ArticleJournal of molecular histology2025
Antitumor effects of Dadas Cress (Lepidium sativum var. sativum) on Ehrlich Ascites tumor cells: an in vitro and in vivo study.
Article in Journal of molecular histology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
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.
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Who cites it
2 citing papers in PubMed.
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Garden cress (Lepidium sativum L.) is widely used in nutrition and traditional medicine for its bioactive properties. Studies show its seeds and leaves have anticancer, antimicrobial, and antidiabetic effects. This study investigated the antitumor potential of an extract from the leaves of Dadaş cress (Lepidium sativum var. sativum), a Turkish variety, against Ehrlich Ascites Tumor (EAT) cells. In the in vitro study, Dadaş cress extract (DCE) was tested at 25, 50, and 100 µg/mL concentrations to evaluate its antitumor activity. Caspase-3/7 activity was measured by fluorometric assay, mitochondrial membrane depolarization by JC-1 dye, and cell cycle by flow cytometry. The 50 µg/mL group had the highest apoptosis rate at 48 h; 100 µg/mL caused the most mitochondrial depolarization at 24 h. After 72 h, the 5-FU group had the highest G0/G1 phase cells, while the 25 µg/mL DCE group had the highest S phase cells. In vivo, groups were control, EAT control, EAT + 5-FU, EAT + DCE (75-150 mg/kg), and DCE only (75-150 mg/kg). Liver and kidney tissues were examined immunohistochemically, biochemically, and genotoxically. DCE significantly lowered TNF-α expression, oxidative stress, and DNA damage in EAT mice. In the 150 mg/kg DCE group, renal tail DNA% dropped from 92.5 to 34.8%, liver tail DNA% from 105.3 to 65.8%. TAS increased, TOS decreased vs. EAT control (p < 0.05). These results suggest DCE protects against EAT-induced damage dose-dependently and has no genotoxicity. The findings suggest that DCE may have antitumor potential.
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Registered trials
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