Rosiglitazone attenuates cerebral vasospasm and provides neuroprotection in an experimental rat model of subarachnoid hemorrhage.

BACKGROUND: Glutamate and oxidative stress play important roles after subarachnoid hemorrhage (SAH). The ability to modulate glutamate transporter 1 (GLT-1) and the antioxidative effect of rosiglitazone have been demonstrated. We investigated the neuroprotective effect of rosiglitazone after SAH. METHODS: SAH was induced by double blood injection. The rats were randomly divided into sham, SAH + vehicle, and SAH + rosiglitazone groups and treated with dimethyl sulfoxide, dimethyl sulfoxide, and 6 mg/kg of rosiglitazone, respectively, at 2 and 12 h after SAH induction and then daily for 6 days. Cerebrospinal fluid dialysates were collected 30 min before SAH induction and then daily for 7 days for glutamate measurement. Mortality, body weight, and neurological scores were also measured daily. On day 7 after SAH, the wall thickness and the perimeter of the basilar artery (BA), neuron variability, GLT-1 levels, glial fibrillary acidic protein (GFAP) expression and activity, and malondialdehyde, superoxide dismutase, and catalase activities were also evaluated. RESULTS: Rosiglitazone improved survival (relative risk = 0.325) and neurological functions and reduced neuronal degeneration (5.7 ± 0.8 vs. 10.0 ± 0.9; P < 0.001) compared with the SAH + vehicle group. Rosiglitazone also lowered glutamate levels by 43.5-fold and upregulated GLT-1 expression by 1.5-fold and astrocyte activity by 1.8-fold compared with the SAH + vehicle group. The increase in BA wall thickness was significantly attenuated by rosiglitazone, whereas the perimeter of the BA was increased. In addition, rosiglitazone abated the 1.9-fold increase in malondialdehyde levels and the 1.6-fold increase in catalase activity after SAH. CONCLUSION: Rosiglitazone reduced SAH mortality, neurological deficits, body weight loss, GFAP loss, and cerebral vasospasm by preventing the neurotoxicity induced by glutamate and oxidative stress.

The effects of Caulerpa microphysa enzyme-digested extracts on ACE-inhibitory activity and in vitro anti-tumour properties.

The aim of this study was to determine the ACE inhibitory activity and its anti-cancer properties of Caulerpa microphysa extracts. C. microphysa samples were digested with Flavourzyme, Alcalase, and pepsin. The ACE inhibitory activity of enzyme-digested C. microphysa decreased in the order of digestion with pepsin>Flavourzyme>Alcalase; that is, pepsin-extracted samples had significantly higher activity than the other enzyme extractions. To test its anti-tumour effects in vitro C. microphysa pepsin-digested extracts were applied to BALB/c mice with transplanted myelomonocytic leukaemia (WEHI-3) and Human promyelocytic leukaemia (HL-60) cell lines. The growth of both cell lines was inhibited, and extracts induced DNA damage, evaluated with a comet assay. The data demonstrate that C. microphysa pepsin-digested extract had the ability to anti-tumour effects. Further application as a health food is worthy of investigation.