scholarly journals Artemisia annua Extract Ameliorates DMBA-induced Breast Cancer in Albino rats; Antioxidant and Genetic Effects

2020 ◽  
Vol 36 (03) ◽  
pp. 451-457
Author(s):  
Hemmat M. M. Faheem ◽  
Sameh M. M. Elnbtete
Keyword(s):  
Breast Cancer ◽  
Artemisia Annua ◽  
Genetic Effects ◽  
Albino Rats

scholarly journals Chrysosplenol d, a Flavonol from Artemisia annua, Induces ERK1/2-Mediated Apoptosis in Triple Negative Human Breast Cancer Cells

2020 ◽  
Vol 21 (11) ◽  
pp. 4090
Author(s):  
Sophia J. Lang ◽  
Michael Schmiech ◽  
Susanne Hafner ◽  
Christian Paetz ◽  
Katharina Werner ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Human Breast Cancer ◽  
High Performance ◽  
Triple Negative ◽  
Artemisia Annua ◽  
Human Breast ◽  
Mitochondrial Membrane Potential Loss

Triple negative human breast cancer (TNBC) is an aggressive cancer subtype with poor prognosis. Besides the better-known artemisinin, Artemisia annua L. contains numerous active compounds not well-studied yet. High-performance liquid chromatography coupled with diode-array and mass spectrometric detection (HPLC-DAD-MS) was used for the analysis of the most abundant compounds of an Artemisia annua extract exhibiting toxicity to MDA-MB-231 TNBC cells. Artemisinin, 6,7-dimethoxycoumarin, arteannuic acid were not toxic to any of the cancer cell lines tested. The flavonols chrysosplenol d and casticin selectively inhibited the viability of the TNBC cell lines, MDA-MB-231, CAL-51, CAL-148, as well as MCF7, A549, MIA PaCa-2, and PC-3. PC-3 prostate cancer cells exhibiting high basal protein kinase B (AKT) and no ERK1/2 activation were relatively resistant, whereas MDA-MB-231 cells with high basal ERK1/2 and low AKT activity were more sensitive to chrysosplenol d treatment. In vivo, chrysosplenol d and casticin inhibited MDA-MB-231 tumor growth on chick chorioallantoic membranes. Both compounds induced mitochondrial membrane potential loss and apoptosis. Chrysosplenol d activated ERK1/2, but not other kinases tested, increased cytosolic reactive oxygen species (ROS) and induced autophagy in MDA-MB-231 cells. Lysosomal aberrations and toxicity could be antagonized by ERK1/2 inhibition. The Artemisia annua flavonols chrysosplenol d and casticin merit exploration as potential anticancer therapeutics.

scholarly journals Effect of Taraxacum officinale extract on PI3K/Akt pathway in DMBA-induced breast cancer in albino rats

2018 ◽  
Vol 38 (6) ◽  
Author(s):  
Mohamed Abdo Nassan ◽  
Mohamed Mohamed Soliman ◽  
Shimaa Ahmed Ismail ◽  
Samir El-Shazly
Keyword(s):  
Breast Cancer ◽  
Mammary Gland ◽  
Breast Cancer Incidence ◽  
Serum Levels ◽  
Taraxacum Officinale ◽  
Pcr Analysis ◽  
Albino Rats ◽  
Root Extract ◽  
Breast Cancer Growth ◽  
Excessive Proliferation

Background: Breast cancer is one of the most prevalent types of cancer and a leading cause of death in women. Materials and methods: An experimental model of breast cancer was induced in female albino rats using single intragastric dose of 7, 12 dimethylbenz (α) anthracene (DMBA) in sesame oil (50 mg/kg b.wt). Four months after DMBA administration, incidence of breast cancer was confirmed by measuring cancer antigen 15-3 (CA15-3) serum levels. Taraxacum officinale ssp. officinale root extract (TOE) was administered in a dose of 500 mg/kg by oral gavage for 4 weeks after breast cancer incidence. Level of CA15-3 as one of the best known breast tumor markers was elevated in all positive breast cancer rats. The genetic effects of TOE on Pdk1–Akt1–Pik3r1–Map3k1–Erbb2–PIk3ca using semi-quantitative RT-PCR analysis were evaluated. In parallel, histopathological changes and immunohistochemical expression of Bcl2 in mammary gland tissues were examined. Results: Level of CA15-3 was normalized in DMBA group administered TOE for 4 weeks. Administration of DMBA increased expression of Pdk1, Akt1, Pik3r1, Map3k1, Erbb2 and PIk3ca. Treatment with TOE normalized the up-regulated mRNA for all examined genes except Pik3ra that was up-regulated. Mammary gland tissues of DMBA group showed excessive proliferation of lining epithelium of acini and ductules with hyperchromatic nuclei with excessive immunostaining of Bcl2 in the proliferated epithelium that was ameliorated by TOE administration. In conclusion, TOE regulated PI3K and Akt pathways involved in suppression of breast cancer growth and proliferation. TOE is effective as anticancer herbal agent.

scholarly journals Acute Toxicity and the Effects of Mangifera indica on Serum IL-6, and IFN-γ in Breast Cancer-Induced Albino Rats

2021 ◽  
pp. 1-6
Author(s):  
Hussaini Mohammed Alhassan ◽  
Hussaini Mohammed Alhassan ◽  
Mohammed Haruna Yeldu ◽  
Usman Musa ◽  
Isiyaku Adamu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Acute Toxicity ◽  
Mangifera Indica ◽  
Phase 1 ◽  
Female Breast Cancer ◽  
Albino Rats ◽  
Cancer Management ◽  
Desirable Outcome ◽  
Group I ◽  
Ifn Γ

Background: Breast cancer is an uncontrolled growth of breast tissue, which develops in cells lining the milk ducts and lobules, it’s the most common neoplasm in the female. Breast cancer has been declared a universal disaster as it is expected to nearly triple between 2020 and 2030, as most available drugs have not shown any desirable outcome. Aims/Objective: This research aimed to evaluate the acute toxicity and effects of M. indica on serum IL-6, and IFN-γ in cancer-induced albino rats. Materials/Methods: Mangifera indica was subjected to plant identification/authentication and extractions, the acute toxicity was determined using Lorke's method. They are 6 groups of 4 rats each. The groups are normal, positive controls, Ascorbic acids, 500mg, 1000mg and 1500mg M. indica groups. All the groups were induced with 65 mg/kg-1 b.w. of 7,12 Dimethylbenzene-(α) anthracene (DMBA), except Group I and observed for 14 days, before treatment with 100mg of AA (Group III), and 500mg, 1000mg, and 1500mg of extracts (Groups IV- VI) respectively. The rats were sacrificed, 24 hours. after the last treatment. Results: The results of acute toxicity study of the extracts in both phase 1 and 2, has shown no signs of behavioural changes and mortality in all the experimental animals. This has proven that methanolic extracts of M. indica is safe. There was a significant down-regulation of serum IL-6, and INF-γ expressions (P>0.005). Conclusion: This research indicated that M. indica extract is safe and possesses anti-tumor, and immunomodulatory effects, it may be used for breast cancer management.

scholarly journals Polyphenols Extracted from Artemisia annua L. Exhibit Anti-Cancer Effects on Radio-Resistant MDA-MB-231 Human Breast Cancer Cells by Suppressing Stem Cell Phenotype, β-Catenin, and MMP-9

Molecules ◽  
2020 ◽  
Vol 25 (8) ◽  
pp. 1916
Author(s):  
Young Shin Ko ◽  
Eun Joo Jung ◽  
Se-il Go ◽  
Bae Kwon Jeong ◽  
Gon Sup Kim ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Human Breast Cancer ◽  
Breast Cancer Cells ◽  
Artemisia Annua ◽  
Janus Kinase ◽  
Human Breast Cancer Cells ◽  
Human Breast ◽  
Artemisia Annua L ◽  
Anti Cancer

Artemisia annua L. has been reported to show anti-cancer activities. Here, we determined whether polyphenols extracted from Artemisia annua L. (pKAL) exhibit anti-cancer effects on radio-resistant MDA-MB-231 human breast cancer cells (RT-R-MDA-MB-231 cells), and further explored their molecular mechanisms. Cell viability assay and colony-forming assay revealed that pKAL inhibited cell proliferation on both parental and RT-R-MDA-MB-231 cells in a dose-dependent manner. The anti-proliferative effects of pKAL on RT-R-MDA-MB-231 cells were superior or similar to those on parental ones. Western blot analysis revealed that expressions of cluster of differentiation 44 (CD44) and Oct 3/4, matrix metalloproteinase-9 (MMP-9) and signal transducer and activator of transcription-3 (STAT-3) phosphorylation were significantly increased in RT-R-MDA-MB-231 cells compared to parental ones, suggesting that these proteins could be associated with RT resistance. pKAL inhibited the expression of CD44 and Oct 3/4 (CSC markers), and β-catenin and MMP-9 as well as STAT-3 phosphorylation of RT-R-MDA-MB-231. Regarding upstream signaling, the JNK or JAK2 inhibitor could inhibit STAT-3 activation in RT-R-MDA-MB-231 cells, but not augmented pKAL-induced anti-cancer effects. These findings suggest that c-Jun N-terminal kinase (JNK) or Janus kinase 2 (JAK2)/STAT3 signaling are not closely related to the anti-cancer effects of pKAL. In conclusion, this study suggests that pKAL exhibit anti-cancer effects on RT-R-MDA-MB-231 cells by suppressing CD44 and Oct 3/4, β-catenin and MMP-9, which appeared to be linked to RT resistance of RT-R-MDA-MB-231 cells.

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