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Objective To study the inhibitory effect of curcumin on the proliferation,migration and invasion of non-small cell lung cancer cell A549,and to discuss further if it is closely related to the expression of c-Jun N-terminal kinase (JNK) and relative protein p38.Methods A549 cells were cultured by conventional method,and then treated with different concentration of curcumin (10,20,40,80 μmol · L-1).The proliferation,migration and invasion of A549 cells were measured by real-time cellular analysis (RTCA).The expression levels of JNK,p-JNK,p38 and P-p38 were detected by real-time PCR and Western blotting.Results Curcumin showed an antiproliferation effect against A549 cells with IC50 =40 μmol · L-1,and curcumin exhibited obviously inhibitory effect on the migration and invasion of A549 cells.Additionally,compared with control group,curcumin suppressed the expression of JNK and p38 at the gene level,and significantly inhibited the expression of JNK,P-JNK,p38 and p38 (P＜0.05) at the protein level.Conclusion These results demonstrated that curcumin can inhibit the proliferation,migration and invasion of A549 cells via reducing the level of JNK,p38 phosphorylation,and blocking JNK signal transduction pathway.
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Objective To investigate the influence of curcumin and its analogue H8 on glucose and lipid metabolism disorder in db/db mice. Methods The type 2 diabetes mouse model (db/db mice) was intragastrically administrated with curcumin and analogue H8 for 8 weeks.The blood biochemical indexes were measured.The expression of PEPCK and G6Pase mRNA was detected by real-time PCR in liver tissues.The expression of PEPCK and G6Pase protein was detected by Western blotting. Results Curcumin analogue H8 reduced blood glucose and lipids in db/db mice (P<0.01) and improved liver function related enzymes significantly.The levels of PEPCK and G6Pase mRNA in db/db mice were significantly decreased (P<0.01) and the expression levels of PEPCK and G6Pase protein were significantly decreased(P<0.01). Conclusion Curcumin analogue H8 improves the glucose and lipid metabolism disorder in db/db mice,and it is related to inhibiting the expression of PEPCK and G6Pase gene and protein.
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Objective To evaluate the inhibitory effect of asiaticoside on bleomycin-induced skin cicatrization. Methods Thirty male C57BL/6 mice were randomly divided into three groups:negative control group,model control group,and asiaticoside group,ten in each group.In model control group and asiaticoside group,1 mg·mL-1bleomycin was subcutaneously injected into the dorsal skin of mice every day;4 h later,1 mL 0.9% sodium chloride solution 1 mL asiaticoside(20 mg·mL-1) was injected into the lesion skin in the model control group and the asiaticoside group,respectively.In the negative control group, the same volume of 0.9% sodium chloride solution was subcutaneously injected into the dorsal skin of the mice at the two time points every day.After 21 days,skin specimens were harvested to observe the histomorphology and detect myofibroblast proliferation and expression of inflammatory factors. Results The skin scar was significantly attenuated in the asiaticoside group as compared with the model control group,and the dermal thickness measured exhibited a gradual decrease in asiaticoside group.The expression of α-antismooth muscle antisbidy and infiltration of inflammatory cells were significantly lower in the asiaticoside group than in the model control group. Conclusion Asiaticoside inhibits the development of skin scar of mice by regulating proliferation and differentiation of myofibroblasts and down-regulating inflammatory cells.
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BACKGROUND:Numerous studies have shown that mesenchymal stem cel s (MSCs) can effectively attenuate the fibrosis of damaged heart, lung and kidney by secreting various bioactive factors. OBJECTIVE:To evaluate the anti-fibrotic therapeutic potential of bone marrow MSCs conditioned media in vitro. METHODS:Normal fibroblasts and hypertrophic scar fibroblasts were treated with bone marrow MSCs conditioned media, then transforming growth factor-βand col agen production were analyzed by ELISA, and mRNA expression level of Smad7 and hydroxyproline content were detected by RT-PCR and colorimetry, respectively. RESULTS AND CONCLUSION:Bone marrow MSCs conditioned media significantly inhibited the production of both transforming growth factor-βand col agen in hypertrophic scar fibroblasts (P<0. 01), and up-regulated the mRNA expression level of Smad7 (P<0. 01), a major inhibitory regulator in the SMAD family. However, the normal fibroblasts were scarcely influenced by bone marrow MSCs conditioned media. These findings indicate that bone marrow MSCs conditioned media is considered a promising candidate for the treatment of hypertrophic scars, which may provide new theoretical supports to reduce cutaneous scarring.
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BACKGROUND:Mesenchymal stem celltransplantation promoted skin repair in trauma via various regulatory mechanisms and inhibited scar formation. At present, many scholars believed that bioactive factors secreted by mesenchymal stem cells played an important role. OBJECTIVE:To investigate the effects of bone marrow mesenchymal stem cellconditioned medium on the proliferation and col agen synthesis of hypertrophic scar fibroblasts. METHODS:Human bone marrow mesenchymal stem cells and hypertrophic scar fibroblasts were isolated and cultured, and bone marrow mesenchymal stem cellconditioned medium was prepared. Hypertrophic scar fibroblasts were cultured in vitro with 12, 24, and 48 hour-col ected conditioned medium for 24 hours, which was compared with blank control group. The proliferation of cells was determined by CCK-8. Type I and type III col agen expression in hypertrophic scar fibroblasts was detected using real-time PCR. RESULTS AND CONCLUSION:Compared with the blank control group, 24 and 48 hour-col ected conditioned medium significantly inhibited the proliferation of hypertrophic scar fibroblasts (P<0.01), and also suppressed col agen synthesis of hypertrophic scar fibroblasts (P<0.01). Results suggested that bone marrow mesenchymal stem cellconditioned medium inhibited the proliferation and col agen synthesis of hypertrophic scar fibroblasts by secreting anti-fibrotic bioactive factors, which may provide new theoretical supports for celltherapy to reduce cutaneous scarring.
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Objective To explore the mechanism and effects of basic fibroblast growth factor( bFGF)on skin wound healing. Methods Fibroblasts( FB)were isolated from normal skin and hypertrophic scar and cultivated by direct adherence method. FB were then treated with different concentrations of bFGF(0,0. 1,1,10,100,1 000 ng·mL-1 )and cultivated with serum-free medium for 72 hours. The proliferation and apoptosis of FB in each group were detected by cell counting and trypan blue staining. Content and gene expression of typeⅠand type Ⅲ collagen and fibronectin were determined by ELISA and RT-PCR,respectively. Results bFGF promoted the proliferation of FB at low concentrations promoted apoptosis of FB at higher concentrations. The proliferation of FB from hypertrophic scar was slower than that from the normal skin. bFGF significantly inhibited type Ⅰ collagen production from hypertrophic scar FB but not from the normal skin. Moreover,bFGF up-regulated fibronectin expression in the normal fibroblasts,but not in the hypertrophic scar. No change in type Ⅲ collagen expression and production was observed in FB from either source. Conclusion bFGF has differential effects and mechanisms on FB of the normal skin and hypertrophic scar,suggesting that bFGF may play a role in early phase of skin wound healing and scar formation.
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Purpose To examine the regulatory effect of recombinant human fibroblast growth factor-21 on the expression of liver X receptor α and glucose transporter protein 1 in the type 2 diabetes mellitus rats.Methods The rat models of type 2 diabetic mellitus were divided into four groups at random, ic. rhFGF-21 every day, after eight weeks of these treatment, Inspect the fasting blood glucose (FBG), fructosamine(FA), triglyceride(TG), T-cholesterol(TC), high density lipoprotein cholesterol(HDL-C) and low density lipoprotein cholesterol(LDL-C) of these rats, then detecting the mRNA expression of LXRα and GLUT1 by RT-PCR.Results (1) rhFGF-21 can reduce blood glucose steadily to near normal levels in diabetic rats. (2) The expression of LXRα and GLUT1 level was significantly higher in the rhFGF-21 treatment group than that in the model group. (3) rhFGF-21 megadoses and middle doses decreased FA, TG, TC,and LDL-C and elevated HDL-C.Conclusion rhFGF-21 could regulate the mRNA expression of LXRα and GLUT1 in diabetes rats, increase basal level glucose transport, then reduce blood glucose, improve lipid metabolize dysfunction.