Evidence map›Paper›PMID 40358878›Full record

ArticleChinese journal of integrative medicine2026

Hydroxychavicol in Combination with 5-Fluorouracil Induced Apoptosis by Inhibiting Purine Metabolism in HT-29 and DLD-1 Cell Lines.

Noor Azleen Mohamad, Amirah Abdul Rahman, Siti Hamimah Sheikh Abdul Kadir, Safaa M Naes, Musalmah Mazlan, Suzana Makpol

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Article in Chinese journal of integrative medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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6 authors.

Noor Azleen MohamadDepartment of Biochemistry & Molecular Medicine, Faculty of Medicine, Universiti Teknologi MARA, Cawangan Selangor, Kampus Sungai Buloh, Sungai Buloh, 47000, Selangor, Malaysia.
Amirah Abdul RahmanDepartment of Biochemistry & Molecular Medicine, Faculty of Medicine, Universiti Teknologi MARA, Cawangan Selangor, Kampus Sungai Buloh, Sungai Buloh, 47000, Selangor, Malaysia. amirahar@uitm.edu.my.
Siti Hamimah Sheikh Abdul KadirDepartment of Biochemistry & Molecular Medicine, Faculty of Medicine, Universiti Teknologi MARA, Cawangan Selangor, Kampus Sungai Buloh, Sungai Buloh, 47000, Selangor, Malaysia.
Safaa M NaesDepartment of Biochemistry & Molecular Medicine, Faculty of Medicine, Universiti Teknologi MARA, Cawangan Selangor, Kampus Sungai Buloh, Sungai Buloh, 47000, Selangor, Malaysia.
Musalmah MazlanDepartment of Biochemistry & Molecular Medicine, Faculty of Medicine, Universiti Teknologi MARA, Cawangan Selangor, Kampus Sungai Buloh, Sungai Buloh, 47000, Selangor, Malaysia.
Suzana MakpolDepartment of Biochemistry, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kampus Kuala Lumpur, Cheras, Kuala Lumpur, 56000, Malaysia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveTo elucidate the effect of hydroxychavicol (HC) in combination with 5-fluorouracil (5-FU) on purine metabolism and apoptosis in colorectal cancer cell lines HT-29 and DLD-1.

methodsThe viability of HT-29 and DLD-1 cells when treated with HC, (0-1,000 µmol/L) 5-FU (0-100 µmol/L) alone, and HC+5-FU for 24 and 48 h was determined. Hypoxanthine (HPX) and xanthine oxidoreductase (XOR) were evaluated, as well as reactive oxygen species (ROS) levels and mitochondrial membrane potential (MMP). The expression levels of genes including nucleoside transporters equilibrative nucleotide transport 1 and 2 (ENT1 and ENT2), the proapoptotic gene Caspase-3 (CASP3), and the anti-apoptotic gene BCL2 were analysed by quantitative polymerase chain reaction.

resultsBoth HPX and XOR levels in cells treated with HC+5-FU were significantly decreased (P<0.05) after 24 and 48 h compared to control cells. ROS levels in HT-29 and DLD-1 treated with HC+5-FU for 24 and 48 h were 26.2% and 21.4%, and 9.1% and 20.5%, respectively, significantly lower than control cells. MMP assays indicated mitochondrial depolarisation. In HT-29 cells, ENT1 and BCL2 were downregulated at 24 h, and CASP3 was upregulated at 48 h. In DLD-1 cells, ENT1 and ENT2 were downregulated, while CASP3 showed a transient decrease at 24 h.

conclusionsThe combination of HC + 5-FU demonstrated synergistic effects in HT-29 and DLD-1 cells, disrupting oxidative balance and purine metabolism, as reflected in reduced hypoxanthine levels, XOR activity, and ROS production. This treatment also induced mitochondrial membrane depolarisation and altered apoptosis-related gene expression, supporting its role in apoptosis induction.

Indexed as

ApoptosisFluorouracilPurinesCaspase 3Cell Line, TumorCell SurvivalGene Expression Regulation, NeoplasticHT29 CellsHumansMembrane Potential, MitochondrialReactive Oxygen SpeciesCaspase 3FluorouracilpurinePurinesReactive Oxygen Species5-fluorouracilapoptosiscolorectal cancerhydroxychavicolpurine metabolism

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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.