Ashwagandha is a medicinal herb long used in Ayurvedic practice, and highly valued for its adaptogenic properties. It bolsters mental and physical stamina, mental resilience, and reduces the effects of stress.
Propolis is a natural substance processed by bees from natural polyphenol-rich material gathered from flowering trees and other plants. It contains a natural compound called caffeic acid phenethyl ester, or CAPE. CAPE is well-regarded as an immune strengthening component. It blocks the release of inflammatory cytokines, and boosts the production of natural anti-inflammatory components in the body.
But in this study, these two ingredients have also shown incredible potential to stop ovarian and cervical cancer, similar to Olaparib, a conventional drug that stops tumor DNA from repairing itself and encouraging further cancer growth. However, even though the drug is convenient, it is prohibitively expensive, at around $14,000 per month. It also causes nausea and fatigue, so if the price wasn’t already a major obstacle, the side effects could be.
The researchers found that a withanolide from ashwagandha (Withaferin A) and CAPE from propolis performed the same actions as Olaparib – inhibiting tumor DNA repair and activating apoptosis (cancer cell death) at low doses when combined together.
As the study authors note, ovarian and cervical cancers are two of the most common cancers in women around the world, so this research shows amazing potential whether the botanical combination is used on its own or as an adjunct medicine.
Sari AN, Bhargava P, Dhanjal JK, et al. Combination of Withaferin-A and CAPE Provides Superior Anticancer Potency: Bioinformatics and Experimental Evidence to Their Molecular Targets and Mechanism of Action. Cancers (Basel). 2020;12(5):1160.
We have earlier reported anticancer activity in Withaferin A (Wi-A), a withanolide derived from Ashwagandha (Withania somnifera) and caffeic acid phenethyl ester (CAPE), an active compound from New Zealand honeybee propolis. Whereas Wi-A was cytotoxic to both cancer and normal cells, CAPE has been shown to cause selective death of cancer cells. In the present study, we investigated the efficacy of Wi-A, CAPE, and their combination to ovarian and cervical cancer cells. Both Wi-A and CAPE were seen to activate tumor suppressor protein p53 by downregulation of mortalin and abrogation of its interactions with p53. Downregulation of mortalin translated to compromised mitochondria integrity and function that affected poly ADP-ribose polymerase1 (PARP1); a key regulator of DNA repair and protein-target for Olaparib, drugs clinically used for treatment of breast, ovarian and cervical cancers)-mediated DNA repair yielding growth arrest or apoptosis. Furthermore, we also compared the docking capability of Wi-A and CAPE to PARP1 and found that both of these could bind to the catalytic domain of PARP1, similar to Olaparib. We provide experimental evidences that (i) Wi-A and CAPE cause inactivation of PARP1-mediated DNA repair leading to accumulation of DNA damage and activation of apoptosis signaling by multiple ways, and (ii) a combination of Wi-A and CAPE offers selective toxicity and better potency to cancer cells.
Here is the link to the complete article: Combination of Withaferin-A and CAPE Provides Superior Anticancer Potency: Bioinformatics and Experimental Evidence to Their Molecular Targets and Mechanism of Action
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