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Study Of DiGan Oral Liquid On Mechanism Of Action For Leulcopenia In Micelnjured By Radiation And Chemistry

Posted on:2003-09-23Degree:DoctorType:Dissertation
Country:ChinaCandidate:D C HeFull Text:PDF
GTID:1104360062995219Subject:Chinese medical science
Abstract/Summary:PDF Full Text Request
Objective Models of mice with leukopenia were made by radiation and chemical drug.The changes were observed as indexes, including circulating white blood cell (WBC) count, SICAM-1, adhesion molecule in marrow hematopoietic system, CD45 modulator genes of cell cycle and apoptosis, the structure of spleen tissue and apoptosis correlative gene expressing, etc.To provide test data and theoretical direct for clinical treatment and new drug explorsion,we investigate the mechanism of Chinese medical compound prescriptption (CMCP)-DG Digian oral Liquid(DG) promoting hematopoietic restoration and enhancing immunological function.Methods e made the leucopenic model with whole body X ray of 6.0 GY dose irradiation by linear accelerator and 3-day continous abdominal abministfation with CTXlOOmg/kg/d.Allocation of animal:There were blank control group.model group, low-dose DG group(the equivalent of five times adult's dose), high-dose DG grour)(the equivalent of ten times adult's dose),positive control group [the former Was batylialcohol(BLC) group,the later was Fu Fang E Jiao Jiang(FEJ)group].The two groups were treated after building .Each index of the radiative injury group was detected on the ninth day after 8-day treat .The indexes of chemical injury group were detected on the ninth day after 8-day treat.(2)The circulating white Blood cell count was routine detected, and the serum SCAM-1 with EliSA, the VGAM-1 expressing of myeloid strotnal cell with immunohistochemical method, the stem cell CD4J with Flow cytometer (FCM), the marrow contents of DNA with ultraviolet spectrophotometry, the mRNA expressing of cyclinD, gene and apoptotic inhibitory and accelaratbr gene of karyocyte and spleen with hyvirdism in situ, the apoptotic rate of spleen tissue with Tunel. The morphological change of the spleen tissue was observed with light microscope and transmission electionmicroscope.We combined function and morphology and relatively analysised the mechanism of DG on injury due to radiation and chemistry for leukopenia.Results 1.Leucopenic model due to radiation. 〤irculating white blood cell count of model group reduced,but Serum SICAM-1 with immunologic functon increased. The marrow contents of DNA,CD45 antigen and VCAM-1 expressing lowered remarkablely in model growp. The mRNA expressing of bcl-2 and cyclinD, of Karyocyte lowered distinctly. The apoptotic rate of spleen tissue increased,as well as the mRNA of bax remarkablely.There were very remarkable difference among the above indexes(p<0.01). Lymphocyte reduced obviously;splenic lymph nodules atrophied;granulocyte and megalocaryocyte reduced seen on light microscope. On transmission electromicroscope, there were manyconcentrated nucleolus or necrotic cells and apoptotic bodies like half-moon shape. 〥ifferent dose of DG groups and Batyl alcohol (BL)group all could promote circulating leukocyte count and marrow contents of DNA, enhance the expressing of CD4S antigen and VCAM-1 and bcl-2 mRNA, lower serum contents of SICAM-land apoptotic rate of spleen tissue and mRNA' expressing of bax. The difference of the above indexes was significant(p<0.01). Between BLA group and model group, the effect of promoting cyclinDl expressing was not obvious(p>0.05). Morphologically: As to treatment groups,the structure of spleen tissue got better obviously; lymphocyte increase0.05). On enhancing white cell count, DG groups were superior to BLA group. 2.Leucopenic model with CTX. ?Circulating white blood cell model group count lowered abviously;serum SICAM-1 highered distinctly; both marrow contents of DNA and CD45 expressing remarkab...
Keywords/Search Tags:Leukopenia, DiGan Oral Liquid, Traditional Chinese medicine treatment, Adhesion molecule of mice, White cell antigen, Apoptotic gene cell cyclin
PDF Full Text Request
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