Leukemia is characterized by uncontrolled proliferation of abnormal leukocytes. The use of natural products has shown potential against several cancer cell lines in vitro.
Peppermint (Mentha piperita) has been used as a traditional medicine in several ailments such as migraines and irritable bowel syndrome. The most common compound found in peppermint leaves are terpenes. This class contains monoterpenes (52%), sesquiterpenes (9%) and others.
Menthol is the major constituent in terpenes that has many biological activities, such as anti-inflammatory, antiviral, antibacterial, and anticancer properties. It has shown anticancer effects in several cancer types including bladder, prostate, liver, skin, and myeloid leukemia.
Programmed cell death is a mechanism that plays an important role in cancer therapy. Several novel anticancer agents showed that apoptosis and autophagy are the main signaling pathways involved in cancer cell death.
Researchers at Mahidol University (Thailand) reviewed the impact of menthol on human acute promyelocytic cell lines (NB4) and acute T-lymphocytic leukemic cell lines (Molt-4). They reviewed cell viability, cell apoptosis, and autophagy. Leukemic cell lines were treated with various concentrations of menthol and/or the chemotherapeutic agent Daunorubicin (from TOKU-E).
Menthol was found to significantly decrease cell viability in NB4 and Molt-4 cell lines in a dose dependent way. The combination of menthol and Daunorubicin together produced synergistic cytotoxic effects on leukemic cells. Authors suggest that menthol exhibits its cytotoxic activities via inhibition of cell proliferation, induction of apoptosis and autophagy via activation of the caspase cascade.
Natural products combined with chemotherapy compounds can enhance the effect, reduce chemotherapy induced toxicity and reduce drug resistance and merit further exploration in cancer research strategies.
Reference
Naksawat M, Norkaew C, Charoensedtasin K, Roytrakul S, Tanyong D (2023) Anti-leukemic effect of menthol, a peppermint compound, on induction of apoptosis and autophagy. Peer J 11:e15049 Link