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Protective effect of alpha‐lipoic acid against apical periodontitis‐induced cardiac injury in rats
Author(s) -
Sehirli Ahmet Ö.,
Aksoy Umut,
Kermeoglu Fatma,
Kalender Atakan,
Savtekin Gokce,
Ozkayalar Hanife,
Sayiner Serkan
Publication year - 2019
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/eos.12618
Subject(s) - lactate dehydrogenase , saline , creatine kinase , periodontitis , alkaline phosphatase , acid phosphatase , superoxide dismutase , lipoic acid , medicine , pharmacology , chemistry , endocrinology , enzyme , biochemistry , oxidative stress , antioxidant
This study was designed to assess the possible protective effect of alpha‐lipoic acid ( ALA ) on apical periodontitis ( AP )‐induced cardiac injury. Wistar albino rats were randomized into four groups: control; ALA ; AP ; and ALA + AP . Rats of the control and ALA groups were not endodontically treated, but saline and ALA (100 mg kg −1 ) were administered. In rats of the AP and ALA + AP groups, the pulp chambers of mandibular first molar teeth were exposed and left open for 30 d to induce AP . Saline and ALA (100 mg kg −1 ) were administered intraperitoneally every 24 h during the experiment. At the end of the experiment, the rats were killed. Establishment of AP was verified by radiographic and histopathological evaluation. Serum alkaline phosphatase ( ALP ), lactate dehydrogenase ( LDH ), creatine kinase ( CK ), and superoxide dismutase ( SOD ) activities were determined using an automated biochemical analyzer, and the structural cardiac injury was assessed pathologically. Serum ALP , LDH , and CK activities were elevated, and SOD activities were decreased, in the AP group. The changed enzyme activities were significantly normalized by treatment with ALA . We conclude that ALA administration alleviated the AP‐induced heart injury and improved cardiac structure and function, and therefore this agent may be of potential therapeutic value in protecting cardiac tissue from systemic injury caused by AP.