ABSTRACT
PURPOSE: The ischemia-reperfusion (I/R) injury seen in the heart can cause severe damage to essential organs such as the brain. Cannabidiol (CBD) obtained from Cannabis sativa is used today to treat various diseases. This study aimed to demonstrate CBD's neuroprotective and therapeutic properties in rats with brain damage caused by I/R in the heart. MATERIALS: Rats were divided into four groups; sham, I/R, I/R + Prophylactic CBD, and I/R + Therapeutic CBD. End of the experiment, brain tissues were collected for biochemical, histopathological, and genetic examinations. RESULTS: I/R damage increased the number of degenerative neurons, caspase-3 and TNF-α immunoexpression, total oxidant status levels, and oxidative stress index. Both prophylactic and therapeutic CBD administration reduced these increased values. In addition, the relative fold changes of AMPK, PGC-1α, SIRT1, and Bcl 2 decreased in the I/R group, and the relative fold change of Bax increased, which are indicators of ER stress and apoptosis. Both administrations of CBD reversed these genes' relative fold changes. CONCLUSION: CBD can be protective against brain injury caused by cardiac I/R damage through antioxidant, anti-inflammatory, and anti-apoptotic mechanisms.
Subject(s)
Acute Coronary Syndrome , Cannabidiol , Reperfusion Injury , Rats , Animals , Cannabidiol/pharmacology , Cannabidiol/therapeutic use , Acute Coronary Syndrome/drug therapy , Oxidative Stress , Antioxidants/pharmacology , Reperfusion Injury/pathologyABSTRACT
Sepsis-induced central nervous system damage is called sepsis-associated encephalopathy (SAE). In addition to neuroinflammation, oxidative stress and apoptosis act in the development of SAE. In the current study, we evaluated the protective effects of lacosamide (LCM) on neuroinflammation induced by lipopolysaccharide (LPS). Twenty-four Wistar albino rats were divided into 3 groups as controls, LPS group (5 mg/kg i.p.), and LPS plus LCM group (5 mg/kg i.p and 40 mg/kg i.p, respectively). In the rat brain, LPS-induced tissue damage was revealed histopathologically as hyperemia and microhemorrhages. LCM pretreatment ameliorated these histopathological changes. LPS decreased brain TAS levels and significantly increased MDA, CRP, HSP, IL-1ß, and TNF-α expressions in the cortex, hippocampus, and cerebellum. Western analysis revealed increased brain tissue levels of TNF-α, NF-Kß, and caspase-3 following LPS. Prophylactic LCM treatment reversed these parameters including oxidative stress, inflammation, and apoptosis in the cortex, hippocampus, and cerebellum.
Subject(s)
Brain/pathology , Inflammation/drug therapy , Lacosamide/pharmacology , Aging , Animals , Apoptosis/drug effects , Cerebellum/drug effects , Cerebellum/metabolism , Cerebral Cortex/drug effects , Cerebral Cortex/metabolism , Cerebral Cortex/pathology , Hippocampus/drug effects , Hippocampus/metabolism , Inflammation/chemically induced , Lacosamide/therapeutic use , Lipopolysaccharides , Oxidative Stress/drug effects , Premedication/methods , Protective Agents/pharmacology , Rats , Sepsis-Associated Encephalopathy/drug therapy , Sepsis-Associated Encephalopathy/pathologyABSTRACT
AIM: To determine the incidence of patent furcal accessory canals in permanent molars of a Turkish population. METHODOLOGY: Two-hundred extracted teeth consisting of 50 maxillary first molars, 50 maxillary second molars, 50 mandibular first molars and 50 mandibular second molars from Turkish patients attending the Oral Surgery Department of the Faculty of Dentistry, Istanbul University, Istanbul, Turkey, were included in the study. After preparation of access cavities and removal of pulp tissue, the teeth were stored in 5.25% sodium hypochlorite for 1 h. Following double-sealing of the access cavities, all tooth surfaces except the furcation regions were covered with nail varnish. The teeth were stored in 0.5% basic fuchsin for 1 week. The teeth were sectioned at the cemento-enamel junction and the presence of patent furcal canals was established by examining the pulp chamber floor with a stereomicroscope (10x) to determine staining. RESULTS: Patent furcal accessory canals were detected in 24% of maxillary first molars, 16% of maxillary second molars, 24% of mandibular first molars, and 20% of mandibular second molars. No statistically significant differences were found between the tooth types. CONCLUSIONS: In a Turkish population, the incidence of patent furcal accessory canals on the pulp chamber floor of maxillary and mandibular first and second molars ranged between 16 and 24%.
Subject(s)
Dental Pulp Cavity/anatomy & histology , Molar/anatomy & histology , Tooth Root/anatomy & histology , Humans , TurkeyABSTRACT
Forty maxillary and four mandibular first premolars that were to be extracted for orthodontic reasons were used in this study to evaluate human pulpal response to hydroxyapatite and Dycal as direct capping materials. After the postoperative periods of 2 days, 30 days and, 60 days, teeth were extracted and prepared for the histologic examination. The results of this study showed that hydroxyapatite does not induce hard tissue bridging at the exposure site in human dental pulp. No hard tissue bridging at the exposure site was observed in any of the teeth capped with hydroxyapatite. Moderate infiltration of the inflammatory cells was seen generally in the teeth capped with hydroxyapatite. However, this study has verified that exposed human dental pulp will heal under Dycal application with hard tissue bridging and with none or minimal inflammatory response.
