ArticleJournal of pharmacopuncture2016
Ethanol Extract of Oldenlandia diffusa - an Effective Chemotherapeutic for the Treatment of Colorectal Cancer in Humans: -Anti-Cancer Effects of Oldenlandia diffusa.
Article in Journal of pharmacopuncture, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- Immune and Tumor Microenvironment Mechanisms ofCancers · 2026Review
- Phytochemistry, pharmacology, and medical uses of Oldenlandia (family Rubaceae): a review.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Novel tetrahydroacridine derivatives with iodobenzoic moieties induce G0/G1 cell cycle arrest and apoptosis in A549 non-small lung cancer and HT-29 colorectal cancer cells.Molecular and cellular biochemistry · 2019Article
- Use of Jianpi Jiedu Herbs in Patients with Advanced Colorectal Cancer: A Systematic Review and Meta-Analysis.Evidence-based complementary and alternative medicine : eCAM · 2018Review
- A Network Pharmacology Approach to Uncover the Multiple Mechanisms ofEvidence-based complementary and alternative medicine : eCAM · 2018Article
- Influences ofBiochemistry research international · 2018Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesOldenlandia diffusa is traditionally used to relieve the symptoms of and to treat various diseases, but its anti-cancer activity has not been well studied. In the present study, the authors investigated the anti-cancer effects of an ethanol extract of Oldenlandia diffusa (EOD) on HT-29 human adenocarcinoma cells.
methodsCells were treated with different concentrations of an EOD, and cell death was assessed by using a 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) assay. Analyses of the sub G1 peak, the caspase-3 and -9 activities, and the mitochondrial membrane depolarizations were conducted to confirm cell death by apoptosis. Also, intracellular reactive oxygen species (ROS) generation was determined using carboxy-H2DCFDA (5-(and-6)-carboxy-20,70-dichlorodihydrofluorescein diacetate).
resultsEOD inhibited the proliferation of HT-29 cells for 24 hours by 78.6% ± 8.1% at 50 μg/mL, 74.4% ± 4.6% at 100 μg/mL, 65.9% ± 5.2% at 200 μg/mL, 51.4% ± 6.2% at 300 μg/mL, and by 41.7% ± 8.9% at 400 μg/mL, and treatment for 72 hours reduced the proliferation at the corresponding concentrations by 43.3% ± 8.8%, 24.3 ± 5.1 mV, 13.5 ± 3.2 mV, 6.5 ± 2.3 mV, and by 2.6 ± 2.3 mV. EOD increased the number of cells in the sub-G1 peak in a dose-dependent manner. The mitochondrial membrane depolarization was elevated by EOD. Also, caspase activities were dose-dependently elevated in the presence of EOD, and these activities were repressed by a pan-caspase inhibitor (zVAD-fmk). The ROS generation was significantly increased by EOD and N-acetyl-L-cysteine (NAC; a ROS scavenger) remarkably abolished EOD-induced cell death. In addition, a combination of sub-optimal doses of EOD and chemotherapeutic agents noticeably suppressed the growth of HT-29 cancer cells.
conclusionThese results indicate that EOD might be an effective chemotherapeutic for the treatment of human colorectal cancer.
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