STIMULASI EKSTRAK PROPOLIS PADA ODONTOBLAST LIKE CELLS YANG DIINDUKSI LACTOBACILLUS ACIDOPHILUS INAKTIF TERHADAP EKSPRESI TLR2 DAN TNFα
DOI:
https://doi.org/10.30659/odj.4.2.85-93Keywords:
Inactive Lactobacillus acidophilus, odontoblast like cells, propolis extractAbstract
Background: Lactobacillus acidophilus, Gram-positive bacterias that enterthe dentinal tissue during the carious process are suspected to influence the immune response in human dental pulp. Odontoblasts situated at the pulp dentin interface are the frst cells encountered by these bacteria and have an important role in this response. Lipoteichoic acid (LTA), a wall component of Gram-positive bacteria, triggered the activation of the odontoblasts. LTA upregulated the expression of its own receptor TLR2, as well as the production of proinflammatory cytokineTNFα. Propolis is a resinous material that holds a great potential as an antiinflammatory agent. Present studies have shown that propolis has a reduction effect towards the proinflammatory cytokines expression and favor pulp healing.
Purpose: To reveal the moleculer mechanism of propolis stimulation on
odontoblast like cells, induced by inactive Lactobacillus acidophilus.
Methods: This review was presented in odontoblasts like cells culture induced by inactive Lactobacillus acidophilus and exposed to propolis extract. Pulp cell culture isolated from human impacted thirds molar that has been extracted. Observation and measurement the expression of TLR2 and TNFα was processed by using immunocytochemistry (ICC) technic.
Result: Data analysis with ANOVA test, a signifcant difference in every group
(p<0,05) was present. The expression of TLR2 and TNFα were shown at low
level percentation on odontoblast like cells, induced by Lactobacillus acidophilus and propolis extract stimulation.
Conclusion: Propolis extract stimulations lower the TLR2 and TNFα expression on odontoblast like cells, induced by inactive Lactobacillus acidophilus
Downloads
Published
Issue
Section
License
Authors who publish with this journal agree to the following terms:
Authors retain copyright and grant the journal right of first publication with the work simultaneously licensed under a Creative Commons Attribution License that allows others to share the work with an acknowledgement of the work's authorship and initial publication in this journal.
Authors are able to enter into separate, additional contractual arrangements for the non-exclusive distribution of the journal's published version of the work (e.g., post it to an institutional repository or publish it in a book), with an acknowledgement of its initial publication in this journal.
Authors are permitted and encouraged to post their work online (e.g., in institutional repositories or on their website) prior to and during the submission process, as it can lead to productive exchanges, as well as earlier and greater citation of published work (See The Effect of Open Access).

This work is licensed under a Creative Commons Attribution 4.0 International License.
