مقالات پذیرفته شده در هفتمین کنگره بین المللی زیست پزشکی
The Effect of Triclabendazole on The Apoptosis of HepG2 Cell Line
The Effect of Triclabendazole on The Apoptosis of HepG2 Cell Line
Sima Orouei,1Mohammad Hossein Gholami,2Teimour Tabari,3Negin Esfandiari,4Reza Najafi,5,*
1. Department of Biology, Science and Research Branch, Islamic Azad University, Tehran, Iran 2. Faculty of Veterinary Medicine, Kazerun Branch, Islamic Azad University, Kazerun, Iran 3. Department of Clinical Sciences, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran 4. Department of Food Hygiene and Quality Control, Division of Epidemiology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran. 5. Department of Pathobiology, Faculty of Veterinary Medicine, Urmia University, Urmia, Iran
Introduction: Being one of the leading causes of cancer-related mortalities worldwide and ranking as the fifth most prevalent in the United States, liver cancer stands as the sole member among the top five deadliest cancers to exhibit an annual rise in its occurrence rate. Liver diseases are more prevalent in developing nations. Triclabendazole, categorized as a novel imidazole compound, has gained FDA approval for the management of fascioliasis. Its actions involve, in part, processes associated with apoptosis. It has been showed that triclabendazole triggers apoptosis by controlling the levels of apoptotic proteins like Bax and Bcl-2, leading to increased cleavage of caspase-8/9/3/7 and PARP. Furthermore, it also promotes the cleavage of GSDME. This study aimed to study the effect of triclabendazole on the apoptosis of HepG2 cells.
Methods: Liver cancer cell line, HepG2, were cultured in complete DMEM (containing 10% FBS, 100 IU/ml penicillin, 100 μg/ml streptomycin, and 2 mM L-glutamine) and treated with 20, 40, 80, 160, and 320 µM concentration of triclabendazole. After 72 hours, they were evaluated for their viability by MTT assay. Giemsa staining and invert microscopy were used to study morphology. Also, real-time PCR was used to assess the expression of apoptotic genes Bax, Bad, and Bcl-2. Data analysis was done by SPSS version 27.
Results: IC50 of triclabendazole was determined to be 80 µM. The highest apoptotic effect was observed at 320 µM eliminating 92% of all HepG2 cells. Real-time PCR results showed an elevation in the expression of Bax and Bad genes and Bcl-2 gene were suppressed and reduced.
Conclusion: Based on the results of the present study, triclabendazole could be considered as an anticancer agent in cancer treatment process. However, this concept is still new in literature and more studies are needed to prove its applicability.