Essential oils of basil cultivars selectively affect the activity of antioxidant enzymes in murine glial cells

Aims: The aim of this work was to reveal some mechanisms of influence of three basil EO on the microglial cells, as recent-years research data state that these oils have anti-aging and neuroprotective action, and as it is supposed, against also some forms of neurodegenerations. Background: The microglial cells play a pivotal role as the neuroprotective agents against neuroinflammation. Ocimum subspecies are a rich source of essential oils (EO) and used to be applied since antiquity for different purposes, including the prevention and treatment of various diseases. Objective: We decided to evaluate the influence of the essential oils extracted from three basil cultivars (O. basilicum var. purpureum, O. basilicum var. thyrsiflora, and O. x citriodorum), possessing remarkable antioxidant capacity on the activity of the main antioxidant enzymes in microglial BV-2 wild type (WT) and Acetyl-CoA oxidase deficient cell lines (Acox1-/-). Method: All manipulations were carried out using murine microglial BV-2 cell lines (BV-2, Acyl-CoA oxidase type 1 (ACOX1) deficient mutants (Acox1-/-) and WT cells). Result: Different data included in the present article are stating that plant origin substances can play a role of regulators of enzymatic antioxidant capacity of cells. EOs extracted from the Ocimum different cultivars are able to trigger the activity of acetyl-CoA oxidase type 1 (or palmytoil-CoA oxidase type 1), which can serve as a basis of regulation of redox deviation in WT cells. Conclusion: So, it can be suggested them to be applied for the prevention of some processes, which can influence on the aging, as the process of ageing is commonly associated with mitochondrial dysfunction, oxidative stress caused by the increased level of free radical production, dysfunction of the microglia, high blood pressure and so on.

Chronic exercise provides renal-protective effects with upregulation of fatty acid oxidation in the kidney of high fructose-fed rats

Excessive fructose intake causes metabolic syndrome and lipid accumulation in the kidney and leads to renal dysfunction and damage. Exercise (Ex) improves lipids regulation, but the mechanisms are unclarified in the kidney. In the present study, male Sprague-Dawley rats were allocated to groups fed with control or high-fructose (HFr) diet. Part of rats in each group underwent aerobic treadmill Ex for 12 wk. Drug treatment was performed as the fenofibrate gavage during the last 4 wk on HFr diet-fed rats. Renal function, histological changes, and expression of regulators involved in fatty acid (FA) metabolism were assessed. In CON diet-fed groups, Ex did not affect renal function or histology and significantly increased renal expression of FA β-oxidation regulators including acyl-CoA dehydrogenases (CADs), acyl-CoA oxidase, peroxisome proliferator-activated receptor (PPAR)-α, and PPAR-γ coactivator (PGC)-1α and lipogenic factors including acetyl-CoA carboxylase (ACCα), FA synthase (FAS), and sterol regulatory element-binding protein 1c. HFr caused albuminuria, lipid accumulation, and renal pathohistological changes, which were attenuated by Ex but not by fenofibrate. HFr decreased renal expression of medium- and short-chain CADs and PPAR-α and increased renal expression of ACCα, FAS, and sterol regulatory element-binding protein 1c. Ex increased expression of CADs, carnitine palmitoyltransferase type I, acyl-CoA oxidase, PPAR-α, and PGC-1α and decreased renal expression of ACCα and FAS in HFr diet-fed rats. The Ex-induced FA metabolism alteration was similar to that in the fenofibrate-treated group. In conclusion, the present study indicates that Ex enhanced renal FA metabolism, which might protect the kidney in lipid dysregulation diseases.