Effects of curcumin and its derivatives on a glioma cell line
DOI:
https://doi.org/10.12923/Keywords:
glioblastoma, oxidative stress, antioxidants, curcumin, demethoxycurcumin, bisdemethoxycurcuminAbstract
Glioblastomas are highly invasive brain tumors associated with oxidative stress (OS) and chronic inflammation. Curcumin (CUR), the principal bioactive compound of Curcuma longa, as well as its natural analogues demethoxycurcumin (DMC) and bisdemethoxycurcumin (BDMC), exhibit promising therapeutic properties.
The aim of this study was to evaluate the antioxidant effects of CUR, DMC, and BDMC in an in vitro model using the LN229 glioma cell line.
LN229 glioblastoma cells and MO3.13 cells as a non-tumor control were cultured in Dulbecco’s Modified Eagle Medium (DMEM) under standard conditions. Cells were treated with CUR, DMC, and BDMC for 24 h and 48 h at concentrations selected based on MTT assay results. Antioxidant capacity was assessed using the ferric reducing antioxidant power (FRAP) assay, while lipid peroxidation and protein oxidation were evaluated by measuring malondialdehyde (MDA) and protein carbonyl group levels, respectively, in cell lysates.
Curcumin, demethoxycurcumin, and bisdemethoxycurcumin reduced LN229 cell viability in a time- and dose-dependent manner. Curcumin exhibited the strongest antioxidant activity, significantly decreasing MDA levels and protein carbonyl content (p < 0.001). Demethoxycurcumin was the most effective compound in reducing protein oxidation after 48 h, whereas bisdemethoxycurcumin increased MDA levels, suggesting
a potential pro-oxidative effect. The FRAP assay confirmed a sustained antioxidant capacity of all compounds, particularly at higher concentrations.
In conclusion, curcumin and its derivatives demonstrated both antioxidant and cytotoxic activities in a time- and dose-dependent manner. Among the tested compounds, curcumin showed the most stable and long-lasting antioxidant and cytotoxic effects, indicating its potential therapeutic value in mitigating oxidative stress–related damage in glioma cells.
References
1. Schwartzbaum JA, Fisher JL, Aldape KD, Wrensch M. Epidemiology and molecular pathology of glioma. Nat Clin Pract Neurol. 2006;2(9):494-503.
2. Ohgaki H, Kleihues P. Epidemiology and etiology of gliomas. Acta Neuropathol. 2005;109(1):93-108.
3. Lin WW, Karin M. A cytokine-mediated link between innate immunity, inflammation, and cancer. J Clin Invest. 2007;117(5):1175-1183.
4. Reuter S, Gupta SC, Chaturvedi MM, Aggarwal BB. Oxidative stress, inflammation, and cancer: How are they linked? Free Radic Biol Med. 2010;49(11):1603-1616.
5. Lewandowska A. Kurkuma. Uzdrawiająca moc. Warszawa: Wydawnictwo RM; 2023. p. 9-48.
6. Ďuračková Z. Some current insights into oxidative stress. Physiol Res. 2010;59:459-469.
7. Kulbacka J, Saczko J. Oxidative stress in cell damage processes. Pol Merkuriusz Lek. 2009;27(157):44-47.
8. Agrawal K, Asthana S, Kumar D. Role of oxidative stress in metabolic reprogramming of brain cancer. Cancers (Basel). 2023;15(20):Article number.
9. Czajka A. Wolne rodniki tlenowe a mechanizmy obronne organizmu. Now Lek. 2006;75(6):582-586.
10. Wierońska JM. Kurkuma – roślinne panaceum. Wszechświat. 2017;117:117-125.
11. Sohn SI, Priya A, Balasubramaniam B, Muthuramalingam P, Sivasankar C, Selvaraj A, et al. Biomedical applications and bioavailability of curcumin—an updated overview. Pharmaceutics. 2017;13(12):2102.
12. Huang C, Lu HF, Chen YH, Chen JC, Chou WH, Huang HC. Curcumin, demethoxycurcumin, and bisdemethoxycurcumin induce caspase-dependent and -independent apoptosis via Smad or Akt signaling pathways in HOS cells. BMC Complement Med Ther. 2020;20(1):68.
13. Benzie IFF, Strain JJ. The ferric reducing ability of plasma (FRAP) as a measure of antioxidant power: The FRAP assay. Anal Biochem. 1996;239(1):70-76.
14. Ledwożyw A, Michalak J, Stępień A, Kądziołka A. The relationship between plasma triglycerides, cholesterol, total lipids and lipid peroxidation products during human atherosclerosis. Clin Chim Acta. 1986;155(3):275-283.
15. Mesquita CS, Oliveira R, Bento F, Geraldo D, Rodrigues JV, Marcos JC. Simplified 2,4-dinitrophenylhydrazine spectrophotometric assay for quantification of carbonyls in oxidized proteins. Anal Biochem. 2014;458:69-71.
16. Walker BC, Mittal S. Antitumor activity of curcumin in glioblastoma. Int J Mol Sci. 2020;21(24):Article number.
17. Wang P, Dai Y, Yang L, Guo Z, Fan W, Wang J. Curcumin inhibits adverse psychological stress-induced proliferation and invasion of glioma cells via downregulating the ERK/MAPK pathway. J Cell Mol Med. 2021;25(15):7190-7203.
18. Giordano A, Tommonaro G. Curcumin and cancer. Nutrients. 2019;11(10):2376.
19. Luo SM, Wu YP, Huang LC, Huang SM, Hueng DY. The anticancer effect of four curcumin analogues on human glioma cells. Onco Targets Ther. 2021;14:4345-4359.
20. Mohamadian M, Ahmadi SS, Bahrami A, Ferns GA. Review on the therapeutic potential of curcumin and its derivatives on glioma biology. Neurochem Res. 2022;47(10):2936-2953.
21. Sandur SK, Pandey CD, Sung B, Ahn KS, Chaturvedi MM, Aggarwal BB. Curcumin, demethoxycurcumin, bisdemethoxycurcumin, tetrahydrocurcumin and turmerones differentially regulate anti-inflammatory and antiproliferative responses through a ROS-independent mechanism. Carcinogenesis. 2007;28(8):1765-1773.
22. Ahmed T, Gilani AH. Therapeutic potential of turmeric in Alzheimer’s disease: Curcumin or curcuminoids? Phytother Res. 2014;28(4):517-525.
23. Buratta S, Chiaradia E, Tognoloni A, Gambelunghe A, Meschini C, Palmieri L, et al. Effect of curcumin on protein damage induced by rotenone in dopaminergic PC12 cells. Int J Mol Sci. 2020;21(8):2761.
24. Jakubczyk K, Drużga A, Janda K, Skonieczna-Żydecka K. Antioxidant potential of curcumin – a meta-analysis of randomized clinical trials. Antioxidants (Basel). 2020;9(11):1092.
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