1-benzoyl-6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline exerts a neuroprotective effect and normalises redox homeostasis in a rat model of cerebral ischemia/reperfusion.

Ischemia is one of the main etiological factors of stroke and is associated with the development of energy deficiency, oxidative stress, and inflammation. An abrupt restoration of blood flow, called reperfusion, can worsen the effects of ischemia. In our study, we assessed the neuroprotective potential of 1-benzoyl-6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline (BHDQ) in cerebral ischemia/reperfusion (CIR) in rats. Wistar rats, divided into 4 groups were used in the study: sham-operated animals; animals with CIR caused by occlusion of the common carotid arteries and subsequent removal of the occlusions; rats treated with BHDQ at a dose of 50 mg/kg in the presence of pathology; sham-operated animals treated with BHDQ. The analysis of the state of energy metabolism in the brain, the level of the S100B protein and the histological assessment of the brain tissue were carried out. The antioxidant potential of BHDQ was assessed by measuring biochemiluminescence parameters, analysing the level of 8-isoprostane, products of lipid and protein oxidation, concentration of α-tocopherol and citrate, and aconitate hydratase activity during CIR in rats. A study of the effect of BHDQ on the regulation of the enzymatic antioxidant system and the inflammatory processes was performed. We demonstrated that BHDQ has a neuroprotective effect in CIR, reducing histopathological changes in the brain, normalizing pyruvate and lactate concentrations, and the transcripts level of Hif-1α gene. The positive effect of BHDQ was probably due to its antioxidant and anti-inflammatory activity, manifested in a decrease in the parameters of the oxidative stress, decreased mRNA of proinflammatory cytokines and NF-κB factor genes. In addition, BHDQ reduced the load on antioxidant protection enzymes, contributing to a change in their activities, decreased the level of antioxidant gene transcripts and expression of Nrf2 and Foxo1 factors toward control. Thus, BHDQ exhibited a neuroprotective effect due to a decrease in the level of oxidative stress and inflammation and the normalization of redox homeostasis on CIR in rats.

Neuroprotective effect of 6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline mediated via regulation of antioxidant system and inhibition of inflammation and apoptosis in a rat model of cerebral ischemia/reperfusion.

The aim of the study was the assessment of the neuroprotective potential of 6-hydroxy-2,2,4-trimethyl-1,2-dihydroquinoline (DHQ) and its effect on inflammation, apoptosis, and transcriptional regulation of the antioxidant system in cerebral ischemia/reperfusion (CIR) in rats. The CIR rat model was constructed using the bilateral common carotid artery occlusion followed by reoxygenation. DHQ was administered at a dose of 50 mg/kg for three days. Histological staining was performed using hematoxylin and eosin. The level of S100B protein, 8-hydroxy-2-deoxyguanosine, and 8-isoprostane was assessed using an enzyme immunoassay. The intensity of apoptosis was assessed based on the activity of caspases and DNA fragmentation. The activity of enzymes was measured spectrophotometrically, the level of gene transcripts was assessed by real-time PCR. DHQ reduced the histopathological changes and normalized levels of S100B, lactate, pyruvate, and HIF-1 mRNA in the CIR rat model. In addition, DHQ decreased the oxidative stress markers in animals with a pathology. The tested compound also inhibited inflammation by decreasing the activity of myeloperoxidase, expression of interleukins and Nfkb2. DHQ-treated rats with CIR showed decreased caspase activity, DNA fragmentation, and AIF expression. DHQ changed activity of antioxidant enzymes to the control values, decreased the expression of Cat, Gsr, and Nfe2l2, which was overexpressed in CIR, and activated the expression of Sod1, Gpx1, Gsta2, and Foxo1. DHQ showed a neuroprotective effect on CIR in rats. The neuroprotective effect involve mechanisms such as the inhibition of oxidative stress, leading to a reduction in the inflammatory response and apoptosis and the modulation of the antioxidant defense components.

[Effect of salt stress on respiration metabolism in higher plants]. / Vliianie solevogo stressa na dykhatel'nyi metabolism vysshikh rastenii.

We studied the activity of NADP-dependent isocitrate dehydrogenase, malate dehydrogenase, succinate dehydrogenase, catalase, and peroxidase as well as the rate of 14CO2 release after introduction of labeled substrates for glycolysis and citrate acid cycle within 24 h after salt stress (1% NaCl) in 10-14 days old germinants of wheat (Triticum aestivum L.) and maize (Zea mays L.) as well as thallus of small duckweed (Wolffia arrhiza (L.) Hork ex Wimmer). Oscillations in the enzymes activity with 4-6 h period have been revealed under stress conditions. Activity of glycolysis decreased in wheat and maize and increased in duckweed under the influence of stress stimulus. Six hours after NaCl action decarboxylation of exogenous citrate and succinate was enhanced in all three plants while the rate of exogenous malate decarboxylation was decreased. We conclude that adaptation of higher plans to salinization is accompanied by rearrangements in oxidative metabolism reflected by oscillations in activity of the enzymes involved in oxidative metabolism.

[Light-dependent changes in the enzyme activity of the ascorbate-glutathione cycle and ascorbate oxidase in the leaves of pea]. / Svetozavisimye izmeneniia aktivnosti fermentov askorbat-glutationovogo tsikla i askorbatoksidazy v list'iakh gorokha.

Light-determined activation of ferments of ascorbate-glutation cycle, ascorbate-oxidase in chloroplasts and cytosol is demonstrated as well as ascorbate-peroxidase, monodehydroascorbate-reductase, glutation-reductase and ascorbate-oxydase in mitochondria. On the other hands activity of mitochondrial dehydroascorbate-reductase increased on reduction of light most likely due to function of electron transport from glutation to dehydroascorbate in mitochondria. Glutation metabolism is proved to be endogenic catalytic process where the amount reconstructed glutation changes slowly with a delay and gradually follow light changes. Light dependable changes of glutation content in chloroplasts ensure resistance of ferment system again hydrogen peroxide and superoxide radicals that generate intensively at light.