Document Type: Research Articles
Oral Biology Research Unit and Center of Excellence in Medicinal Herbs for Treatment of Oral Diseases,Thammasat University (Rangsit campus), Pathum Thani, Thailand.
Faculty of Dentistry, Thammasat University (Rangsit campus), Pathum Thani, Thailand.
3Department of Chemistry, Faculty of Science, Ramkhamhaeng University, Bangkok, Thailand.
Background: Propolis, a resinous substance produced by the honeybee, has a wide spectrum of potent biological
activities. However, anti-cancer activity of propolis obtained from Trigona sirindhornae, a new species of stingless
bee, has not yet been reported. This study concerned cytotoxicity of propolis extracts from T. sirindhornae against two
head and neck squamous cell carcinoma (HNSCC) cell lines. Materials and Methods: A dichloromethane extract
of propolis (DMEP) was prepared generating 3 fractions: DMEP-A, DMEP-B, and DMEP-C. Genetically-matched
HNSCC cell lines derived from primary (HN30) and metastatic sites (HN31) in the same patient were used to study
cytotoxic effects of the DMEPs by MTT assays. The active compounds in the DMEPs were analyzed by reversephase
high performance liquid chromatography. Results: DMEP-A exhibited cytotoxic activity on HN30 cells with
significantly decreased viability at 200 μg/ml compared with the control (p<0.05). However, no significant cytotoxic
effect was evident in HN31 cells. DMEP-B and DMEP-C significantly decreased the viability of both cell lines from
100–200 μg/ml and 50–200 μg/ml, respectively (p<0.05). Interestingly, HN31 cells were more toxically sensitive
compared with the HN30 cells when treated with DMEP-B and DMEP-C. IC50 values for DMEP-B with HN30 and
HN31 cells were more than 200 μg/ml and 199.8±1.05 μg/ml, respectively. The IC50 of DMEP-C to HN30 and HN31
cells was found to be 114.3±1.29 and 76.33±1.24 μg/ml, respectively. Notably, apigenin, pinocembrin, p-coumaric acid,
and caffeic acid were not detected in our propolis extracts. Conclusion: T. sirindhornae produced propolis displays
cytotoxic effects against HNSCC cells s. Moreover, DMEP-B and DMEP-C differentially inhibited the proliferation
of a metastatic HNSCC cell line.