1、a Case Of Lichen Planus Induced By Imatinib Mesylate 2、influence Of Long Term Arsenite Stimulation On HaCaT Cell Proliferation, Apoptosis And Ginsenoside Rg3’s Intervention Effects Of Arsenic On HaCaT Cells

Background: Lichen planus is a common chronic inflammatory disease in the skin, hair follicles, mucosal, finger(toe) of unknown cause.Lesions is usually itchy flat polygonal purple papules, with characteristic pathological changes.Erasmus Wilson reported and named LP in 1869.The exact causes are unknown,including autoimmune, genetic,infectious, mental, drugs, metabolic and endocrine doctrine.The common drug cause of lichen planus include sulfa,streptomycin, penicillamine, gold or mercury preparations,chlorpropamide, tolbutamide and so on.Imatinib mesylate(IM) is the first-line treatment for chronic myeloid leukemia(CML) and Gastrointestinal intestine stromal tumor(GIST).Imatinib mesylate induced lichen planus eruption is rare.There are reports in the literature in recent years.Most reports agree that lichen planus eruption caused imatinib mesylate is self-limiting.It is not necessary to stop the drug.Case presentation: A 71-year-old male had whole body multiple itchy flat polygonal purple papules for five months.Patients because “ small intestinal stromal tumor ”underwent tumor resection and radiofrequency ablation of liver metastases six months ago.During not taking other drugs.He noticed that back of hands appeared purple papules, plaques with itching about two weeks later.Used topical corticosteroids ointment have poor treatment,gradually expand to the whole body.Histological examination of the forearm show hyperkeratosis,granular layer thickening,irregularacanthosis hypertrophy,the epidermis axon terminal hyperplasia of serrated, basal cell liquefaction degeneration,banded inflammatory cells mainly Lymphocytes were infiltrated in the superficial dermis.Diagnosis:Lichen planus.Conclusion:1.Imatinib mesylate induced lichen planus is rare in clinical, should be paid attention;2.Imatinib mesylate induced lichen planus is severein exposed parts,with light-sensitive,Should pay attention to avoid to expose to the sun;Background:Arsenic(As) is both a human carcinogen and an effective anti-cancer drugs.The common form of skin cancer induced by arsenic exposure is Bowen’s disease(squamous cell carcinoma in situ), basal cell carcinoma and invasive squamous cell carcinoma of the skin black spot disease symptoms are diffuse change, leucomelanosis and keratosis. Ha Ca T cells are immortalized cutin cell lines, which has no tumor characteristics. Continued exposure to low concentrations of arsenic make Ha Ca T cells acquire malignant phenotype.Arsenic-induced skin cancer cell research model has been already recognized. Studies have found that arsenic stimulation can promote Ha Ca T cell proliferation,Inhibition of Ha Ca T cells apoptosis.Prompt apoptosis resistance may be one of arsenic make Ha Ca T cells to malignant transformation mechanism.Ginseng is a kind of Chinese herbal medicine.Ginsenoside Rg3 trace from red ginseng extract the active chemical components. The exact molecular mechanism of ginsenoside Rg3 is unclear, experiments showed that ginsenosides Rg3 can kill a variety of potent cancer cells, it is possible to effectively inhibit tumor cell proliferation and metastasis, inducing the mammalian cell cycle arrest and apoptosis. At present the ginseng saponins Rg3 intervention arsenic induce Ha Ca T cells apoptosis induced malignant transformation.It is not reported.In this experiment, we prepared the arsenic lead Ha Ca T cells to malignant phenotype.Analysis of arsenic stimulation at different times,which Ha Ca T cell proliferation, cell cycle and apoptosis.Clear and definite that long-term exposure to arsenic effects on proliferation and apoptosis of Ha Ca T cell.On this basis,use flowcytometry to test different concentrations of ginsenoside Rg3 intervention on arsenic Ha Ca T cells.Explore the prospects of ginsenoside Rg3 used to relieve skin damage caused by chronic arsenic poisoning.ObjectiveTo study the long-term low concentrations of arsenic stimulation Ha Ca T cell proliferation, cell cycle, apoptosis and ginsenoside Rg3 intervention on arsenic culture Ha Ca T cells.MethodsHa Ca T cells to low concentrations of 100 n M arsenic as the cells were collected after 22 weeks of continuous culture. The cell viability and proliferative activity of Ha Cat normal cell treat ginsenosides Rg3 in the concentration range of(0-200) μg / ml,evaluated with Cell Counting kit-8(CCK8) assay.The cell viability activity and Cytotoxicity of low concentrations of arsenic culture Ha Ca T cells treated with ginsenosides Rg3 in the concentration range of(0-100) μg / ml, evaluated with Cell Counting kit-8(CCK8) assay.The apoptosis of low concentrations of arsenic culture Ha Ca T cells(0 weeks, 22 weeks) treated with ginsenosides Rg3 in the concentration of(5,10,20,40,80) μg / ml was quantified by flow cytometry.ResultGinsenosides Rg3 in the concentration range of(0-100) μg / ml on the normal Ha Ca T cells were not significantly apoptosis(P>0.05);Cell cycle analysis showed that to low doses of arsenic exposed Ha Ca T cells increased the percentage of cells in G2-phase and(G2+S)phase contrast of normal Ha Ca T cells; Long-term exposure to low doses of arsenic Ha Ca T cells less apoptosis than normal Ha Ca T cells;Ginsenoside Rg3 induced Long-term exposed to low doses of arsenic Ha Ca T cells with growth inhibition and apoptosis,a positive correlation with the degree of apoptosis and drug concentration.Conclusions:1.Low-dose arsenic continuous culture Ha Ca T cell can promote proliferation.2.Low-dose arsenic constant stimulation inhibits Ha Ca T cell apoptosis.2. Ginsenoside Rg3 inhibit arsenic stimulate Ha Ca T cells caused by excessive growth.3.Ginsenoside Rg3 can intervene arsenic induced apoptosis resistance.