Nanostructured titanium dioxide (TiO2) with a crystallite size from 10 to 85 nm, photocatalytically active for organic reactions under illumination with visible light, has been prepared by a sol–gel process using a titanium tetrabutoxide solution in ethanol with an initial pH of 6. According to X-ray diffraction characterization results, the as-prepared titanium dioxide was amorphous. Annealing in a hydrogen atmosphere for 1 h at 400°C led to the formation of an anatase phase, and annealing in the temperature range from 600 to 800°C resulted in the anatase–rutile phase transition. The crystallite size of titanium dioxide increased from 10 to 75 nm as the annealing temperature was raised from 400 to 1000°C (furnace annealing for 1 h) and from 60 to 85 nm as the annealing time at a temperature of 800°C was increased from 30 to 240 min. Diffuse reflection spectra showed that the band gap of TiO2 decreased from 3.3 to 2.6 eV as the annealing temperature was raised from 200 to 1000°C. The specific surface area data obtained by BET measurements showed that the samples annealed at the highest temperature (1000°C) had the smallest surface area, which dropped from 307 to 1 m2/g. The efficiency of the synthesized TiO2 tested as a catalyst for oxidative $$S_{{\text{N}}}^{{\text{H}}}$$ cross-coupling of acridine with indole demonstrated an in crease in product yield from 35 to 80% as the annealing temperature was raised to 800°C. Varying the 800°C annealing time from 30 to 180 min had no effect on the reaction product yield, which ranged from 70 to 80%.

The recovery period after traumatic brain injury (TBI) is often complicated by secondary damage that may last for days or even months after trauma. Two proteins, Hsp70 and glyceraldehyde-3-phosphate dehydrogenase (GAPDH), were recently described as modulating post-traumatic processes, and in this study, we test them as targets for combination therapy using an inhibitor of GAPDH aggregation (derivative of hydrocortisone RX624) and an inducer of Hsp70 synthesis (the pyrrolylazine derivative PQ-29). The protective effect of the combination on C6 rat glioblastoma cells treated with the cerebrospinal fluid of traumatized animals resulted in an increase in the cell index and in a reduced level of apoptosis. Using a rat weight drop model of TBI, we found that the combined use of both drugs prevented memory impairment and motor deficits, as well as a reduction of neurons and accumulation of GAPDH aggregates in brain tissue. In conclusion, we developed and tested a new approach to the treatment of TBI based on influencing distinct molecular mechanisms in brain cells.

The risk of progression of most sporadic neurodegenerative diseases, including Alzheimer’s disease, increases with age. Traditionally, this is associated with a decrease in the efficiency of cell protection systems, in particular, molecular chaperones. Thus, the development of small molecules able to induce the synthesis of chaperones is a promising therapeutic approach to prevent neural diseases associated with ageing. Here, we describe a new compound IA-50, belonging to the class of indolylazines and featured by a low size of topological polar surface area, the property related to substances with potentially high membrane-penetrating activity. We also estimated the absorption, distribution, metabolism and excretion characteristics of IA-50 and found the substance to fit the effective drug criteria. The new compound was found to induce the synthesis and accumulation of Hsp70 in normal and aged neurons and in the hippocampi of young and old mice. The transgenic model of Alzheimer’s disease, based on 5xFAD mice, confirmed that the injection of IA-50 prevented the formation of β-amyloid aggregates, loss of hippocampal neurons and the development of memory impairment. These data indicate that this novel substance may induce the expression of chaperones in neural cells and brain tissues, suggesting its possible application in the therapy of ageing-associated disorders.

Traumatic brain injury (TBI) often causes massive brain cell death accompanied by the accumulation of toxic factors in interstitial and cerebrospinal fluids. The persistence of the damaged brain area is not transient and may occur within days and weeks. Chaperone Hsp70 is known for its cytoprotective and antiapoptotic activity, and thus, a therapeutic approach based on chemically induced Hsp70 expression may become a promising approach to lower post-traumatic complications. To simulate the processes of secondary damage, we used an animal model of TBI and a cell model based on the cultivation of target cells in the presence of cerebrospinal fluid (CSF) from injured rats. Here we present a novel low molecular weight substance, PQ-29, which induces the synthesis of Hsp70 and empowers the resistance of rat C6 glioma cells to the cytotoxic effect of rat cerebrospinal fluid taken from rats subjected to TBI. In an animal model of TBI, PQ-29 elevated the Hsp70 level in brain cells and significantly slowed the process of the apoptosis in acceptor cells in response to cerebrospinal fluid action. The compound was also shown to rescue the motor function of traumatized rats, thus proving its potential application in rehabilitation therapy after TBI.