Abstract
BackgroundConsidering the advantages of using medicinal herbs as supplementary treatments to sensitize conventional anti-cancer drugs, studying functional mechanisms and regulatory effects of Echinacea purpurea (as a non-cannabinoid plant) and Cannabis sativa (as a cannabinoid plant) are timely and required. The potential effects of such herbs on lung cancer cell growth, apoptosis, cell cycle distribution, cellular reactive oxygen species (ROS) level, caspase activity and their cannabinomimetic properties on the CB2 receptor are addressed in the current study.MethodsThe cytotoxic effect of both herb extracts on the growth of lung cancer cells (A549) was assessed using the MTT assay. The annexin-V-FITC staining and propidium iodide (PI) staining methods were applied for the detection of apoptosis and cell cycle distribution using flow cytometry. The cellular level of ROS was measured using 7′-dichlorofluorescin diacetate (DCFH-DA) as a fluorescent probe in flow cytometry. The caspase 3 activity was assessed using a colorimetric assay Kit.ResultsEchinacea purpurea (EP) root extract induced a considerable decrease in A549 viable cells, showing a time and dose-dependent response. The cell toxicity of EP was accompanied by induction of early apoptosis and cell accumulation at the sub G1 phase of the cell cycle. The elevation of cellular ROS level and caspase 3 activity indicate ROS-induced caspase-dependent apoptosis following the treatment of A549 cells by EP extract. The observed effects of EP extract on A549 growth and death were abrogated following blockage of CB2 using AM630, a specific antagonist of the CB2 receptor. Increasing concentrations of Cannabis sativa (CS) induced A549 cell death in a time-dependent manner, followed by induction of early apoptosis, cell cycle arrest at sub G1 phase, elevation of ROS level, and activation of caspase 3. The CB2 blockage caused attenuation of CS effects on A549 cell death which revealed consistency with the effects of EP extract on A549 cells.ConclusionsThe pro-apoptotic effects of EP and CS extracts on A549 cells and their possible regulatory role of CB2 activity might be attributed to metabolites of both herbs. These effects deserve receiving more attention as alternative anti-cancer agents.Graphical abstract
Highlights
Considering the advantages of using medicinal herbs as supplementary treatments to sensitize conventional anti-cancer drugs, studying functional mechanisms and regulatory effects of Echinacea purpurea and Cannabis sativa are timely and required
The pro-apoptotic effects of Echinacea purpurea (EP) and Cannabis sativa (CS) extracts on A549 cells and their possible regulatory role of cannabinoid receptor 2 (CB2) activity might be attributed to metabolites of both herbs
EP extract induced the time and dose-dependent cell death in A549 cells To determine the possible effect of EP extract on human lung cancer cell growth, A549 cells were incubated with EP extract (50–900 ng/mL) for 24, 36, and 48 h, and the cell viability was measured using MTT assay
Summary
Considering the advantages of using medicinal herbs as supplementary treatments to sensitize conventional anti-cancer drugs, studying functional mechanisms and regulatory effects of Echinacea purpurea (as a non-cannabinoid plant) and Cannabis sativa (as a cannabinoid plant) are timely and required. The endocannabinoid system (ECS) is an extensive lipid signaling complex system that is involved in regulating numerous physiological mechanisms and pathological processes in the human body [1] This system consists of cannabinoid receptors, eicosanoid compounds called endogenous cannabinoids or endocannabinoids, and enzymes that synthesize and break down these compounds [2]. Cannabinoids are terpenoid lipid-based chemicals isolated from Cannabissativa (Marijuana) which has been proven to exert its effects by specific binding to cannabinoid receptors [3] Both cannabinoid receptors and naturally occurring cannabinoids, known as phytocannabinoids, have potential therapeutic applications based on their pivotal roles in regulating immunologic responses, alleviating inflammation, tumor cell proliferation, angiogenesis, invasion, and migration [4,5,6,7].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
