Correlation Between BFGF And Platelet Abnormalities In Mice

Objective: This study aims to explore the relationship between basic fibroblast growth factor(b FGF)and mouse platelet abnormalities,as well as the expression level of interleukin-6 in platelet abnormalities,and to evaluate the effect of b FGF antibody on thrombocytosis,in order to better understand the pathogenesis of platelet abnormalities and provide scientific basis for clinical treatment.Methods: Fifteen male Balb /c mice were randomly divided into PBS buffer control group(Group A,n=5),b FGF experimental group(Group B,n=5),and b FGF antibody neutralization group(Group C,n=5)after adaptive feeding in an animal laboratory for one week.Groups B and C were given b FGF for four consecutive days,while Group A was given the same dose of PBS buffer.The above methods of administration were all administered intraperitoneally(once a day).Before 120 minutes of administration on the first and third days of the experiment,A Mice in groups B and C were administered with Mouse Ig G,Mouse Ig G,and b FGF antibodies,respectively.After the completion of the last injection,the number of peripheral blood cells and bone marrow pathology of the three groups of mice were measured every 24 hours,and the concentration of serum interleukin-6(IL-6)was measured by ELISA.Then,a comparison between the mouse platelet count and IL-6 level was performed,and P<0.05 was considered statistically significant.Results:The experiment showed that mice treated with b FGF could increase the number of platelets in the circulating blood,but the morphology of platelets did not change.The corresponding mice treated with specific b FGF antibodies could neutralize and antagonize the b FGF induced platelet increase,manifested as a decrease in the number of circulating platelets in the mice compared to before;There is a correlation between platelet count and IL-6 levels in mice(r=0.633,P<0.05).Bone marrow histology showed that the bone marrow of b FGF experimental group showed megakaryocyte proliferation,increased volume,and neovascularization.There was no significant change in group B and group C.Conclusion: 1.b FGF is an important mediator causing thrombocytosis,but platelet morphology remains unchanged during the increase in count.The use of b FGF antibodies can counteract the effect of b FGF induced thrombocytosis.2.There is a correlation between platelet count and serum IL-6 levels.3.The use of b FGF cytokines will cause the megakaryocyte of bone marrow to become larger and form new blood vessels.