Effects Of Pterostilbene On Activities And Protein Expression Of Cytochrome P450 1a1 (Cyp1a1) And Glutathione S-Transferase (Gst) In BenzoAPyrene-Induced Ht-29 Colorectal Cancer Cell Line
- Author:
Ahmad Rohi GHAZALI
1
;
Wee Xian LEE
;
Xiang Yi CHENG
;
Asmariah AHMAD
;
Tava Shelan NAGAPAN
Author Information
1. Programme of Biomedical Science School of Diagnostics and Applied Health Sciences Faculty of Health Sciences Universiti Kebangsaan Malaysia Jalan Raja Muda Abdul Aziz 50300 Kuala Lumpur, Malaysia
- Publication Type:Journal article
- Keywords:
Pterostilbene;
Cytochrome P450 1A1;
Glutathione S-Transferase;
Benzo[a]pyrene;
HT-29 colorectal cell line
- From:Malaysian Journal of Health Sciences
2018;16(Special Issue (Article)):27-33
- CountryMalaysia
- Language:English
-
Abstract:
Drug Metabolizing Enzyme (DME) has been a target of natural chemopreventive agents to inhibit, retard and reverse theprocess of carcinogenesis. Pterostilbene, an analog to resveratrol has been reported to possess various pharmacologicalbenefits including chemoprevention. In our study, benzo[a]pyrene-induced HT-29 colorectal cell line was used as theDME model. The activity of phase I enzyme CYP1A as determined by the 7-ethoxyresorufin O-deethylation (EROD) assaywas found to be inhibited significantly by pterostilbene at 50 µM, 75 µM and 100 µM (p ≤ 0.01, p ≤ 0.05, p ≤ 0.01respectively) compared to the benzo[a]pyrene treated group. Meanwhile, pterostilbene induced glutathione-S-transferase(GST) activity significantly (p ≤ 0.01) at 50 µM as compared to the untreated. In addition, However, the protein expressionof CYP1A1 and GST in pterostilbene treated group was not significantly affected compared to untreated. On the otherhand, pterostilbene at 25 and 75 µM were able to increase the protein expression of transcription factor Nrf2 significantly(p ≤ 0.01). Results indicated that pterostilbene could reduce metabolic activation of procarcinogens and increase thedetoxification process which can be potentially developed as chemopreventive agent.
