RESUMEN
This study examined the effect of astilbin on the proliferation of rat aortic smooth muscle cells (RASMCs) induced by angiotensin Ⅱ (Ang Ⅱ) and explored the possible mechanisms.Cell proliferation model of RASMCs was induced by treatmente with Ang Ⅱ.Cells were randomly divided to 8 groups.Normally cultured VSMCs serves as blank control group; in Ang Ⅱ model group,cells were treated with AngⅡ at 10-7 mol/L; in three astilbin groups,cells were treated with 10,15,30 mg/L of astilbin; in three Ang Ⅱ +astilbin groups,cells were treated with Ang Ⅱ (at 1 0-7 mol/L) and astilbin at 10,15,30 mg/L.Cell proliferation ability was detected by MTT method and the cell cycles and proliferation index were flow cytometrically determined.The expression of c-myc mRNA was assessed by using reverse transcription polymerase chain reaction (RT-PCR),and the expression of NF-κB in RASMCs was immunocytochemically observed.Our results showed that MTT metabolism in RASMCs in the basic and Angll stimulated situation was inhibited by astilbin,and the cells numbers of G0/G1 phase were increased and that of G2/S phase were decreased markedly.Not only highly expression of c-myc gene stimulated by Ang Ⅱ could be inhibited by Astilbin significantly,but also the expression of NF-κB protein can be down regulated by Astilbin.We are led to conclude that astilbin astilbin can inhibit the Ang Ⅱ -mediated proliferation of RASMCs by blocking the transition of RASMCs from Go/G1 phase to S phase and by down-regulating the expression of NF-κB,c-mvc gene.
RESUMEN
This study explored the possibility that the components in melanoma cytoplasm induce murine BMSCs transformation and expression of Melan-A by morphologically observing the changes of BMSCs and immunocytochemically detecting Melan-A in the cells after culturing BMSCs in medium containing melanoma cytoplasm components (MCC).MCC of B16 melanoma cells was prepared and BMSCs were cultured and induced by adding the MCC into culture medium.The cells were morphologically observed and Melan-A was immunohistochemically detected to confirm BMSCs transformation.MCC-induced BMSCs underwent morphological changes.A number of melanin granules appeared in the cytoplasm of the cells and some were released into surrounding areas.Several cells that might come from one cell formed a cluster,and their granules,together with those secreted by other induced BMSCs,formed a so-called “sphere-formed structure”.The induced BMSCs expressed Melan-A.We are led to conclude that there might be some factors in the cytoplasm of melanoma cells that might induce BMSCs transformation toward melanogenic cell,or even melanoma.
RESUMEN
The inhibitory effect of astilbin on transplant arteriosclerosis in murine model of thoracic aorta transplantation was examined.Model of rat thoracic aorta transplantation was established.Ninety rats were divided into three groups.In isograft group,the thoracic aorta of Brown Norway (BN) rat was anastomosed with the abdominal aorta of another BN rat.In allograft group,the thoracic aorta of BN rat was anastomosed with the abdominal aorta of Lewis rat.In astilbin group,the rats receiving allo-transplantation were given astiibin 5 mg/kg per day for a time of 28 days.The donor thoracic aorta and the recipient abdominal aorta were anastomosed by means of a polyethylene cannula (inner diameter:1.5 mm,length:3 mm length).The grafts were histologically examined for structural changes.The areas of arterial lumen and endatrium were calculated.Our results showed that,in the allograft group,28 days after aliografting,conspicuous proliferation of smooth muscles and infiltration with a great number of inflammatory cells were found in the tunica intima and tunica media.Astilbin significantly inhibited the proliferation of smooth muscles and ameliorated the infiltration of inflammatory cells thereyby prevent against the development of transplant arteriosclerosis.It is concluded that asltilbin can effectively prevent the development of arteriosclerosis in allotrausplant by inhibiting the proliferation of smooth muscles and inhibit the proliferation of smooth muscles in tunica of intima and media and reducing infiltration of the inflammatory cells.
RESUMEN
Cigarette smoking is intimately related with the development of chronic obstructive pulmonary diseases, and alveolar epithelium is a major target for the exposure of cigarette smoke ex- tract. In order to investigate the effect of cigarette smoke extract on the proliferation of alveolar epithelial cell type Ⅱand its relationship with P21WAF1, the alveolar epithelial type Ⅱ cell line (A549) cells were chosen as surrogate cells to represent alveolar epithelial type Ⅱ cells. MTT assay was used to detect cell viability after interfered with different concentrations of cigarette smoke ex-tract. It was observed cigarette smoke extract inhibited the growth of A549 cells in a dose- and time-dependent manner. The morphological changes, involving the condensation and margination of nuclear chromatin, even karyorrhexis, were observed by both Hoechst staining and electronic mi-croscopy. Flow cytometry analysis demonstrated the increased cell percentages in G1 and subG1phases after the cells were incubated with cigarette smoke extract. The expression of p21WAF1 protein and mRNA was also significantly increased as detected by the methods of Western blot or reverse transcription-polymerase chain reaction respectively. In conclusion, cigarette smoke extract inhibits the proliferation of alveolar epithelial cell type Ⅱ and blocks them in G1/S phase. The intracellular accumulation of P21WAF1 may be one of the mechanisms which contribute to cigarette smoke ex-tract-induced inhibition of cell proliferation.