Biocompatibility of a newly developed ethylenediamine modified poly (DL-latic acid) (EMPLA) with osteoblasts was investigated by means of cell morphology and cell proliferation. Films of PLA and EMPLA were made by solvent casting. Osteoblasts obtained from crania of neonatal Wistar rats were cultured on surfaces of PLA and EMPLA, with glass as control. The cell morphology was observed by phase contrast microscope and the cell proliferation was determined by MTT assay. The morphology observations revealed that the osteoblasts cultured on EMPLA spread wider than those on PLA, and much more cells were confluent on EMPLA, compared to those on PLA and glass. The growth curves showed the osteoblasts on EMPLA grew faster than did those on PLA and glass. The results exhibited that the biocompatibility of EMPLA with osteoblasts is better than that of PLA and glass, which suggested wide applications of EMPLA in biomedical area, especially in tissue engineering.
Animals ; Animals, Newborn ; Biocompatible Materials ; chemistry ; pharmacology ; Cell Proliferation ; Cells, Cultured ; Ethylenediamines ; chemistry ; pharmacology ; Lactic Acid ; chemistry ; pharmacology ; Materials Testing ; methods ; Osteoblasts ; cytology ; Polyesters ; Polymers ; chemistry ; pharmacology ; Rats ; Rats, Wistar

Estrogen replacement therapy in postmenopausal women may reduce the risk of Alzheimer's disease, possibly by ameliorating neuronal degeneration. In the present study, we examined the neuroprotective spectrum of estrogen against excitotoxicity, oxidative stress, and serum-deprivation-induced apoptosis of neurons in mouse cortical cultures. 17beta-estradiol as well as 17alpha-estradiol and estrone attenuated oxidative neuronal death induced by 24 hr exposure to 100 microM FeCl2, excitotoxic neuronal death induced by 24 hr of exposure to 30 microM N-methyl-D-aspartate (NMDA) and serum-deprivation induced neuronal apoptosis. Furthermore, estradiol attenuated neuronal death induced by Abeta25-35. However, all these neuroprotective effects were mediated by the anti-oxidative action of estrogens. When oxidative stress was blocked by an antioxidant trolox, estrogens did not show any additional protection. Addition of a specific estrogen receptor antagonist ICI182,780 did not reverse the protection offered by estrogens. These findings suggest that high concentrations of estrogen protect against various neuronal injuries mainly by its anti-oxidative effects as previously shown by Behl et al. Our results do not support the view that classical estrogen receptors mediate neuroprotection.
Amyloid beta-Protein/pharmacology ; Animal ; Antioxidants/pharmacology* ; Antioxidants/metabolism ; Apoptosis/drug effects* ; Cells, Cultured ; Chelating Agents/pharmacology ; Chromans/pharmacology ; Estradiol/pharmacology ; Estrogens/pharmacology* ; Estrogens/metabolism ; Estrone/pharmacology ; Ethylenediamines/pharmacology ; Excitatory Amino Acid Agonists/pharmacology ; Ferric Compounds/pharmacology ; Lactate Dehydrogenase/analysis ; Mice ; N-Methylaspartate/pharmacology ; Neurons/metabolism ; Neurons/drug effects* ; Neurons/cytology ; Organ of Corti/cytology ; Peptide Fragments/pharmacology ; Staurosporine/pharmacology

Estrogen replacement therapy in postmenopausal women may reduce the risk of Alzheimer's disease, possibly by ameliorating neuronal degeneration. In the present study, we examined the neuroprotective spectrum of estrogen against excitotoxicity, oxidative stress, and serum-deprivation-induced apoptosis of neurons in mouse cortical cultures. 17beta-estradiol as well as 17alpha-estradiol and estrone attenuated oxidative neuronal death induced by 24 hr exposure to 100 microM FeCl2, excitotoxic neuronal death induced by 24 hr of exposure to 30 microM N-methyl-D-aspartate (NMDA) and serum-deprivation induced neuronal apoptosis. Furthermore, estradiol attenuated neuronal death induced by Abeta25-35. However, all these neuroprotective effects were mediated by the anti-oxidative action of estrogens. When oxidative stress was blocked by an antioxidant trolox, estrogens did not show any additional protection. Addition of a specific estrogen receptor antagonist ICI182,780 did not reverse the protection offered by estrogens. These findings suggest that high concentrations of estrogen protect against various neuronal injuries mainly by its anti-oxidative effects as previously shown by Behl et al. Our results do not support the view that classical estrogen receptors mediate neuroprotection.
Amyloid beta-Protein/pharmacology ; Animal ; Antioxidants/pharmacology* ; Antioxidants/metabolism ; Apoptosis/drug effects* ; Cells, Cultured ; Chelating Agents/pharmacology ; Chromans/pharmacology ; Estradiol/pharmacology ; Estrogens/pharmacology* ; Estrogens/metabolism ; Estrone/pharmacology ; Ethylenediamines/pharmacology ; Excitatory Amino Acid Agonists/pharmacology ; Ferric Compounds/pharmacology ; Lactate Dehydrogenase/analysis ; Mice ; N-Methylaspartate/pharmacology ; Neurons/metabolism ; Neurons/drug effects* ; Neurons/cytology ; Organ of Corti/cytology ; Peptide Fragments/pharmacology ; Staurosporine/pharmacology

Human immunodeficiency virus type 1 (HIV-1) viral infectivity factor (Vif), one of the accessory proteins, which is a small basic phosphoprotein, is essential for viral replication and pathogenesis. The best well-characterized function of Vif is its ability to neutralize the host cell antiviral factor, apolipoprotein B mRNA editing enzyme catalytic polypeptide like 3G (APOBEC3G), which makes the viral particles more infective. In addition, Vif can regulate the reverse transcription and the advanced stage of replication of the virus particle, as well as induce the termination of cell cycle at G2 stage and so on. The designed drug aimed directly at Vif can efficiently block the maturation and infectivity of HIV-1. In this review, the structure, function and especially the related inhibitors of Vif are reviewed.
APOBEC-3G Deaminase ; Amino Acid Sequence ; Anti-HIV Agents ; pharmacology ; Cytidine Deaminase ; metabolism ; Ethylenediamines ; pharmacology ; HIV-1 ; physiology ; Humans ; Reverse Transcription ; Virus Replication ; vif Gene Products, Human Immunodeficiency Virus ; antagonists & inhibitors ; genetics ; metabolism ; physiology