette smoke on pulmonary function are not necessarily related to increased airway resistance. Pulmonary function alterations seen after brief cigarette smoke exposure may be sustained for a relatively long period of time.

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