scholarly journals Efficacy of Vitex agnus in lowering prolactin level in mammary tumor induced SD rats

Biomedicine ◽  
2020 ◽  
Vol 39 (2) ◽  
pp. 380-386
Author(s):  
Maninder Kour ◽  
Kumar Megur Ramakrishna Bhat ◽  
Vinodini Nithyanandamadom Anatharaya ◽  
Shrijeet Chakraborty ◽  
Reshma Kumara Chandra

Introduction and Aim: Breast cancer accounts for about 30% of all cancers in women. The present study aims to see the role of prolactin and Vitex agnus fruit extract in breast cancer progression in mammary tumor induced Sprague Dawley (SD) rats. Materials and Methods: Thirty-day old inbred SD female rats of body weight 70-80 grams were taken for this study. The rats were induced with N- Methyl-Nitroso-Urea for mammary tumor development. After the development of palpable and visible tumor the rats were treated with anti-prolactin drug (Cabergoline) and a prolactin lowering herb Vitex agnus Castus (VAC) for two months. After the treatment the rats were sacrificed for antioxidants estimation and histopathological section examination. Results: The rats treated with anti-prolactin drug showed benign tumors with hyperplasia and lactational change proving the presence of prolactin in the tumor tissue, whereas the plant extract showed mammary tumor regression by the presence of foamy macrophages in the histopathological sections. Results also showed treatment with cabergoline increased the GSH level and decreased the MDA level compared to tumor induced group. Conclusion: Prolactin may have a potential role in progression of breast cancer and Vitex agnus extract showed a prolactin lowering effect and facilitated in regression of the tumor.  

2020 ◽  
Vol 151 ◽  
pp. 01058
Author(s):  
Siti Aisyah ◽  
Ekowati Handharyani ◽  
Nurliani Bermawie ◽  
Agus Setiyono

The purpose of the research was to study the potency of Murraya koenigii leaves extract to overcome the mammary tumor in Sprague Dawley rat. Thirty-five female rats were divided into seven groups: control (P1), tumor without therapy (P2), methotrexate group (P3), curative groups (P4 and P5) were given extract after the tumor was formed, and preventive groups (P6 and P7) were given extract before the tumor was formed with dose of 300 and 400 mg/kg, respectively. The induction of mammary tumor in rats were carried out using 7,12 dimethylbenz(α) anthracene (DMBA) subcutaneously. Bodyweight and tumor size were measured every week for 4 weeks. At the end of treatment, rats were euthanized and mammary glands were collected for histopathological examination. The result showed tumor size in P2 was significantly higher (p<0.05) than in other groups. On the other hand, tumor size in P4 and P6 were significantly smaller (p<0.05) compared to P5 and P7. Histopathological changes showed PMN cells, 1-3 layers of cuboid epithelial and solid collagen fibers proliferation in P2, while in P3 to P7 showed moderate collagen fibers proliferation. In conclusion, the administration of the extract at a dose of 300 mg/kg can decelerate tumor development in Sprague Dawley rat mammary gland.


2020 ◽  
Vol 28 (4) ◽  
Author(s):  
Urmila Banik ◽  
Sarfarz Ahamed ◽  
Swe Swe Latt ◽  
Nur Asyilla Che Jalil ◽  
Wan Faiziah Wan Abdul Rahman ◽  
...  

Natural products are becoming primary investigative molecules creating hope for finding new powerful classes of anticancer agents for breast cancer. One of the most remarkable of these is honey. To explore the mechanism of action of any anticancer agent the initial step is to analyse its effect in the histopathological tissue section. This study was designed to describe the histopathology of N-methyl- N-nitrosourea (MNU) induced breast cancer in Sprague Dawley rat (SD rats) treated with crude honey. Female rats were distributed into 4 groups: Group0 (normal), Group1 (MNU control), Group2 and 3: Tualang and Manuka honey-treated, respectively. Rats were sacrificed and histopathology of both non-treated and treated tumours was done. Lower histological grade, infrequent combination histologic pattern (p&lt;0.001), prominent cytoplasmic vacuolization (p&lt;0.001), aggregates of atypical macrophages (p&lt;0.001) and lesser necrosis (p= 0.005) were major outcomes in treated cancers. This data will aid in the histopathological interpretation of honey-treated breast cancer model and future anticancer study of honey.


2017 ◽  
Vol 35 (15_suppl) ◽  
pp. e14090-e14090
Author(s):  
Debra A. Tonetti ◽  
Rui Xiong ◽  
Jiong Zhao ◽  
Lauren Gutgesell ◽  
Arkadiusz Z. Dudek ◽  
...  

e14090 Background: The high prevalence of treatment resistance for estrogen receptor positive (ER+) breast cancer cause more deaths than all other breast cancers, despite the availability of endocrine therapeutics including selective ER downregulators (SERDs). Before tamoxifen, high dose estradiol (E2) delivered clinical efficacy slightly superior to tamoxifen. While recent clinical trials have shown efficacy of low dose E2, unacceptable side effects including vaginal bleeding, endometrial hypertrophy, and the negative perceptions of both patients and physicians limit acceptance. In preclinical models, tamoxifen resistant (TR) breast cancer is sensitive to treatment by E2. TTC-352 is an orally bioavailable selective human ERα partial agonist (ShERPA) designed to mimic E2 in causing tumor regression of TR breast cancer xenografts without uterine proliferation caused by E2 and tamoxifen. Methods: The published preclinical efficacy studies were extended to multiple TR ER+ cell lines in 3D spheroid cell cultures comparing to E2 and the SERD GDC0810. The maximum tolerated dose (MTD) was determined in Sprague-Dawley rats at: 200, 300, 600, 1000 and 2000 mg/kg by oral gavage (N = 3). Animals were observed for 7 days prior to necropsy. A single MTD range finding study was performed in dogs at: 50, 100, and 200 mg/kg TTC-352, administered orally in gelatin capsules. Based on these results, a 7-day repeated dose studies were completed at 30, 100, 300 and 1000 mg/kg/day in rats (3/sex/dose) and 15, 75, and 150 mg/kg (2/sex/dose) in dogs. Results: Growth of three TR ER+ breast cancer cell cultures in 3D was inhibited by TTC-352, which mimicked E2 and was equivalent to GDC0810. In female rats MTD was 1000 mg/kg and TTC-352 was well tolerated following a single oral dose of 200, 300, 600 mg/kg. The oral administration of TTC-352 at doses of 30, 100, and 300 mg/kg/day in rats (both sexes) and 15, 75 or 150 mg/kg/day in dogs (both sexes) for seven days was generally well tolerated. Conclusions: TTC-352 has demonstrated efficacy in preclinical models of TR breast cancer. Completed rat and dog studies indicated favorable tolerability and rapid absorption up to 300 mg/kg/day in rats and 150 mg/kg/day in dogs.


2021 ◽  
Author(s):  
Zhengzheng Xiao ◽  
Guoliang Yao ◽  
Yongxuan Liu ◽  
Chunling Zhao

Abstract There has been controversy regarding folate- and vitamin B12-deficient diet (FVD)-induced hyperhomocysteinemia (HHcy) associated with breast cancer risk in most published epidemiological studies. Thus, the present study designed experiments to assess the causal association between FVD-induced HHcy and mammary tumor risk, as well as to identify the relative underlying mechanism. In this study, mammary tumor development was examined in mouse mammary tumor virus (MMTV)-erb-b2 receptor tyrosine kinase 2 (ErbB2) mice fed with a control AIN-93G diet or a FVD diet. MMTV-ErbB2 mice fed with the FVD diet displayed elevated blood levels of the amino acid homocysteine, a shorter tumor latency and an increased tumor multiplicity compared with the controls. The expression levels of key markers in the receptor tyrosine kinase and estrogen receptor (ER) signaling pathways, including phosphorylated (p)-Akt, p-Erk, p-ERα and Cyclin D1, were elevated in mammary tissues from MMTV-ErbB2 mice fed the FVD diet compared with mice fed with control diet. These data suggested that FVD-induced HHcy may promote mammary tumor development and decrease tumor latency, possibly by activating the epidermal growth factor receptor/ErbB2 and ERα signaling pathways. Therefore, examining the signaling mechanisms and identifying the relative metabolic pathways underlying mammary tumor promotion following FVD-induced HHcy may provide a novel strategy for breast cancer prevention and treatment.


Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Fatima Ryalat ◽  
N Cruz-Diaz ◽  
W Graham ◽  
T Gwathmey-Williams ◽  
P E Gallagher ◽  
...  

Aldosterone plays a significant role in hypertension and target organ damage. Aldosterone antagonists are used in the management of heart failure. However, neither the influence of age nor sex on aldosterone pathophysiology is well understood. We investigated the changes in circulating aldosterone with age and its association with cardiovascular function, using male and female hypertensive renin transgenic (mRen2)27 rats and SD rats at 20 and 50 weeks of age. Both male (22 ± 3 vs. 12 ± 2 ng/dL, n = 9 - 12, p < 0.05) and female (59 ± 10 vs. 23 ± 8 ng/dL, n = 6 - 10, p < 0.05) hypertensive rats had higher serum aldosterone compared with SD rats at 20 weeks of age. At 50 weeks of age, the difference persisted in the hypertensive female rats (63 ± 8 vs. SD: 33 ± 7 ng/dL, n = 6 - 7, p < 0.05), but not in the males. SD male rats have higher systolic blood pressure (SBP) as they age, and consequently develop cardiac diastolic dysfunction associated with higher aldosterone at 50 weeks compared to 20 weeks (28 ± 3 vs. 12 ± 2 ng/dL, n = 7 - 9, p < 0.05). This aging effect on aldosterone was not significant in the other groups. We showed previously that SD males treated with polyphenol rich muscadine grape extract (MGE) have lower aldosterone, less aortic stiffness and better cardiac diastolic function (E/e’) than controls at the older age; the MGE effect was not seen in (mRen2)27 males. Sex differences in aldosterone were not significant in the SD rats at either time point. However, (mRen2)27 female rats had higher aldosterone than (mRen2)27 males at both 20 weeks (59 ± 10 vs. 22 ± 3 ng/dL, n = 10 - 12, p < 0.05) and 50 weeks (63 ± 8 vs. 31 ± 7 ng/dL, n = 6 - 7, p < 0.05), despite the lack of significant differences in SBP. (mRen2)27 female rats preserve cardiac function better than males throughout their life span, while males develop indices of heart failure. Our data suggest that lower aldosterone levels in hypertensive males compared with females do not protect against the higher lifetime burden of elevated SBP and also may reflect different mechanisms controlling circulating aldosterone between sexes. In addition, data suggest a potential therapeutic effect of MGE in the management of age-associated moderate hypertension.


1991 ◽  
Vol 39 (2) ◽  
pp. 193-202 ◽  
Author(s):  
Cor J.M.'Arts ◽  
Albert Th.J.J. de Bie ◽  
Henk van den Berg ◽  
Pieter van 't Veer ◽  
Gijsbert S.J. Bunnik ◽  
...  

F1000Research ◽  
2021 ◽  
Vol 10 ◽  
pp. 902
Author(s):  
Kusmardi Kusmardi ◽  
Elvan Wiyarta ◽  
Numlil Khaira Rusdi ◽  
Andi Muh. Maulana ◽  
Ari Estuningtyas ◽  
...  

Background: Research in natural substances for their anticancer potential has become increasingly popular. Lunasin, a soybean protein, is known to inhibit cancer progression via various pathways.  The aim of this study was to investigate the effect of Lunasin Extract (LE) on the expression of Intercellular Adhesion Molecule 1 (ICAM-1) and epithelial cadherins (E-Cadherin) in breast cancer. Methods: In this true-experimental in vivo study, 24 Sprague-Dawley rats that were induced by 7,12-Dimethylbenz[a]anthracene (DMBA), were used. Based on the therapy given, the groups were divided into, normal, positive control (PC), negative control (NC), adjuvant, curative, and preventive. Lunasin was extracted from soybean seeds of the Grobogan variety in Indonesia. Tissue samples were obtained, processed, stained with anti-ICAM-1 and anti-E-Cadherin antibodies, examined under a microscope, and quantified using H-score. The data were analyzed using ANOVA, which was then followed by Duncan's test. Results: Statistically significant difference in ICAM-1 expression was observed between the following groups: adjuvant and NC, normal and NC, PC and NC, adjuvant and preventive, normal and preventive, PC and preventive, adjuvant and curative, normal and curative, PC and curative. E-Cadherin expression was significantly different between preventive and NC, adjuvant and NC, PC and NC, normal and NC, adjuvant and curative, PC and curative, normal and curative, normal and preventive. Significant negative correlation was found between ICAM-1 and E-Cadherin [-0.616 (-0.8165; -0.283)] with p = 0.001. Conclusion: Preventive dose of LE was able to reduce ICAM-1 expression while increasing E-Cadherin expression.


2012 ◽  
Vol 82 (4) ◽  
pp. 298-302 ◽  
Author(s):  
Abigail Daily ◽  
Shuqian Liu ◽  
Saloni Bhatnagar ◽  
Rouzan G. Karabakhtsian ◽  
Jeffrey A. Moscow

We have previously described the down-regulation of thiamine transporter gene expression in breast cancer, and others have shown an epidemiologic relationship between obesity and breast cancer. To further explore the relationship of thiamine, fat, and breast cancer, we exposed FVB/N-Tg(MMTVneu)202Mul/J female mice to four diets that varied in fat and thiamine content (15 mice per group). The high-fat (HF) diet contained 60 % of calories from fat and the normal-fat (NF) diet contained 10 % of calories from fat. The normal-thiamine (NT) diet contained 6 mg thiamine per 4057 kcal and the low-thiamine (LT) diet contained 2 mg thiamine/4057 kcal. Tumor latency was 203 days from date of birth for the HF/NT group, 210 days for the HF/LT group, 225 days for the NF/NT group, and 295 days for the NF/LT group (p = 0.01). The time to endpoint of a mammary tumor volume > 1000 mm3 was 231 days for the HF/NT group, 238 days for the HF/LT group, 257 days for the NF/NT group, and undefined (>310 days) for the NF/LT group (p < 0.001). The high-fat groups were heavier than the normal-fat groups, and the low-thiamine group had a lower serum thiamine level than the normal-thiamine group. There were no differences in the number of pulmonary metastases between groups. This study demonstrates a potential role for dietary thiamine, and an interaction between thiamine and fat, in breast cancer progression.


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