Herbal Cascara Sagrada's Emodin Which Kills Pancreatic Cancer Cells

By Kyle J. Norton

Scientists may have found a functional herb bioactive compound which processes anti-pancreatic cancer activity with no side effects, some scientists suggested.

Pancreatic cancer is a medical and chronic condition characterized by the irregular cells growth in the tissue of the pancreas.

In the early stage, pancreatic cancer starts on the cells of the surface of the inner lining of pancreatic tissue. At the advanced stage, cancerous cells of the pancreas can travel a distance away to invade other healthy tissue and organs.

The exact causes of the alternation of DNA of pancreatic cells are unknown. However, epidemiological studies suggested that genetic preposition and acquired gene mutations are associated with the increased incidence of cancer.

Some researchers suggested long-term use of tobacco, being overweight and obesity, exposure to workplace chemicals, age, gender and family history are some prevalent risk factors of pancreatic cancer.

According to the statistic, pancreatic cancer is the eighth most common cancer in women and the fourth leading cause of cancer death in men and women. cancer accounts for 7% of all cancer deaths.

 

The 5 years survival rate at stage 1 and 2 is 61% and 52% respectively.
Cascara sagrada is a species of buckthorn, genus Rhamnus, belonging to the family Rhamnaceae, native to western North America.

The herbal’s bark has been used in traditional medicine for gastrointestinal support. and it is thought to have a laxative and natural cleansing effect.

Besides the main compound of anthraquinones, the herb also contains anthraquinone glycosides, (emodin, frangulin, iso-emodin, aloe-emodin, and chrysophanol), rhein, aloin, malic acid, tannic acid, cascarosides A, B, C, and D, and hydroxy anthracene derivatives (HAD), etc.

In the study to reaffirm the Emodin anti-pancreatic cancer effect through inducing apoptosis of pancreatic cancer cells and inhibit tumor growth, researchers at the Zhejiang University School of Medicine, launched an investigation to find out whether emodin could inhibit the angiogenesis of pancreatic cancer tissues and its mechanism.
In vitro and in vivo Emodin inhibited pancreatic cancer cell growth, induced apoptosis, and enhanced the anti-tumor effect of gemcitabine on pancreatic cancer cells by inhibiting the activity of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), the protein in response to cellular survival

Emodin inhibited tumor angiogenesis in vitro and in implanted pancreatic cancer tissues, decreased the expression of angiogenesis-associated factors and reduced eNOS phosphorylation in cell proliferation.

However, Emodin had no effect on VEGFR expression in vivo.

 

Dr. Lin SZ, the lead author said, “emodin has a potential anti-tumor effect on pancreatic cancer via its dual role in the promotion of apoptosis and suppression of angiogenesis”.

 

Additionally, in the examine the effects of an X-linked inhibitor of apoptosis (XIAP) and NF-κB in chemotherapy resistance in pancreatic cancer, researchers conducted an investigation of SW1990 cells treated by sodium chloride, gemcitabine, emodin or their combination (gemcitabine plus emodin).

 

The combination therapy of gemcitabine plus emodin)  are more effective in inducing a significantly inhibited SW1990 cell growth and a higher percentage of apoptosis than monotherapy.

 

Gemcitabine upregulated the expression of XIAP and NF-κB, while emodin or emodin plus gemcitabine downregulated them compared to the control group in vitro.

 

In SW1990 cells established orthotopic pancreatic tumor models in nude mice. The combination of emodin and gemcitabine showed a significant reduction in the tumor to tumor (T/NT) ratio, Standardized uptake value (SUV) and tumor weight compared to monotherapy.

 

Dr. Wang ZH, the lead author after taking into account of co and confounders wrote:” emodin enhances the antitumor effect of gemcitabine in SW1990 pancreatic cancer in vitro and in vivo, which may be via the downregulation of NF-κB expression, thus inhibiting the expression of XIAP.”.

 

Taken altogether, herbal Cascara sagrada process high amount of bioactive ingredient Emodon may be considered a function in the prevention and an adjunct therapy combined with chemo intervention of treatment of pancreatic cancer, pending to the results of large example size and multi-center studies.

 

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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.

References
1. Antitumor activity of emodin against pancreatic cancer depends on its dual role: promotion of apoptosis and suppression of angiogenesis by Lin SZ, Wei WT, Chen H, Chen KJ, Tong HF, Wang ZH, Ni ZL, Liu HB, Guo HC, Liu DL. (PubMed)
2. Enhanced antitumor efficacy by the combination of emodin and gemcitabine against human pancreatic cancer cells via downregulation of the expression of XIAP in vitro and in vivo by Wang ZH, Chen H, Guo HC, Tong HF, Liu JX, Wei WT, Tan W, Ni ZL, Liu HB, Lin SZ.(PubMed)
3. [Toxic hepatitis following consumption of the herbal medicinal product Cascara Sagrada].[Article in Danish]” by Jacobsen C, Semb S, Kromann-Andersen H(PubMed)
4. “Cascara sagrada-induced intrahepatic cholestasis causing portal hypertension: case report and review of herbal hepatotoxicity” by Nadir A, Reddy D, Van Thiel DH. (PubMed)
5. “Occupational respiratory allergic disease induced by Passiflora alata and Rhamnus purshiana” by Giavina-Bianchi PF Jr, Castro FF, Machado ML, Duarte AJ. (PubMed)