naphthoquinones and Cerebral-Hemorrhage

To investigate the effects of shikonin on CD36 expression and phagocytic ability of microglia, and its protective effect on neurons and the possible mechanism within.. The effects of shikonin on CD36 expression and phagocytic ability of microglia were detected by Western blot method, and cerebral haemorrhage was isolated by flow cytometry in the experiment. The protective effect of neurons was observed through neuron-microglia co-culture technique. Meanwhile, the effect of hydrogen peroxide on the expression of catalase was detected, and the concentration of hydrogen peroxide was measured in the isolated cerebral haemorrhage model. The t test was used to compare data between 2 groups, and one-way ANOVA was applied to multiple sets of data.. Compared with the control group, the CD36 expression and phagocytic ability of microglia was increased by shikonin in the isolated cerebral haemorrhage model, while inflammatory factors such as tumour necrosis factor a (TNF-a) and interleukin 1b (IL-1b) attenuated the effects of the drug. The amount of neuron apoptosis/necrosis was significantly reduced by the drug, while the expression of catalase in microglia was increased, but the secretion of hydrogen peroxide was decreased in the neuron-microglia co-culture system.. Shikonin can enhance the CD36 expression and the ability to phagocytose erythrocyte of microglia. Simultaneously, shikonin performs protective effects on neuronal cells and promotes the absorption of haematoma. Therefore, shikonin is probably an innovative medicine to treat cerebral haemorrhage.

Topics: CD36 Antigens; Cerebral Hemorrhage; Humans; Microglia; Naphthoquinones

The changes developing in the perifocal area of hematoma and perspectives of antioxidant and chelate therapy were studied on the model of experimental hemorrhagic stroke and in clinical conditions. Microcirculatory, ischemic and inflammation disturbances with a certain time sequence were found in the perifocal areas. These changes, along with hypostasis and oxidative stress, form the pathobiochemical cascade of changes in hemorrhagic stroke and are potential therapeutic targets. Administering of an antioxidant and chelate drug histochrome reduces the intensity of changes in the perifocal area in the experimental conditions. In clinical conditions, it accelerates the dynamics of brain and meningeal symptoms regression and improves the blood rheological properties.

Topics: Animals; Antioxidants; Brain Ischemia; Cerebral Hemorrhage; Chelating Agents; Male; Naphthoquinones; Platelet Aggregation Inhibitors; Rats; Rats, Wistar

Presented are the results of the use of histochrome in animals with experimental hemorrhagic stroke. An influence of the compound on cerebral edema and the dynamics of hemoglobulin converting as well as a role of MRT in diagnostic of experimental hemorrhagic stroke in different periods of the disease are discussed.

Topics: Animals; Cerebral Hemorrhage; Disease Models, Animal; Follow-Up Studies; Magnetic Resonance Imaging; Male; Motor Activity; Naphthoquinones; Rats; Rats, Wistar; Severity of Illness Index; Treatment Outcome