Influence of Various Light Regimes on Morphofunctional Condition of Transplantable Melanoma B16.

A study of the morphofunctional condition of mice with transplantable melanoma B16 under the influence of a normal daylight regime, constant lighting and constant darkness was conducted. It was shown that exposure to constant lighting leads to intensification of the proliferation of melanoma cells, more significant growth and spread of the tumor, the development of more pronounced secondary changes, the presence of perivascular growth and an increase in perineural invasion. At the same time, keeping of animals in constant darkness significantly reduced the intensity of the proliferative process in the tumor and lead to tumor regression in the absence of signs of lympho-, intravascular and intraneural invasion. Intergroup differences in tumor cell status were confirmed by the results of micromorphometric studies. It was also shown that the expression of clock genes was suppressed by an exposure to constant light, while an influence of constant darkness, on contrary, led to its intensification.

Urokinase-Type Plasminogen Activator Enhances the Neuroprotective Activity of Brain-Derived Neurotrophic Factor in a Model of Intracerebral Hemorrhage.

Brain-derived neurotrophic factor (BDNF) is a classic neuroprotective and pro-regenerative factor in peripheral and central nervous tissue. Its ability to stimulate the restoration of damaged nerve and brain tissue after ischemic stroke and intraventricular hemorrhage has been demonstrated. However, the current concept of regeneration allows us to assert that one factor, even if essential, cannot be the sole contributor to this complex biological process. We have previously shown that urokinase-type plasminogen activator (uPA) complements BDNF activity and stimulates restoration of nervous tissue. Using a model of intracerebral hemorrhage in rats, we investigated the neurotrophic and neuroprotective effect of BDNF combined with uPA. The local simultaneous administration of BDNF and uPA provided effective neuroprotection of brain tissue after intracerebral hemorrhage, promoted survival of experimental animals and their neurological recovery, and decreased lesion volume. The study of cellular mechanisms of the observed neurotrophic effect of BDNF and uPA combination revealed both known mechanisms (neuronal survival and neurite growth) and new ones (microglial activation) that had not been shown for BDNF and uPA. Our findings support the concept of using combinations of biological factors with diverse but complementary mechanisms of action as a promising regenerative approach.