Abstract:
Stress causes the development of post-stress pathological reactions,
which culminate in dysmetabolic disorders, against the background of which most diseases of
humans and animals develop. Bone tissue has been found to be one of the most sensitive
organs and tissues to the effects of dysmetabolic syndrome.
Aim. Study of the effect of stress on the activity of the proteolytic enzyme elastase in
bone tissue and determination of the possibility of preventing elastase activation using antistress agents.
Methods. Stress was induced in rats by holding the animals at −20 °C for 30 minutes
and elastase activity was investigated on the 4th day after stress. Antioxidant preparations
EkSoVit, Quercetin and ascorbic acid were used as anti-stressors, which were administered
into the oral cavity 3 days before stress and 3 days after stress in the form of an oral gel in
doses (mg/kg): EkSoVit 0.43 and 1.07, Quercetin 0.128 and 0.257 and ascorbic acid 0.257.
Results. In rats without stress, the elastase activity in the femur was (μk-kat/kg) 6.66;
in rats after stress 9.61; in rats with stress that received EkSoVit, 8.16 and 6.90; in rats with stress that received quercetin, 7.20 and 5.60; in rats with stress that received ascorbic acid,
7.20. The antielastase activity in vivo was: EkSoVit – 49.15 and 126.05; quercetin – 112.10
and 135.93 and ascorbic acid – 81.63. The antielastase efficacy of antistressants was after
conversion of antielastase activity to a dose of 1 g/kg: for EkSoVit 114.3 and 117.8; for
quercetin 875.8 and 528.9; for ascorbic acid 317.8.
Conclusion. After stress, the activity of the proteolytic enzyme elastase increases in
bone tissue. The use of anti-stress agents with antioxidant action significantly prevents the
activation of elastase. The most effective anti-elastase drug was quercetin (vitamin P).
