Factors Enhancing Apoptosis in Vivo through a Caspase-3. Bax. PARP-1 and NFkB Expression in Mice Gingival Epithelium.

• Main Author: Ernie Maduratna, Saraswati
• Format: Article PeerReviewed
• Language: English; English
• Published: Medical Laboratory Technology | Medicine, Research & Experimental | 2014
• Subjects: R Medicine; RK Dentistry
• Online Access: http://repository.unair.ac.id/73080/1/ernie%204.pdf; http://repository.unair.ac.id/73080/2/ernie%204%20makalah.pdf; http://repository.unair.ac.id/73080/; https://ejournals.ph/article.php?id=2768
• Institution: Universitas Airlangga

Aggregatebacter actinomycetemcomitans serotype b in periodontal pockets indicates future periodontal disease progression. A. actinomycetemcomitans serotype-b has virulence factors, such as leukotoxin and cytolethal distending toxin (CDT) which may induce rapid tissue destruction by promoting apoptosis of a number of host cell types. This study tested the hypothesis that periodontal destruction is induced by crude toxin A. actinomycetemcomitans (Aa) serotype b based on apoptosis mechanism associated with caspase-3, Bax, PARP-1, and NF- ΚB expression. Thirty adult mice Swiss Webster strain were randomly divided into two groups (toxin and control). Gingival epitheliums were inoculated with crude toxin Aa serotype b and euthanized at base and 24 hours after inoculation. Apoptotic cells in gingival epithelium were measured by a TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end labeling) assay. The induction of caspase-3, Bax, PARP-1 and NF-ΚB was evaluated by immunohistochemistry. After Aa serotype b toxin was induced, the apoptotic cell in gingival epithelium was 8-fold higher than controlled mice (P < 0.05). The results show that the induction of caspase-3, Bax, PARP-1 was 2-fold higher and NF-ΚB was up to 3-fold higher than controlled mice (P < 0.05). Besides, Aa- serotype-b induced periodontal destruction in mice gingival epithelium significantly through acaspase-3- dependent mechanism.