scholarly journals Capsaicin Encapsulated Chitosan Nanoparticles Augments Anticarcinogenic and Antiproliferative Competency Against 7,12 Dimethylbenz(a)anthracene Induced Experimental Rat Mammary Carcinogenesis

2021 ◽  
pp. 126-144
Author(s):  
Kalaiyarasi Dhamodharan ◽  
Manobharathi Vengaimaran ◽  
Mirunalini Sankaran
Keyword(s):  
Chitosan Nanoparticles ◽  
Immunohistochemical Analysis ◽  
Mammary Carcinogenesis ◽  
Female Rats ◽  
Tissue Sections ◽  
Tumor Bearing ◽  
Normal Ranges ◽  
Hydrophobic Agent ◽  
Abnormal Cell Proliferation ◽  
Mammary Tissues

Background: Capsaicin is a powerful phytochemical spotted in chilies, starkly tied up with a bunch of health benefits but its clinical applications in cancer therapy are limited due to its poor solubility, and low bioavailability. Nanotechnology offers a strategy to discover new formulations for hydrophobic agent. Aim: The main intent of the current research was to investigate the effect of Capsaicin encapsulated chitosan nanoparticles (CAP@CS-NP) on 7,12-Dimethylbenz(a)anthracene (DMBA) induced mammary carcinogenesis in rats. Methodology: Mammary tumor was induced in female rats by injecting DMBA (25mg/kg b.wt) at the first week of the experiment. After 7 weeks, CAP@CS-NP (4mg/kg b.wt) was administered orally to DMBA induced tumor bearing rats for 21 days (thrice per week). The experiment was terminated at the end of the 14th week and their plasma and tissue sections were analyzed. Results: We found that significantly elevated levels of lipid peroxidation and diminished levels of antioxidant status in plasma, liver and mammary tissues. Increased levels of detoxification phase I enzymes and dropped levels of phase II enzymes in liver and mammary tissues in DMBA induced tumor bearing rats. As a result, oral administration of CAP@CS-NP suppressed the tumor growth, significantly raised body weight and restored abnormal enzymatic levels to near normal ranges. Additionally, histopathological and immunohistochemical analysis were also confirmed that CAP@CS-NP protects DMBA mediated cellular disruption and also inhibits abnormal cell proliferation. Conclusion: These findings suggest that nano encapsulation of CAP@CS-NP could be useful in targeted drug delivery and act as a promising chemotherapeutic agent to treat mammary carcinogenesis.

Codelivery of STAT3 and PD-L1 siRNA by hyaluronate-TAT trimethyl/thiolated chitosan nanoparticles suppresses cancer progression in tumor-bearing mice

Life Sciences ◽  
2021 ◽  
Vol 266 ◽  
pp. 118847
Author(s):  
Shima Bastaki ◽  
Surendar Aravindhan ◽  
Nasrin Ahmadpour Saheb ◽  
Mahsa Afsari Kashani ◽  
Aleksei Evgenievich Dorofeev ◽  
...  
Keyword(s):  
Cancer Progression ◽  
Chitosan Nanoparticles ◽  
Thiolated Chitosan ◽  
Tumor Bearing

scholarly journals Effects of CX3CL1 inhibition on murine bleomycin-induced interstitial pneumonia

2020 ◽  
Vol 18 ◽  
pp. 205873922095990
Author(s):  
Soichi Yamada ◽  
Shion Miyoshi ◽  
Junko Nishio ◽  
Satoshi Mizutani ◽  
Zento Yamada ◽  
...  
Keyword(s):  
Interstitial Pneumonia ◽  
T Cell Activation ◽  
Lung Tissue ◽  
Cell Activation ◽  
Immunohistochemical Analysis ◽  
Inflammatory Cells ◽  
Lavage Fluid ◽  
Novel Therapy ◽  
Tissue Sections

Background: Treatment for interstitial pneumonia (IP) associated with collagen diseases has not been established. There is a need to elucidate the pathogenesis of IP and develop a novel therapy. We aimed to clarify the role of chemokine (C-X3-C motif) ligand 1 (CX3CL1, also known as fractalkine) in IP. Methods: Bleomycin (BLM) was intratracheally administered to C57BL/6 mice to induce IP. For treatment with control Ab or anti-CX3CL1 mAb, the mice were administered either Ab three times per week for 2 weeks from the day of BLM administration until euthanasia. Expressions of CX3CL1 and its unique receptor CX3CR1 in the lung tissue were examined by immunohistochemical analysis. Cellular infiltration and lung fibrosis were evaluated based on hematoxylin-eosin-staining and Sirius red staining of the lung tissue sections, respectively. Bronchoalveolar lavage fluid (BALF) cells were analyzed by flow cytometry. Results: CX3CL1 and CX3CR1 were strongly expressed in the lung tissue from mice with BLM-induced IP (BLM-IP). Treatment with anti-CX3CL1 mAb did not significantly alter inflammatory cell infiltration or fibrosis in the lung tissue. However, the number of M1-like macrophages in BALF was decreased and surface CD3 expression on T cells was increased by anti-CX3CL1 mAb treatment. Conclusions: Inhibition of CX3CL1 decreased inflammatory cells and may attenuate T cell activation in BALF. CX3CL1 inhibitor may have the potential to suppress the infiltration and activation of immune cells in IP.

scholarly journals Cyclic Food Restriction Alters Substrate Utilization and Abolishes Protection from Mammary Carcinogenesis in Female Rats

1996 ◽  
Vol 126 (5) ◽  
pp. 1398-1405 ◽  
Author(s):  
Anthony R. Tagliaferro ◽  
Anne M. Ronan ◽  
Loren D. Meeker ◽  
Henry J. Thompson ◽  
Amy L. Scott ◽  
...  
Keyword(s):  
Food Restriction ◽  
Mammary Carcinogenesis ◽  
Substrate Utilization ◽  
Female Rats

scholarly journals Prolactin Suppression of Gonadotropin-Releasing Hormone Initiation of Mammary Gland Involution in Female Rats

Endocrinology ◽  
2016 ◽  
Vol 157 (7) ◽  
pp. 2750-2758 ◽  
Author(s):  
Duangjai Rieanrakwong ◽  
Titaree Laoharatchatathanin ◽  
Ryota Terashima ◽  
Tomohiro Yonezawa ◽  
Shiro Kurusu ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Mast Cells ◽  
Epithelial Cells ◽  
Female Rats ◽  
Local Administration ◽  
Boyden Chamber ◽  
Plasma Prolactin ◽  
Mammary Gland Involution ◽  
Prolactin Suppression ◽  
Mammary Tissues

It has been demonstrated that mammary gland involution after lactation is initiated by accumulation of milk in alveoli after weaning. Here, we report that involution is also dependent on mammary GnRH expression that is suppressed by PRL during lactation. Reduction of plasma prolactin (PRL) by the withdrawal of suckling stimuli increased GnRH and annexin A5 (ANXA5) expression in the mammary tissues after lactation with augmentation of epithelial apoptosis. Intramammary injection of a GnRH antagonist suppressed ANXA5 expression and apoptosis of epithelial cells after forcible weaning at midlactation, whereas local administration of GnRH agonist (GnRHa) caused apoptosis of epithelial cells with ANXA5 augmentation in lactating rats. The latter treatment also decreased mammary weight, milk production, and casein accumulation. Mammary mast cells were strongly immunopositive for GnRH and the number increased in the mammary tissues after weaning. GnRHa was shown to be a chemoattractant for mast cells by mammary local administration of GnRHa and Boyden chamber assay. PRL suppressed the mammary expression of both ANXA5 and GnRH mRNA. It also decreased mast cell numbers in the gland after lactation. These results are the first to demonstrate that GnRH, synthesized locally in the mammary tissues, is required for mammary involution after lactation. GnRH is also suggested to introduce mast cells into the regressing mammary gland and would be in favor of tissue remodeling. The suppression of these processes by PRL is a novel physiological function of PRL.

scholarly journals Galanin-Like Peptide (GALP) Is a Target for Regulation by Leptin in the Hypothalamus of the Rat

Endocrinology ◽  
2000 ◽  
Vol 141 (7) ◽  
pp. 2703-2706 ◽  
Author(s):  
Anders Juréus ◽  
Matthew J. Cunningham ◽  
Molly E. McClain ◽  
Donald K. Clifton ◽  
Robert A. Steiner
Keyword(s):  
In Situ Hybridization ◽  
Leptin Receptor ◽  
Fold Increase ◽  
Female Rats ◽  
Dorsomedial Nucleus ◽  
Physiological Regulation ◽  
Tissue Sections ◽  
Galanin Receptors ◽  
Neuroendocrine Functions

Galanin-like peptide (GALP), which was recently isolated from the porcine hypothalamus, shares sequence homology with galanin and binds with high affinity to galanin receptors. To study the distribution and regulation of GALP-expressing cells in the brain, we cloned a 120 base-pair cDNA fragment of rat GALP and produced an antisense riboprobe. In situ hybridization for GALP mRNA was then performed on tissue sections throughout the forebrain of adult ovariectomized female rats. We found GALP mRNA-containing cells in the arcuate nucleus (Arc), caudal dorsomedial nucleus, median eminence and the pituitary. Because GALP mRNA in the Arc appeared to overlap with the known distribution of leptin receptor mRNA, we tested the hypothesis that GALP expression is regulated by leptin. Using in situ hybridization, we compared the number of GALP mRNA-containing cells among groups of rats that were fed ad lib or fasted for 48 h and treated with either leptin or vehicle. Fasting reduced the number of identifiable cells containing GALP mRNA in the Arc, whereas the treatment of fasted animals with leptin produced a 4-fold increase in the number of cells expressing GALP message. The presence of GALP mRNA in the hypothalamus and pituitary and its regulation by leptin suggests that GALP may have important neuroendocrine functions, including the physiological regulation of feeding, metabolism, and reproduction.

Chemoprevention of mammary carcinogenesis in female rats by rofecoxib

2003 ◽  
Vol 202 (2) ◽  
pp. 131-136 ◽  
Author(s):  
Peter Kubatka ◽  
Ivan Ahlers ◽  
Eva Ahlersová ◽  
Eva Adámeková ◽  
Pauline Luk ◽  
...  
Keyword(s):  
Mammary Carcinogenesis ◽  
Female Rats

Estrogen influences satellite cell activation and proliferation following downhill running in rats

2008 ◽  
Vol 104 (2) ◽  
pp. 347-353 ◽  
Author(s):  
Deborah L. Enns ◽  
Peter M. Tiidus
Keyword(s):  
Satellite Cells ◽  
Cell Activation ◽  
Myogenic Differentiation ◽  
Immunohistochemical Analysis ◽  
Treadmill Running ◽  
Female Rats ◽  
Downhill Running ◽  
Glucuronidase Activity ◽  
Estrogen Exposure ◽  
Satellite Cell Activation

To investigate the influence of estrogen on postexercise muscle repair processes, we examined the effects of estrogen supplementation (0.25-mg pellet) on numbers of myofibers positive for markers of total, activated, and proliferating satellite cells in rat skeletal muscles 72 h following downhill running. Ovariectomized female rats ( n = 44) were divided into four groups ( n = 11 per group): sham (no estrogen) controls (SC); sham, exercised (SE); estrogen-supplemented controls (EC); and estrogen-supplemented, exercised (EE). After 8 days of estrogen exposure, animals were exposed to 90 min of treadmill running at 17 m/min (−13.5°). Seventy-two hours later, soleus and white vastus muscles were removed and immunostained for total [paired box homeotic gene 7 (Pax7)], [activated myogenic differentiation factor D (MyoD)], and proliferating [5-bromo-2′-deoxyuridine (BrdU)] satellite cells. β-Glucuronidase activity was increased ( P < 0.05) in both muscles following exercise; however, the postexercise elevations in enzyme activity were attenuated in the EE group compared with the SE group in the soleus ( P < 0.05). Immunohistochemical analysis revealed that exercised groups displayed increased numbers of myofibers containing total, activated, and proliferating satellite cells compared with control groups ( P < 0.05). Furthermore, greater numbers of fibers positive for markers of total, activated, and proliferating satellite cells were observed postexercise in EE animals compared with SE animals for both muscles ( P < 0.05). The results demonstrate that estrogen may potentially influence postdamage repair of skeletal muscle through activation of satellite cells.

Chemopreventive effect of diclofenac on mammary carcinogenesis in Sprague-Dawley rats

Biologia ◽  
2013 ◽  
Vol 68 (4) ◽  
Author(s):  
Peter Orendáš ◽  
Ivan Ahlers ◽  
Bianka Bojková ◽  
Monika Kassayová ◽  
Peter Kubatka ◽  
...  
Keyword(s):  
Tap Water ◽  
Mammary Carcinogenesis ◽  
Female Rats ◽  
Sprague Dawley ◽  
Short Term ◽  
Antiinflammatory Drugs ◽  
Sprague Dawley Rats ◽  
Term Administration ◽  
Chemopreventive Effect

AbstractChemopreventive effect of non-steroidal antiinflammatory drugs (NSAIDs) in mammary carcinogenesis was reported in several studies. In this study, the effect of a nonselective cyclooxygenase inhibitor diclofenac (DICLO) in the prevention of N-methyl-N-nitrosourea (NMU)-induced mammary carcinogenesis in Sprague-Dawley female rats was evaluated. NMU was administered to animals intraperitoneally in two doses of 50 mg kg−1 b.w. within postnatal days 42-48. In experiment A (short-term administration), DICLO was administrated intramuscularly (5 mg kg−1 b.w.) every other day, starting 3 days before and for subsequent 25 days after first NMU injection. In experiment B (long-term administration), DICLO was administered in tap water (0.01 mg ml−1) continually, starting 7 days before and for subsequent 22 weeks after first NMU dose. The study was terminated 22 weeks after the first dose of NMU in both experiments. After DICLO treatment, tumor frequency per group was reduced in both variants of drug administration: in experiment A by 38% and in experiment B by 39.5%. Moreover, DICLO decreased tumor incidence by 11.5% and delayed tumor latency by 14 days in experiment B. In our preventive-curative experiments DICLO decreased some parameters of NMU-induced rat mammary carcinogenesis, mainly the tumor frequency.

Lipotrope‐modified diets enhance nitrosomethylurea‐induced mammary carcinogenesis in female rats

1993 ◽  
Vol 20 (3) ◽  
pp. 215-221 ◽  
Author(s):  
Chang B. Choi ◽  
Myung G. Baik ◽  
Wanda L. Keller ◽  
Chung S. Park
Keyword(s):  
Mammary Carcinogenesis ◽  
Female Rats
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