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1.
AIM:To induce lymphoid stem cells and/or T-cell precursors to differentiate into functional mature T lymphocyte, and to increase the surface marker of T lymphocytes such as CD3+, while embryonic stem(ES) cells differentiated into hematopoietic stem/progenitor cells(HSPCs) in vitro. When they were injected into lethally irradiated mice, these differentiated cells had the advantage in immune reconstitution. METHODS:Embryonic stem cells formed embryoid bodies(EBs) in the medium containing methycellulose, hematopoietic growth factors(HGFs) was added to the culture system on the 6th day, thymopeptide was added at the same time. Flow cytometry were performed to detect the surface marker CD34+ and CD3+ of the differentiated cells. Finally the differentiated cells were injected into lethally irradiated mice, 60 days later, the incidence rate of graft versus host disease(GVHD) was taken as the mark of cell mediated immunity, PCR was performed to detect the sex determining region of the Y-chromosome(Sry) in bone marrow cells and spleen cells of the survival host female mice. RESULTS:The percentage of CD3+ T lymphocytes was 10.52% and the incidence rate of GVHD was 0% on the 13th day, but they respectively rose up to 22.93% and 100% if thymopeptide was added in the procedure of inducing ES cells to differentiate into HSPC in vitro. CONCLUSION:The quantity of CD3+ T lymphocytes increased in medium containing thymopeptide when ES cells differentiated into CD34+ HSPC.  相似文献   

2.
AIM: To observe the expression of Akt/GSK-3β/Snail signaling pathway-related molecules in cisplatin-resistant cell line A549/DDP mediated by transforming growth factor-β1 (TGF-β1), and to explore the association of Akt/GSK-3β/Snail signaling pathway with epithelial-mesenchymal transition (EMT). METHODS: The A549/DDP cells were divided into TGF-β1 (+) group, TGF-β1 (-) group and LY294002 group. The morphological changes of A549/DDP cells treated with TGF-β1 were observed under microscope. The protein expression of E-cadherin and N-cadherin was determined by the methods of immumofluorescence and Western blot. The protein levels of Akt, p-Akt, GSK-3β, p-GSK-3βSer9 and Snail were also detected by Western blot. RESULTS: The A549/DDP cells in TGF-β1 (+) group were dispersive, showed a spindle-like shape and developed pseudopodia. This transformation was conformed to classic EMT markers. Compared with TGF-β1 (-) group, the protein expression of E-cadherin in TGF-β1 (+) group was significantly decreased (P<0.05), and N-cadherin was significantly increased (P<0.05). The protein levels of p-Akt, p-GSK-3βSer9 and Snail were also significantly increased (P<0.05). Compared with TGF-β1 (+) group, the protein levels of p-Akt, p-GSK-3βSer9 and Snail were significantly decreased in LY294002 group (P<0.05). No difference of Akt and GSK-3β expression between TGF-β1 (-) group and TGF-β1 (+) group was observed. CONCLUSION: The mechanism of EMT in A549/DDP cells might be related to Akt/GSK-3β/Snail signaling pathway activated by TGF-β1.  相似文献   

3.
AIM: To investigate whether gap junction participates in transforming growth factor β1(TGF-β1)-induced proliferation of spontaneous hypertensive rat (SHR) vascular smooth muscle cells (VSMCs). METHODS: The thoracic aorta of the rats were sampled. The primary SHR VSMCs were isolated and cultured in vitro. The cells were divided into 4 groups: control group, TGF-β1 group,18α-glycyrrhetinic acid(18α-GA) group and TGF-β1+18α-GA group. The proliferation of SHR VSMCs was observed by the methods of MTT and flow cytometry. The protein expression and co-localization of connexin(Cx)43 and Cx40 in SHR VSMCs were detected by immunofluorescence staining. The protein levels of Cx43 and Cx40 in the cells were also measured by Western blotting. The method of molecular dye transfer (scrape dye transfer method) was applied to detect the function of gap junction in SHR VSMCs. RESULTS: The protein expression of Cx43 and Cx40 in SHR VSMCs was positive and co-localized in the cytoplasm. Compared with control group, the percentage of S-phase detected by cell cycle and A value detected by MTT in TGF-β1 group were obviously increased (P<0.05), indicating that the proliferation of the cells was enhanced. However, the proliferation of the cells decreased in 18α-GA group (P<0.05). Compared with TGF-β1 group, the percentage of S-phase and A value in TGF-β1+18α-GA group were both significantly decreased (P<0.05), indicating that the proliferation of the cells decreased. Compared with control group, the protein expression of Cx43 in TGF-β1 group was increased (P<0.05), whereas the protein expression of Cx40 was not changed (P>0.05), and the protein expression of Cx43 and Cx40 in 18α-GA group were decreased (P<0.05). Compared with TGF-β1 group, the expression of Cx43 in TGF-β1+18α-GA group was significantly decreased (P<0.05),but no difference of the Cx40 protein levels between the two groups was observed. Compared with control group, the function of gap junction detected by scrape dye transfer method in TGF-β1 group was enhanced (P<0.05), and weakened in 18α-GA group (P<0.05). Compared with the TGF-β1 group, the function of gap junction in TGF-β1+18α-GA group was significantly attenuated (P<0.05). CONCLUSION: TGF-β1 enhances the function of gap junction to stimulate the proliferation of SHR VSMCs through the expression of Cx43 protein. The expression of Cx40 protein may not play a major role in this process.  相似文献   

4.
AIM:To study the effect of Bene Jones protein (BJP) from multiple myeloma(MM) patient and TGF-β1 on cultured renal proximal tubular cell(PTC) proliferation.METHODS:[H3]TdR incorporation was used to study the effect of λBJP and TGF-β1 on cultured rat NRK.52E PTC proliferation, the expression of TGF-β1 in the supernatant of PTC cultured with BJP was assessed with ELISA.RESULTS:① [H3]TdR incorporation of PTC was inhibited by BJP in a dose-dependent manner, when co-cultured with 100-800 μmol/L BJP and 2.0 μg/L TGF-β1, the [H3]TdR incorporation was lower than that of BJP alone, especially when BJP≥400 μmol/L;②The expression of TGF-β1 in the supernatant of PTC cultured with BJP was increased, especially when BJP≥400 μmol/L(P＜0.05);③ The [H3]TdR incorporation of PTC was also inhibited by exogenous TGF-β1 in a dose-dependent manner.CONCLUSION:λBJP has antiproliferative effect on rat PTC in vitro, The effect is related with stimulating the PTC to produce excessive TGF-β1, which also has antiproliferative effect on PTC in some degree.  相似文献   

5.
AIM: To investigate whether aorta-derived CD105+ cells show characteristics of mesenchymal stem cells, and if dexamethason enhances this kind of CD105+ cells to differentiate into adipocytes. METHODS: The distribution of CD105 in aorta was assessed by imunohistochemistry. The aorta wall cells were isolated and immunophenotypes were identified by FACS. CD105+ cells were sorted using MACS CD105 micromagnetic beads. The differentiation of CD105+ cells into adipocytes and osteoblasts was induced under different conditions and indicated by staining of Oil red O, detecting of alkaline phosphatase activity, calcium accumulation stained with silver nitrate and transmission electron microscope analysis, respectively. RESULTS: The endothelial cells, a part of medial smooth muscle cells and adventital fibrblasts were CD105 positive. The isolated aortic arch cells were positive for CD105, CD106, CD44, CD29, and negative for CD45, CD11a, CD11b and HLADR. The CD105+ cells differentiated into adipocytes contained Oil-Red-O-positive lipid droplets, the osteocytes with calcium deposition and alkaline phosphatase activity. Ultrastructurally, it was observed that some needle-shaped crystal calcium deposition similar to bone spicules was inside the cytoplasm of induced osteocytes. When the dexamethason was absent in the adipogenic medium, there were no adipocytes with lipid droplets. CONCLUSION: The results demonstrated that CD105+ cells showed characters of MSCs reside in aortic wall, and was able to differentiate into adipocytes and osteocytes in vitro. Dexamethason enhanced aorta-derived CD105+ with characters of MSCs to differentiate into adipocytes. These suggested that MSCs might be related with atherosclerosis.  相似文献   

6.
AIM:To explore the localization and expression of transforming growth factor-β1,2 (TGF-β1,2) and alpha-smooth muscle actin (α-ASMA) in fetal and adult skins. METHODS:Skins of 15 cases of fetuses with different gestational ages and 5 cases of adults were taken, embedded with paraffin wax, and sectioned. Immunohistochemistry method and pathological method were used to detect the expression intensity and distribution of TGF-β1,2 and α-ASMA. RESULTS: Positive immunohistochemical signals of TGF-β1, 2 and α-ASMA were found in fetal and adult skins. In skins derived from young fetus, the positive signals of these three proteins were very weak. Along with the increment in gestational age, the positive cellular rates of TGF-β1,2M and α-ASMA were elevated progressively. In elder fetal and adult skins, TGF-β1,2 were mostly distributed in epidermal cells, endothelial cells and some fibroblasts, while α-ASMA was mainly located in myofibroblasts and sweat gland epithelial cells. CONCLUSION:The endogenous TGF-β1,2might be involved in the cutaneous development at embryonic stage, in the cutaneous structure maintenance at adult stage, and in the wound healing after injury.  相似文献   

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9.
AIM: To investigate the role of adrenomedullin (AM) in diabetic nephropathy. METHODS: We observed the changes in the expression and secretion of AM, TGF-β1 in the cultured human mesangial cells under high glucose condition and the contents of the laminin and type IV collagen in the supernatants. The effect of intervention with AM was also observed. RESULTS: High glucose condition resulted in increase in the expression and secretion of AM、 TGF-β1、 laminin and type IV collagen. AM reversed the influence of high glucose on the cultured human mesangial cells. CONCLUSION: These results showed that high glucose condition is one of stimulating factors of AM and the renal protective action of AM may be associated with suppression of TGF-β1 and reducing excessive accumulat ion of laminin and type IV collagen.  相似文献   

10.
AIM: To investigate whether transforming growth factor-β1 (TGF-β1) participates in hypoxia-induced bronchial epithelial-mesenchymal transition (EMT) through lysyl oxidase (LOX). METHODS: Sprague-Dawley (SD) rats were exposed to hypoxia to establish the animal model and were treated with LOX inhibitor β-aminopropionitrile (β-APN). Furthermore, primary rat bronchial epithelial cells were cultured in vitro and exposed either to normoxia or to hypoxia. TGF-β1, TGF-β1 receptor inhibitor (SB431542) or β-APN was used in the cell experiments. The content of collagen was measured by colorimetric method. The expression of TGF-β1, LOX, and 2 EMT-related proteins (namely, the epithelial marker E-cadherin and the mesenchymal marker vimentin) were determined by immunohistochemistry and We-stern blot, respectively. RESULTS: The expression of TGF-β1, vimentin and LOX and cross-linking of collagen were enhanced in hypoxia-exposed rat and in hypoxia-exposed bronchial epithelial cells, but the enhancement was impaired by the treatment with β-APN. In contrast, the expression of E-cadherin was reduced in hypoxia-exposed rat, and was reversed by treatment with β-APN. In vitro experiments demonstrated that TGF-β1 and hypoxia led to the morphological phenotype characteristic of EMT in rat bronchial epithelial cells, in which the morphology of rat bronchial epithelial cells was switched from cobble-stone shape in normoxia-exposed group to spindle fibroblast-like morphology in hypoxia-or TGF-β1-exposed group (P<0.01). Additionally, both β-APN and SB431542 partially prevented TGF-β1 and hypoxia induced EMT in rat bronchial epithelial cells. TGF-β1was able to dose-dependently up-regulate LOX expression in rat bronchial epithelial cells, which was blocked by concurrent incubation with SB431542. The up-regulation of TGF-β1, vimentin, LOX and cross-linking of collagen and down-regulation of E-cadherin in hypoxia-exposed rat bronchial epithelial cells was significantly reversed by incubation with SB431542. CONCLUSION: TGF-β1 regulates hypoxia-induced EMT in bronchial epithelial cells via activation of the LOX.  相似文献   

11.
AIM: To observe the expression of transforming growth factor β1 (TGF-β1), MAPK1/3 and fibronectin (FN) in the development of renal tubulointerstitial disease. METHODS: Wistar male rats were randomly divided into normal control group, diabetic group of 1week, 2 weeks, 4 weeks and 8 weeks. Diabetic model was induced by peritoneal injection of streptozotocin. Immunohistochemistry was employed to detect the expression of TGF-β1, MAPK1/3 and FN in the kidney. TGF-β1 protein in the renal cortex was checked by Western blot. BG, Scr and UP were analysed by biochemical methods, and the morphological changes in renal tubulointerstitium were also examined under microscopy on sections stained with HE and PAS. RESULTS: The expression of MAPK1/3 and FN was observed, but not the expression of TGF-β1 in normal renal tissue. Positive staining of TGF-β1 was observed in the renal tubulo-interstitium in 1-week diabetic group and thereafter it increased in the course of diabetes. A continuous increase in the expression of MAPK1/3 and FN was also observed in two - week diabetic rats. Chronologically the expression of TGF-β1,MAPK1/3 and FN and the ratio of KW/BW were positively correlative with each other in diabetic animals except one -week diabetic rats. There was also a positive correlation between MAPK1/3 and FN in l -week diabetic rats. CONCLUSION: Our data suggest that TGF-β1 appears in the renal tubulointerstitium in early period of diabetes and then its signal is mediated by MAPK1/3 cascades to accelerate production of FN ,and in turn leads to renal hypertrophy and tubulointerstitial fibrosis.  相似文献   

12.
AIM: To investigate the effect of ozone bath on the pathological changes and the expression of cytokines, platelet-derived growth factor (PDGF), transforming growth factor-β3 (TGF-β3), and tumor necrosis factor-α (TNF-α), in the wounds of deep second-degree burns in rats. METHODS: Male clean-grade SD rats (n=80) were randomly divided into 2 groups, ozone bath group and routine dressing group (control group), with 40 rats in each group. Deep second-degree burn wound was established on the back of the rats, and then the examinations were conducted at 3 d, 7 d, 14 d and 21 d after burn. For the routine dressing group, the wound was cleaned by normal saline and covered with iodophor vaseline gauze every 2 d. For the ozone bath group, before the dressing, the rats were put into the clean foam box to accept ozone fumigation for 20 min (50 mg/L), and then accepted dressing change as the same as that in control group every 2 d. At each time point, the tissue specimens from these rat wounds (at wound center) were taken. The rats in ozone bath group received cleaning by saline cotton and then the ozone bath fumigation, while the rats in control group only received cleaning by saline. After that, the tissue specimens were taken again for HE staining, immunohistochemical staining and semiquantitative observation combined with image data analysis. The concentrations of the cytokines PDGF, TGF-β3 and TNF-α in the wound were measured by double-antibody sandwich ELISA. RESULTS: In ozone bath group, the wounds were smooth with clear edge and slight inflammatory reaction, swelling and exudation were weaker, and the wound healing rate was higher than that in control group with significant difference. Under microscopic observation with HE staining, slighter inflammatory reaction in ozone bath group was observed than that in control group at each time point, and the numbers of fresh capillaries, fibroblasts and epithelial cells were significantly larger than those in control group. The expression levels of PDGF and TGF-β3 in the wound tissue homogenate in ozone bath group were higher, and the expression level of TNF-α was significantly lower than those in control group at each time point with significant difference. CONCLUSION: The ozone bath therapy improves the local pathological changes and promotes the expression of cytokines PDGF and TGF-β3, which are associated with wound healing, as well as reduces the expression of inflammatory mediator TNF-α in the rats with deep second-degree burns, thus promoting the wound healing and anti-inflammatory responses.  相似文献   

13.
AIM: To investigate the regulatory effects of phosphatylinositol 3-kinase/protein kinase B (PI3K/PKB) signaling pathway on the expression of osteopontin (OPN) in transforming growth factor-β1 (TGF-β1)-induced human hepatic stellate cells. METHODS: Human hepatic stellate cell line LX-2 was cultured in DMEM and stimulated by TGF-β1 at the final concentration of 2.5, 5, 10 and 20 μg/L for 24 h or at final concentration of 10 μg/L for 12 h, 24 h and 48 h. LX-2 cells were pretreated with wortmannin, a specific inhibitor of PI3K/PKB signaling pathway, at final concentration of 0.1 μmol/L for 1 h, followed by incubation with TGF-β1 at final concentration of 10 μg/L for 24 h. The cells were collected. The expression of OPN was detected by real-time PCR and Western blotting. RESULTS: In LX-2 cells, the expression of OPN was apparently elevated when incubated with TGF-β1. With the increase in TGF-β1 concentration or the extension of incubation hours, the expression of OPN was increased gradually in a dose-and time-dependent manner with certain limits. LX-2 cells pretreated with wortmannin and incubated with TGF-β1 had a significant decrease in the OPN expression as compared with control group (P<0.01). CONCLUSION: The expression of OPN in TGF-β1-induced LX-2 cells is regulated by the PI3K/PKB signaling pathway.  相似文献   

14.
AIM: To study the effect of natural killer(NK)-cells on graft-versus-host disease(GVHD), graft rejection, engraftment and reconstituting of hematopoiesis in mouse allogeneic bone marrow transplantation. METHODS: Lethally irradiated BALB/c(H-2d) mice were transplanted with C57/6j(H-2b) bone marrow containing donor peripheral T cells and/or NK cells. Recipients CD34+ cell counts and the expression of H-2Kb＋ cell were detected by flow cytometry, peripheral white blood cell(WBC) was detected by auto-cytometry, and the recipients survival rates, GVHD, engraftment and hematopoiesis recovery were then observed. RESULTS: In the group of transplanted with NK cells infusion, the incidence of GVHD was evidently lessened, the survival rates, WBC and CD34+ cell counts and the expression of H-2Kb＋ cell were significantly high than that without NK cells infusion. CONCLUSION: In mouse allogeneic bone marrow transplantation, alloreactivity NK cells prevents GVHD, reduces graft rejection, and promotes engraftment and reconstituting of hematopoiesis.  相似文献   

15.
AIM:To investigate the antagonistic effect of thalidomide (THD) on the activation of connective tissue growth factor (CTGF) gene promoter induced by transforming growth factor-β1 (TGF-β1) in human embryonic lung fibroblasts (HELF). METHODS:Luciferase reporter vector driven by CTGF gene promoter was used to detect the effects of TGF-β1 and THD on the activity of CTGF gene promoter, and DNA pull-down assay with CTGF gene promoter as a probe was used to analyze the changes of CTGF promoter-binding proteins under different conditions. RESULTS:TGF-β1 increased the activity of reporter driven by CTGF gene promoter (P<0.01), while THD significantly inhibited TGF-β1-induced increase in the reporter activity dose-dependently (P<0.01). At the same time, THD had inhibitory effect on the TGF-β1-induced change of CTGF gene promoter-binding proteins (P<0.05). CONCLUSION:Regulation of CTGF gene promoter-binding proteins takes part in TGF-β1-induced activation of CTGF gene promoter, while THD has antagonistic effect on this process.  相似文献   

16.
AIM:To investigate the effect of tea-polyphenols (TP) on the activation of NF-κB and the expression of TGF-β1 mRNA in THP-1 cells (a human acute monocytic leukemia cell line). METHODS:THP-1 cells were incubated with the different concentrations of TP, VLDL, LDL or ox-LDL. In the THP-1 cellls, the nuclear malposition rate of NF-κB was detected with immunohistochemistry technique, the positive index of the TGF-β1 mRNA expression was detected by hybridization in situ, and accumulation of total cholesterol (TC) in cells incubated with 0.4-40 μg/L TP was determined with oxidase assay. RESULTS:The nuclear malposition rate of NF-κB, the positive index of the TGF-β1 mRNA expression and TC in THP-1 cells incubated with 0.4-40 μg/L of TP were lower than those with 0 μg/L of TP in TP-V group, TP-L group and TP-O (P＜0.05). The differences of these markers in THP-1 cells incubated with more than 40 μg/L TP in TP-V group, TP-L group and TP-O were not statistically significant, compared with TP-C group (P＞0.05). CONCLUSION:TP inhibited the activation of NF-κB, the expression of TGF-β1 mRNA and the foam cell formation in the mono-macrophage.  相似文献   

17.
AIM: To investigate the effects of all-trans-retinoic acid (ATRA) on the proliferation and differentiation of transforming growth factor β1(TGF-β1)-stimulated human embryonic lung fibroblasts (HFL-I).METHODS: The HFL-I cells were cultured in vitro and were pretreated with ATRA for 3 days at the concentrations of 0.1 μmol/L, 1 μmol/L and 10 μmol/L. The proliferation of HFL-1 cells was detected by MTT method. The mRNA expression of α-smooth muscle actin(α-SMA) in HFL-I cells stimulated with TGF-β1 for 0 h, 6 h, 12 h, 24 h, 48 h and 72 h was detected by RT-PCR and the protein expression of α-SMA at the time points of 1,3 and 5 days was detected by Western blotting. The mRNA expression of α-SMA in HFL-I cells pretreated with different concentrations of ATRA for 24 h was detected the by RT-PCR and the protein expression at time point of 3rd day was detected by Western blotting. RESULTS: Different concentration of ATRA inhibited the proliferation of HFL-I in a dose-dependent manner (P<0.05). Both mRNA and protein expression of α-SMA in HFL-I cells pretreated with TGF-β1 was up-regulated (P<0.05). ATRA down-regulated the mRNA and protein expression of α-SMA induced by TGF-β1 in a dose-dependent manner (P<0.05). CONCLUSION: ATRA inhibits the proliferation and TGF-β1-stimulated differentiation in HFL-I cells by down-regulating the mRNA and protein expression of α-SMA.  相似文献   

18.
AIM: To investigate the effects of curcumin (Cur) on the expression of High mobility group box 1 protein (HMGB1), interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α) in amyloid-β (Aβ)-induced primary rat microglial cells. METHODS: Microglia were derived from the cerebral cortices of postnatal rat brains. The cells were identified by immunocytochemistry using mouse anti rat Iba-1 monoclonal antibody. A cell model using primary rat microglial cells incubated with Aβ25-35 as an inflammation model of Alzheimer's disease (AD) was set up. The morphological characters of primary rat microglial cells were observed. The concentration of Aβ25-35 and the treatment concentration of curcumin were selected by CCK-8 assay. Cultured primary rat microglial cells were divided into 5 groups:normal cell group, Aβ25-35 group, Cur group, Aβ25-35+Cur group and Aβ25-35+DMSO group. The expression of HMGB1, NF-κB, and receptor for advanced glycation end products (RAGE) was detected by Western blot. The levels of HMGB1, IL-1β, and TNF-α in the culture supernatant were measured by ELISA. RESULTS: The purity of primary microglias determined by Iba-1 immunofluorescence was more than 95%. The protein levels of HMGB1, RAGE and NF-κB were significantly increased after Aβ25-35 stimulation. After treatment with Cur, the protein levels of HMGB1, RAGE and NF-κB were significantly decreased (P<0.05). The levels of HMGB1, IL-1β and TNF-α in the supernatant were significantly increased after Aβ25-35 stimulation. Cur significantly decreased the level of HMGB1, IL-1β and TNF-α in the supernatant. CONCLUSION: Curcumin significantly inhibits neuroinflammation stimulated by Aβ25-35 in primary rat microglial cells.  相似文献   

19.
HAN Yuan-yuan  LIU Yi-min  WANG Yu 《园艺学报》2012,28(12):2266-2282
AIM: To investigate the mechanism that intranasal transforming growth factor beta 1 (TGF-β1) reduces the occurrence of spontaneous seizures after status epilepticus (SE) induced by pilocarpine. METHODS: The rats received recombinant human TGF-β1 or the same volume of PBS, and were treated with pilocarpine to induce SE. All the rats were put into a special cage for video monitoring 7 days later. The determinations of glial fibrillary acidic protein (GFAP) and ionized calcium-binding adaptor molecule 1 (Iba1) positive cells by the method of immunohistochemistry were performed to evaluate the activation levels of the gliocytes in hippocampus. The neuron loss was measured by Nissl staining. RESULTS: TGF-β1 reduced the average frequency, severity and duration of spontaneous seizures. The activated glia cells in the hippocampus were significantly reduced in TGF-β1 group compared with pilocarpine group at 14 days after SE (P<0.05). TGF-β1 significantly attenuated the loss of pyramidal neurons in hippocampal CA3 area at 14 days after SE (P<0.01). CONCLUSION: Intranasal TGF-β1 reduces spontaneous recurrent seizures by inhibiting the activation of glia cells and attenuating the loss of pyramidal neurons.  相似文献   

20.
AIM:To investigate the anti-hepatic fibrosis effect of chelerythrine on mice and the regulation of transforming growth factor-β (TGF-β)/Smads signaling pathway. METHODS:C57BL/6N mice (n=50) were randomly divided into control group, model group and chelerythrine groups (10 mg·kg-1·d-1, 20 mg·kg-1·d-1 and 40 mg·kg-1·d-1, ig). The mouse model of hepatic fibrosis was established by intraperitoneal injection of carbon tetrachloride (CCl4) in combination with the olive oil for 8 weeks. At the 5th week, different doses of chelerythrine was used to treat hepatic fibrosis in the mice. At the 14th week, hepatic index was detected. Histopathological changes and the degree of hepatic fibrosis were observed by hematoxylin-eosin staining and Van Gieson staining. The serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and hyaluronic acid (HA), and hepatic hydroxyproline (Hyp) content were assayed by spectrophotometry and ELISA. The mRNA expression of TGF-β1, Smad3, Smad4 and Smad7 in the liver was detected by RT-qPCR, and the protein expression of TGF-β1, Smad4 and Smad7 was determined by Western blot. RESULTS:The degree of hepatic fibrosis changed markedly in model group compared with control group. The hepatic index, the serum levels of ALT and AST, and the contents of HA and Hyp were significantly increased (P<0.05). The mRNA expression of TGF-β1, Smad3 and Smad4 was significantly up-regulated, while the mRNA expression of Smad7 was significantly down-regulated (P<0.05). The protein expression of TGF-β1 and Smad4 was significantly up-regulated, while the protein expression of Smad7 was significantly down-regulated (P<0.05). Compared with model group, the changes of the above indexes in chelerythrine groups were inhibited. CONCLUSION:Chelerythrine protects the mouse liver from CCl4-induced fibrogenesis injury by regulating TGF-β/Smads signaling pathway.  相似文献   

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