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Indwiani Astuti
Department of Pharmacology and Therapy, Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta
Immunology & microbiology Neuroscience

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Journal : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

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Cytotoxicity of α-terpineol in HeLa cell line and its effects to apoptosis and cell cycle Rasuane Noor; Indwiani Astuti; . Mustofa
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 46, No 01 (2014)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (649.907 KB) | DOI: 10.19106/JMedScie004601201401

Abstract

α-Terpineol is a natural compound of terpenoid alcohols class. However, it can be synthesizedfrom α-pinene of turpentin content. α-Terpineol has been reported as potential anticancer agentdue to its activity on inhibition of cells growth and induction of tumor cell death. However, itsanticancer activity in HeLa cervical cancer cells line has never been studied, yet. The aim of thisstudy was to evaluate the cytotoxicity of α-terpineol and its effects to apoptosis and cell cycle.This was a quasi-experimental study with post-test only with non-equivalent control groupdesign. Cytotoxicity of á-terpineol was evaluated using MTT cell viability assay. The effect of α-terpineol on cell apoptotis was tested using acridine orange-ethidium bromide staining method,whereas its effect on cell cycle was evaluated by flowcytometry method. The results showedthat α-terpineol had cytotoxicity against HeLa cell with an IC50 value about 12.46 μg/mL.Furthermore, α-terpineol induced the HeLa with an IC50 value about 13.12 μg/mL. Cell accumulationat G1 phase during cell cycle after incubation with α-terpineol (52.78)was observed. In conclusion,α-terpineol is potential as an anticancer due to its ability to induce cell apoptosis and to inhibitthe cell cycle at G1 phase.
Mechanism of cytotoxic activity of chalcone derivatives against K562 leukemia cell lines Arina Novilla; . Mustofa; Indwiani Astuti; . Jumina; Hery Suwito
Journal of the Medical Sciences (Berkala Ilmu Kedokteran) Vol 49, No 4 (2017)
Publisher : Journal of the Medical Sciences (Berkala Ilmu Kedokteran)

Show Abstract | Download Original | Original Source | Check in Google Scholar | Full PDF (310.272 KB) | DOI: 10.19106/JMedSci004904201701

Abstract

Two chalcone derivatives i.e. (E)-1-(4-aminophenyl)-3-(2,3dimethoxyphenyl)-prop-2-en-1-one (Compound-1), and (E)-1-(4-aminophenyl)-3-phenylprop-2-en-1-one) (Compound-2),has been proven to have potential cytotoxic activity. The aim of this study was toevaluate the effect of these compounds on PI3K/Akt signalling pathway in K562 celllines. After incubation with the tested compounds, AKT, caspase-3, STAT3 and cyclinD1 concentrations were measured using ELISA. Furthermore, cell cycle was analysedusing flowcytometry. Imatinib and isotretinoin were used as positive control, whereascell culture without treatment was used as negative control. The AKT concentration aftertreatment with Compound-1 and -2 was significantly lower than that control, imatiniband isotretinoin (p<0.05). The apoptotic indices after treatment with Compound-1 and-2 were significantly higher than control, however they were lower than imatinib andisotretinoin (p<0.05). The caspase-3 concentration after treatment with Compound-1 at5 and 10 μg/mL and Compound-2 at 10 μg/mL was significantly higher than that controland imatinib, however it was lower than isotretinoin (p<0.05). The STAT3 concentrationafter treatment with Compound-1 and -2 was significantly lower than that control andisotretinoin at 50 μg/mL (p<0.05) and similar with imatinib (p>0.05). The cyclin D1concentration after treatment with Compound-1 and -2 was significantly lower than thatcontrol, imatinib and isotretinoin (p<0.05). In addition, Compound-1 and -2 arrested G0/G1 and G2/M phase in K562 cell lines, with comparable results to imatinib and isotretinoin.In conclusion, the mechanism of cytotoxic activity of Compound-1 and -2 are through thePI3K/Akt signalling pathway inhibition, apoptosis induction by upregulation of apoptoticmarkers, and inhibition of cell cycle progression by regulating cell cycle-related factors.
Co-Authors . Jumina Arina Novilla Hery Suwito Mustofa Mustofa Rasuane Noor