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INFLUENCE OF THE ACTING SUBSTANCE SODIUM DICLOFENAC ON BONE MARROW CELLS. | LitMetric

In humans and mammals, the homeostasis system is supported by many organs and systems, but hematopoietic remains one of the most important. A negative effect on the hematopoietic system is rejected by many factors, but the first place remains for drugs, which one in three are non-steroidal anti-inflammatory drugs (NSAIDs). The most popular among them remains the active substance "Diclofenac Sodium", which is part of many drugs. The purpose of the work is to study the action of the active substance Diclofenac sodium and its effect on the erythrocyte series of bone marrow cells of white laboratory mice in an experiment. The studies were conducted on white laboratory mice, males, 6 months old, 60 grams. The animals were divided into three groups, the first received 0.09 mg of Diclofenac sodium in the quadriceps of the thigh, the second - 0.18 mg and the third physiological solution for 96 hours. After observing all the rules of bioethics, the animals were slaughtered and the bone marrow was examined using pure immuno-magnetic separation techniques. During the study, it became known that in the first group the number of erythroblasts increased by 75%, while in the second group by 166.5%, due to the blocking of differentiation into more mature cells. The number of reticular cells decreased by 33.4%, while in the second group by 60%. A decrease in the erythrokaryocyte maturation index in the first group by 42.6% whereas in the second by 32.5%, primarily due to immature red blood cell precursors. In the first group, the leuko-erythrokaryoid ratio decreased by 9.5%, while in the second group by 12.3%. The number of megakaryocytes due to the predominant blockade of cyclooxygenase-2 increased in the first group by 266.6%, while in the second by 733.3%. It was found that the most favorable effect on red bone marrow cells has a dose of 0.09 mg, while 0.18 mg has a toxic effect and contributes to the development of cardiovascular complications.

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