Testing a Novel Heat-Shock Protein Inducer in the Cellular Model of Traumatic Brain Injury Response

Abstract

Traumatic brain injury (TBI) induces multiple pathological processes affecting various brain cells. the accumulation of toxic factors in interstitial and cerebrospinal fluid may be a consequence of TBI and massive cell death. The accumulation process, causing so-called “secondary damage,” is not transient and often lasts within days and weeks. We believe that Hsp70 protein can play an important role in reducing the severity of posttraumatic pathological complications. Chaperone Hsp70 is known for its cytoprotective activity, and, therefore, an approach involving its increase in in cells exposed to proapoptotic and proinflammatory factors may turn out to be extremely promising. In support of this idea, we studied the effect of the low molecular weight substance KD-29, which is able to induce the synthesis of Hsp70 in the cellular model of the posttraumatic process. We used rat C6 glioma cells to study the cytotoxic effect of rat cerebrospinal fluid obtained after TBI. We found that the drug KD-29 significantly inhibited the apoptosis process and increased the proliferative activity of C6 cells under conditions of modeling posttraumatic processes.