Overexpression of adiponectin alleviates intracerebral hemorrhage-induced brain injury in rats via suppression of oxidative stress.

Oxidative stress and blood-brain barrier (BBB) dysfunction contribute to brain injury after intracerebral hemorrhage (ICH). Adiponectin (APN) inhibits oxidative stress in the CNS, but the role of APN in ICH is not clear. Thus, we elucidated the possible neuroprotective effect of APN in ICH-induced brain injury in rats and investigated the neuroprotective mechanisms. A lentivirus-carrying APN gene was injected into rats 14 days before ICH induced via intracerebral injection of autologous blood. The effects of lentiviral overexpression of APN on brain injury were evaluated 24 h after ICH. Superoxide dismutase (SOD), glutathione (GSH), and the ratio of oxidized glutathione to reduced glutathione (GSSG/GSH) and malondialdehyde (MDA) were measured. Oxidative stress-related proteins were measured by Western blot and qRT-PCR. APN overexpression improved neurological function, reduced brain edema, preserved the BBB and increased the expression of APN and decreased the expression of NADPH oxidase-2 (NOX 2) compared with null vector controls (p < 0.01). SOD, GSH, and GSSG/GSH increased, and MDA was reduced. Furthermore, tetrabromocinnamic acid (TBCA, a NADPH oxidase activator) blocked the effect of APN on cerebral protection and antioxidant activity. Our results demonstrate the importance of APN in regulating oxidative stress and BBB function and suggest APN may be a novel treatment for brain damage after ICH.

KEYWORDS: {{ getKeywords(articleDetailText.words) }}