Evidence map›Paper›PMID 33446187›Full record

ArticleBMC complementary medicine and therapies2021

The pro-apoptosis effects of Echinacea purpurea and Cannabis sativa extracts in human lung cancer cells through caspase-dependent pathway.

Fatemeh Hosami, Azadeh Manayi, Vahid Salimi, Farshad Khodakhah, Mitra Nourbakhsh, Britt Nakstad, Masoumeh Tavakoli-Yaraki

Abstract read
In one paragraph

Article in BMC complementary medicine and therapies, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

16 citing papers in PubMed, 1 synthesis or guideline pooled it.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Fatemeh HosamiDepartment of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Azadeh ManayiMedicinal Plants Research Center, Faculty of Pharmacy, Tehran University of Medical Sciences, Tehran, Iran.
Vahid SalimiDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Farshad KhodakhahDepartment of Virology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
Mitra NourbakhshDepartment of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Britt NakstadDivision of Pediatric and Adolescent Medicine, Institute of Clinical Medicine, University of Oslo, Oslo, Norway.
Masoumeh Tavakoli-YarakiDepartment of Biochemistry, School of Medicine, Iran University of Medical Sciences, Tehran, Iran. tavakoli.m@iums.ac.ir.ORCID http://orcid.org/0000-0003-4449-9248

Funding

Iran University of Medical Sciences (Grant Number: 97-3-4-12920).
6 · The paper itself

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.

Indexed as

A549 CellsApoptosisCannabisCaspase 3Cell Cycle CheckpointsEchinaceaHumansPlant ExtractsReactive Oxygen SpeciesSignal TransductionCaspase 3Plant ExtractsReactive Oxygen SpeciesApoptosisCannabinoid receptor 2Cannabis sativaCaspase 3Cell cycleEchinaceae purpureaPhyto cannabinoidsReactive oxygen species

Identifiers

PMID33446187
PMCPMC7809807

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.