Neuroinflammation is a process associated with degeneration and loss of neurons in different parts of the brain. The most important damage mechanisms in its formation are oxidative stress and inflammation. This study aimed to investigate the protective effects of cannabidiol (CBD) against neuroinflammation through various mechanisms. Thirty‑two female rats were randomly divided into 4 groups as control, lipopolysaccharide (LPS), LPS + CBD and CBD groups. After six hours following LPS administration, rats were sacrificed, brain and cerebellum tissues were obtained. Tissues were stained with hematoxylin‑eosin for histopathological analysis. Apelin and tyrosine hydroxylase synthesis were determined immunohistochemically. Total oxidant status and total antioxidant status levels were measured, and an oxidative stress index was calculated. Protein kinase B (AKT), brain-derived neurotrophic factor (BDNF), cyclic‑AMP response element‑binding protein (CREB) and nuclear factor erythroid 2‑related factor 2 (NRF2) mRNA expression levels were also determined. In the LPS group, hyperemia, degeneration, loss of neurons and gliosis were seen in all three tissues. Additionally, Purkinje cell loss in the cerebellum, as well as neuronal loss in the cerebral cortex and hippocampus, were found throughout the LPS group. The expressions of AKT, BDNF, CREB and NRF2, apelin and tyrosine hydroxylase synthesis all decreased significantly. CBD treatment reversed these changes and ameliorated oxidative stress parameters. CBD showed protective effects against neuroinflammation via regulating AKT, CREB, BDNF expressions, NRF2 signaling, apelin and tyrosine hydroxylase synthesis.

OBJECTIVE: Multiple sclerosis (MS) is a chronic inflammatory autoimmune disease of the central nervous system (CNS). Although it is not clear how autoimmune responses occur, it is known that peripheral blood cells may promote the initiation and exacerbation of the inflammatory response in MS. The aim of this study was to evaluate the sensitivity and specificity of neutrophil-lymphocyte ratio (NLR), monocyte-lymphocyte ratio (MLR), platelet-lymphocyte ratio (PLR), erythrocyte distribution width (RDW) and systemic immune inflammation index (SIII) in MS and to determine their relationship with disability. MATERIAL AND METHODS: In this single-center, retrospective case-control study, 104 patients with MS and 65 healthy individuals were included. Disability was assessed with the Expanded Disability Status Scale (EDSS) score, and patients were classified as mild (EDSS<3), moderate (3.5 ≤ EDSS ≥4.5), and severe (EDSS≥5) disabilities. NLR, MLR, PLR, RDW and SIII values were calculated according to the complete blood counts of the patients and the control group. Inflammation markers between the control group and MS patients, MS subtypes, and relapsing-remitting MS (RRMS) attack and remission periods were compared. the relationship between these markers and duration of illness, number of attacks and disability was examined. RESULTS: MLR and RDW were higher in MS than the controls. There was no significant difference in these values between MS subtypes. It was observed that RDW increased as the disease duration, number of attacks and EDSS increased. CONCLUSIONS: In our study, in evaluating inflammation it was seen that MLR and RDW were more determinative than PLR, NLR and SIII. The fact that RDW is higher in MS patients and is affected by disease disability indicates that RDW may have an important role in the follow-up of MS patients and in evaluating the degree of disability.