The present study was conducted to investigate the effect of hepatocyte growth factor (HGF) on cortical neurons exposed to oxygen-glucose deprivation/reperfusion (OGD/R). Primary cultured cerebral cortical neurons were prepared from Sprague-Dawley rats. The cells were used for experiments after culture for 12 d in vitro.
View Article and Find Full Text PDFZhongguo Ying Yong Sheng Li Xue Za Zhi
February 2008
Aim: To explore the mechanisms of hypoxic preconditioning on protecting cultured astrocytes from hypoxia injury.
Methods: Cultured astrocytes were divided randomly into several groups: control(C), hypoxia(H) and hypoxic preconditioning (HP). Cells MTT metabolic activity, qualitation of apoptosis and modality to explore the protection effects of hypoxic preconditioning.
Zhong Nan Da Xue Xue Bao Yi Xue Ban
October 2007
Objective: To explore the effect of thrombin precondition (TPC) on the rat cerebral astrocytes(As) cultured in oxygen-glucose deprivation (OGD).
Methods: Astrocytes were pretreated with thrombin (TB) at various concentrations (0.005 approximately 5.
Zhong Nan Da Xue Xue Bao Yi Xue Ban
October 2007
Objective: To observe the effect of thrombin on the cytotoxicity of astrocytes injured by hypoxia/reoxygenation(H/R) and to explore its relationship with inducible nitric oxide synthase (iNOS).
Methods: Primary astrocytes were cultured in DMEM with 10% approximately 15% calf serum and divided into 6 groups: a control group, a Tm control group, an H/R group, a Tm+H/R group, a hirudin (HR) control group, and a Tm+HR+ H/R group. The cell damage and viability were detected by the 3-(4, 5-di-methyl-thazol-2-yl)-2, 5 diphenyl-tetrazol-iumbromide (MTT) conversion method.
Colloids Surf B Biointerfaces
February 2008
Hepatocyte growth factor (HGF) has been revealed to exert multipotent activities on a variety of cells. In this study, we investigated whether HGF had a direct neuroprotection on cultured cerebral cortical neurons subjected to hypoxia/reoxygenation (H/R) and explored the intracellular signalings mediated the effects. The decrease in cell viability and increase in number of apoptotic cells resulting from H/R were significantly prevented by HGF pre-treatment.
View Article and Find Full Text PDFObjective: To assess the effects of treatment of Amanita mushroom poisoning with Glossy anoderma Decoction (, GGD).
Methods: Twelve patients with acute Amanita mushroom poisoning received conventional treatment (penicillin and reduced glutathione) combined with oral administration of GGD (treated group), which was prepared out of 200 g Glossy ganoderma decocted in water to 600 mL, and 200 ml was given once, three times a day for 7 successive days; while conventional treatment alone was given to the other 11 patients assigned to the control group. The therapeutic efficacy and changes in serum levels of total bilirubin (TBil), bile acids (BA), alanine transaminase (ALT), and aspartate transaminase (AST) activities in the two groups were compared.
Zhong Nan Da Xue Xue Bao Yi Xue Ban
June 2005
Objective: To explore the effect of hepatocyte growth factor (HGF) on oxygen-glucose deprived injury and apoptosis of astrocytes.
Methods: The injury of primary cultured rat cerebral cortical astrocytes was induced by oxygen-glucose deprivation. Astrocytes were treated with HGF at various final concentrations of 20 - 100 ng/mL.
Zhongguo Zhong Xi Yi Jie He Za Zhi
April 2003
Objective: To observe the effect of Ganoderma lucidum decoction in treating Russula subnigricans poisoning (RSP) patients.
Methods: The 14 patients of RSP in the treated group were treated with GLD (GLD, one dose was prepared by 100 g of Ganoderma lucidum decocted with water to 600 ml), on the base of conventional treatment, and 11 patients received conventional therapy in the previous year were taken as control. The clinical efficacy and parameters in them were compared, including the urine N-acetyl-D-glucosaminidase (NAG, which reflects the injury of kidney), the red blood cell and protein in urine, the alanine transaminase (ALT, which reflects the injury of liver), and the aspartate aminotransferase (AST, which reflects the injury of heart).