Objective:To explore the effect of ligustrazine on CD34 antigen expression of bone marrow cells in immune-induced aplastic anemia（AA）mice.Methods:The model of immune aplastic anemia mice was in duced by means of 6.0...Objective:To explore the effect of ligustrazine on CD34 antigen expression of bone marrow cells in immune-induced aplastic anemia（AA）mice.Methods:The model of immune aplastic anemia mice was in duced by means of 6.0GY60γ-rayirr adi at ion and lym phocyte infusion through tail vein.Immuneinduce dAA micewere divided into 3 groups:thenormal group,the AA control group and the ligustrazine group.Miceof the ligustrazine group were fed by 4 mg of ligustrazine in jecti on twicea day bygastro gavage.On the 10 thday,CD34 an tigen expression intensity of bone marrow cell membrane was measured by flowcy tometer an alysis system.Results:CD34 antigen expressionin tensity of ligustrazine group was 77.6±6.5,with no statistic difference from that in normal group（80.0±2.6),while that of the control group was muchhigher（68.6±4.5,P＜0.05).Conclusion:Ligustrazine could promote proliferation of stem and progenitor cell of AA mice through in fluencing on bone marrowmicro-environment so as to increase the CD34antigen expression of bone marrow cells.展开更多
Immunologically mediated aplastic anemia in mice were used as animal models to study the the curative effect of Zaizhang-Ⅰin term of the changes of two pathogenetic aspects in aplastic mice,namely the defciency of he...Immunologically mediated aplastic anemia in mice were used as animal models to study the the curative effect of Zaizhang-Ⅰin term of the changes of two pathogenetic aspects in aplastic mice,namely the defciency of hematopoietic stem cells and the disturbance of immunology. Our results demonstrated that in aplastic mice, after treatment by Zaizhang-Ⅰ,the loss of mature hematopoietice cells (WBC, RBC, Plt) were reduced, and marrow cellular cytosis,and their clinical findings were improved, indicating a partial remission. The present data show that its curative mechanism lies in the action of promoting the recovery of colony forming unit-spleen (CFU-S) and reversing immunologically-induced plasma colony forming unit granulocyte/macrophage (CFU-GM ) inhibitory activity. Natural killer cells activity (Nka) and interleukin-2 tumor necrosis factors (TNF) were also examined to further understand the mechanism by which Zaizhang-Ⅰreverse plasma hematopoietic activity.展开更多
The kidneys and the blood system mutually exert influence in maintaining homeostasis in the body. Because the kidneys control erythropoiesis by producing erythropoietin and by supporting hematopoiesis, anemia is assoc...The kidneys and the blood system mutually exert influence in maintaining homeostasis in the body. Because the kidneys control erythropoiesis by producing erythropoietin and by supporting hematopoiesis, anemia is associated with kidney diseases. Anemia is the most prevalent genetic disorder, and it is caused by a deficiency of glucose 6-phosphate dehydrogenase(G6PD), for which sulfhydryl oxidation due to an insufficient supply of NADPH is a likely direct cause. Elevated reactive oxygen species(ROS) result in the sulfhydryl oxidation and hence are another potential cause for anemia. ROS are elevated in red blood cells(RBCs) under superoxide dismutase(SOD1) deficiency in C57BL/6 mice. SOD1 deficient mice exhibit characteristics similar to autoimmune hemolytic anemia(AIHA) and systemic lupus erythematosus(SLE) at the gerontic stage. An examination of AIHA-prone New Zealand Black(NZB) mice, which have normal SOD1 and G6 PD genes, indicated that ROS levels in RBCs are originally high and further elevated during aging. Transgenic overexpression of human SOD1 in erythroid cells effectively suppresses ROS elevation and ameliorates AIHA symptoms such as elevated anti-RBC antibodies and premature death in NZB mice. These results support the hypothesis that names oxidative stress as a risk factor for AIHA and other autoimmune diseases such as SLE. Herein we discuss the association between oxidative stress and SLE pathogenesis based mainly on the genetic and phenotypic characteristics of NZB and New Zealand white mice and provide insight into the mechanism of SLE pathogenesis.展开更多
文摘Objective:To explore the effect of ligustrazine on CD34 antigen expression of bone marrow cells in immune-induced aplastic anemia（AA）mice.Methods:The model of immune aplastic anemia mice was in duced by means of 6.0GY60γ-rayirr adi at ion and lym phocyte infusion through tail vein.Immuneinduce dAA micewere divided into 3 groups:thenormal group,the AA control group and the ligustrazine group.Miceof the ligustrazine group were fed by 4 mg of ligustrazine in jecti on twicea day bygastro gavage.On the 10 thday,CD34 an tigen expression intensity of bone marrow cell membrane was measured by flowcy tometer an alysis system.Results:CD34 antigen expressionin tensity of ligustrazine group was 77.6±6.5,with no statistic difference from that in normal group（80.0±2.6),while that of the control group was muchhigher（68.6±4.5,P＜0.05).Conclusion:Ligustrazine could promote proliferation of stem and progenitor cell of AA mice through in fluencing on bone marrowmicro-environment so as to increase the CD34antigen expression of bone marrow cells.
文摘Immunologically mediated aplastic anemia in mice were used as animal models to study the the curative effect of Zaizhang-Ⅰin term of the changes of two pathogenetic aspects in aplastic mice,namely the defciency of hematopoietic stem cells and the disturbance of immunology. Our results demonstrated that in aplastic mice, after treatment by Zaizhang-Ⅰ,the loss of mature hematopoietice cells (WBC, RBC, Plt) were reduced, and marrow cellular cytosis,and their clinical findings were improved, indicating a partial remission. The present data show that its curative mechanism lies in the action of promoting the recovery of colony forming unit-spleen (CFU-S) and reversing immunologically-induced plasma colony forming unit granulocyte/macrophage (CFU-GM ) inhibitory activity. Natural killer cells activity (Nka) and interleukin-2 tumor necrosis factors (TNF) were also examined to further understand the mechanism by which Zaizhang-Ⅰreverse plasma hematopoietic activity.
基金Supported by The Strategic Young Researcher Overseas Visits Program for Accelerating Brain Circulation from the Japan Society for the Promotion of Sciences
文摘The kidneys and the blood system mutually exert influence in maintaining homeostasis in the body. Because the kidneys control erythropoiesis by producing erythropoietin and by supporting hematopoiesis, anemia is associated with kidney diseases. Anemia is the most prevalent genetic disorder, and it is caused by a deficiency of glucose 6-phosphate dehydrogenase(G6PD), for which sulfhydryl oxidation due to an insufficient supply of NADPH is a likely direct cause. Elevated reactive oxygen species(ROS) result in the sulfhydryl oxidation and hence are another potential cause for anemia. ROS are elevated in red blood cells(RBCs) under superoxide dismutase(SOD1) deficiency in C57BL/6 mice. SOD1 deficient mice exhibit characteristics similar to autoimmune hemolytic anemia(AIHA) and systemic lupus erythematosus(SLE) at the gerontic stage. An examination of AIHA-prone New Zealand Black(NZB) mice, which have normal SOD1 and G6 PD genes, indicated that ROS levels in RBCs are originally high and further elevated during aging. Transgenic overexpression of human SOD1 in erythroid cells effectively suppresses ROS elevation and ameliorates AIHA symptoms such as elevated anti-RBC antibodies and premature death in NZB mice. These results support the hypothesis that names oxidative stress as a risk factor for AIHA and other autoimmune diseases such as SLE. Herein we discuss the association between oxidative stress and SLE pathogenesis based mainly on the genetic and phenotypic characteristics of NZB and New Zealand white mice and provide insight into the mechanism of SLE pathogenesis.
基金the National Natural Science Foundation of China (No. 81202839)the National Natural Science Foundation of China (No. 81774080)+1 种基金the “Taishan Scholar” Project Special Fundthe Study Abroad Funding by the Shandong health science and technology association and the Affiliated Hospital of Shandong University of Traditional Chinese Medicine.
