Sunday 31 May 2020

Elecampane (Inula helenium) Exerts cytotoxicity in Acute Lymphoblastic Leukemia (ALL) Cell Lines

By Kyle J. Norton

Cytotoxicity is the process in the induction of cell death through toxins.

In other words, cell cytotoxicity is the process to use certain chemicals or mediator cells to destroy living cells.

In normal cells, cytotoxicity can cause the death of healthy cells

In cancer cells, cytotoxicity can be benefits to humans by destroying the cancer cells and prevent them from proliferation.

Most cases of cytotoxicity of a substance are to determine the potential toxicity of the quality of the substance, including plant extracts or biologically active compounds isolated from plants.

In other words, the aim of the cytotoxic studies is to find the minimal quality that is essential for the successful development of pharmaceutical or cosmetic preparation that induces cellular toxicity for the treatment of cancer.

Before the preparation can be used in humans, bioassays associated with a number of different cell lines in vitro and vivo have been used to assess the cytotoxicity of many herbal plants, including those of African medicinal plants.

For example, cytotoxicity induced by oxidative stress due to the imbalanced ratio of free radicals and antioxidant enzymes produced by the body can cause protein, lipid and cellular damage that leads to chronic low-grade inflammatory diseases and cancer.


However, stimulation of ROS and antioxidants production to induce cytotoxicity to the tumors can also cause cancer cell death without damage to nearby healthy cells.

On finding a natural ingredient for the prevention and treatment of leukemia, scientists examined the effects of Ergolide isolated from Inula oculus Christi against leukemic cell lines.

Elecampane, also known as Horse-heal (Inula helenium) is a perennial composite plant, genus nulla, belonging to Asteraceae, native to Southern Europe, and Asia. 

The plant has been used in traditional and herbal medicine in treating bronchitis or emphysema, night sweats, pulmonary tuberculosis, irritating cough, catarrhal discharges, etc.

According to tested analysis,
* Ergolide induced cytotoxic effect on the tested cells by increasing the ROS production during early hours after treatment of cells followed by cell cycle arrest in G0/G1 phase and autophagy induction.
* However, Ergolide did not exert anti cytotoxicity against non-tumorous cells and did not cause noticeable hemolysis.

* Interestingly, according to the N-acetyl-L-cysteine (NAC) assay, Ergolide induces cell death through a ROS-dependent manner by altering the expression of pro-apoptotic related genes. 

* Furthermore, Ergolide intensified vincristine cytotoxicity against acute lymphoblastic leukemia (ALL) cell lines.

Based on the results, researchers suggest, "Ergolide could be considered as a potent natural compound against leukemic cells by inducing cell cycle arrest followed by dose-dependent cell death".

Taken altogether, Elecampane processed abundantly Ergolide, may be considered a remedy for the treatment of acute lymphoblastic leukemia, pending to the confirmation of the larger sample size and multicenter human study.

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Author Biography
Kyle J. Norton (Scholar, Master of Nutrition, All right reserved)
Health article writer and researcher; Over 10.000 articles and research papers have been written and published online, including worldwide health, ezine articles, article base, health blogs, self-growth, best before it's news, the karate GB daily, etc.,.
Named TOP 50 MEDICAL ESSAYS FOR ARTISTS & AUTHORS TO READ by Disilgold.com Named 50 of the best health Tweeters Canada - Huffington Post
Nominated for shorty award over last 4 years
Some articles have been used as references in medical research, such as international journal Pharma and Bioscience, ISSN 0975-6299.

Sources
(1) Ergolide, a potent sesquiterpene lactone induces cell cycle arrest along with ROS-dependent apoptosis and potentiates vincristine cytotoxicity in ALL cell lines by Yami A1, Hamzeloo-Moghadam M2, Darbandi A3, Karami A4, Mashati P4, Takhviji V4, Gharehbaghian A. (PubMed)

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