An important task of pharmacology is to find effective agents to improve retinal microcirculation and resistance to ischemia. The purpose of the study is to pharmacologically evaluate the retinoprotective effect of 2-ethyl-3-hydroxy-6-methylpyridine nicotinate in a rat model of retinal ischemia–reperfusion. A retinal ischemia–reperfusion model was used, in which an increase in intraocular pressure (IOP) to 110 mmHg was carried out within 30 min. The retinoprotective effect of 2-ethyl-3-hydroxy-6-methylpyridine nicotinate at a dose of 3.8 mg/kg, in comparison with nicotinic acid at a dose of 2 mg/kg and emoxipine at a dose of 2 mg/kg, was estimated by the changes in the eye fundus during ophthalmoscopy, the retinal microcirculation level with laser Doppler flowmetry (LDF), and electroretinography (ERG) after 72 h of reperfusion. The use of 2-ethyl-3-hydroxy-6-methylpyridine nicotinate prevented the development of ischemic injuries in the fundus and led to an increase in the retinal microcirculation level to 747 (median) (lower and upper quartiles: 693;760) perfusion units (p = 0.0002) in comparison with the group that underwent no treatment. In the group with the studied substance, the b-wave amplitude increased significantly (p = 0.0022), and the b/a coefficient increased reliably (p = 0.0002) in comparison with the group with no treatment. Thus, 2-ethyl-3-hydroxy-6-methylpyridine nicotinate has established itself as a potential retinoprotector.
1 June 2007 in Bulletin of Experimental Biology and Medicine
Introduction: Erythropoietin interacts ETwith EPOR/βcR(CD131) and activates the non-canonical pathway JAK/STAT and PI3K/AKT. Phosphorylated STAT subunits were found to get dimerized and translocated into the nucleus to activate the expression of the Runx-2 and TGF-β genes. The purpose of the study was to evaluate the effectiveness of osteogenesis when using epoetin alpha as an osteoinducer in an experimental model of a bone organoid. Materials and Methods: The study was conducted on human mesenchymal stem cells (hMSC) and trabecular bone organoids (TBO). Photometry and microscopy were used to assess the effects of drugs on proliferation and differentiation of hMSС and the formation of osteogenic tissue in TBO. The volume of connective tissue structures and the activity of mitochondria was determined in cells that form fibrovascular osteogenic tissue in TBO. Results: Epoetin alpha was found to have a dose-dependent osteoinductive effect in TBO. At a dose of 200 IU/mL, epoetin alpha has an inhibitory effect, whereas at a dose of 20 IU/mL, it activates the proliferation and differentiation of hMSC in the osteogenic direction by inducing osteogenesis in TBO. Conclusion: Epoetin alpha has a protective effect on osteogenesis in TBO inducing the proliferation of osteoblasts and endotheliocytes, stimulating the growth of connective tissue structures of the bone organoid with the formation of osteogenic tissue along with increasing the activity of mitochondria and reducing intracellular generation of reactive oxygen species.