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Clinical studies have demonstrated that decreased adiponectin is associated with the development of Type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD). We focused on determining the neuroprotective effect offered by adiponectin against streptozotocin-induced brain damage in ICV-STZ rat model. We found that adiponectin supplements significantly restored the cognitive deficits in ICV-STZ rat model including shorter escape latency, more crossing times and increased time spent in the target quadrant. Adiponectin supplements also increased number of dendritic branches and mushroom percentage. In addition, adiponectin supplements attenuated tau hyperphosphorylation at multiple AD-related sites through activation of protein Ser9-phosphorylated glycogen synthase kinase-3β (Ser9-GSK-3β) with increased the Akt and PI3K activity. Our data suggest that adiponectin supplements have neuroprotective effects on the ICV-STZ rat model, which may be mediated by the activation of the PI3K/Akt/GSK-3β signaling pathway. [ABSTRACT FROM AUTHOR]

Acute lung injury (ALI) is a common emergency and severe case in clinic. High mobility group protein box 1 (HMGB1) can be treated as a new anti-inflammatory treatment target. Toll-like receptor 4 (TLR4) is an important receptor of HMGB1. Ketamine is a widely used intravenous anesthetic with good anti-inflammatory and immune regulating function. Whether it can protect ALI through inhibiting HMGB1 and TLR4 expression in lung tissue still needs further investigation. Male SD rats were randomly divided into control, lipopolysaccharide (LPS) group and ketamine intervention group with 15 rats in each group. The rats were euthanatized at 24 h after modeling and the bronchoalveolar lavage fluid (BALF) was collected for HMGB1 and TLR4 level detection. Western Blot was applied to analyze HMGB1 and TLR4 protein expression in the lung tissue. HMGB1 and TLR4 concentration in BALF were 5.369 ± 1.564 ng/ml and 43.980 ± 7.524 pg/ml in the control, respectively. They were 12.358 ± 4.681 ng/ml and 102.538 ± 8.412 pg/ml in LPS group, and 7.399 ± 2.346 ng/ml and 87.208 ± 7.558 pg/ml in ketamine intervention group, respectively. Their levels increased significantly in LPS group and down-regulated after ketamine intervention. HMGB1 and TLR4 protein expression in lung tissue elevated obviously in LPS group, and decreased after ketamine treatment. HMGB1 and TLR4 protein level showed positive correlation in lung tissue (r = 0.921, P < 0.001). Ketamine can inhibit HMGB1 and TLR4 expression in ALI, and alleviate LPS induced rat lung injury.

Objective: To investigate changes in serum neuron-specific enolase (NSE) concentration in patients before, during and after surgery for acute craniocerebral trauma, and examine the effects of propofol and isoflurane on these changes., Methods: Ten patients scheduled for urinary operation without cerebral injury were enrolled in the control group. Thirty patients with acute cerebral trauma were randomly allocated to propofol group (n=15) and isoflurane group (n=15). Serum concentrations of NSE before surgery, 2 h after the surgery began, and after completion of surgery were measured in all the patients by enzyme-linked immunoadsorbent assay. Glasgow scores of patients with cerebral trauma were also estimated and recorded., Results: Serum concentration of NSE in patients with cerebral trauma were significantly higher than those in the control group before the surgery (P<0.01). The Glasgow score was inversely correlated with serum NSE concentration (r=-0.494, P<0.01). Serum NSE level after completion of surgery was significantly lower in propofol group than in isoflurane group (P<0.05). NSE levels at 2 h after the initiation of the surgery and after the completion of surgery were higher than those before the surgery., Conclusions: Serum NSE concentration increases in patients with acute cerebral injury in parallel to the severity of brain damage. Application of propofol by intravenous pumping can reduce the increase in serum NSE, alleviate cerebral injury, and protect the brain tissues of patients undergoing surgery for acute craniocerebral trauma.