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Magnetic anisotropy energy (MAE) plays a key role for 2D magnetic materials, which have attracted significant attention for their promising applications in spintronic devices. Based on first-principles calculations, we have investigated the influence of surface adsorption on the ferromagnetism and MAE of monolayer CrI3. We find that Li adsorption can dramatically enhance its ferromagnetism, and tune its easy magnetization axis to the in-plane direction from original out-of-plane at certain coverage of Li. The monotonic enhancement of in-plane magnetism in CrI3 as the coverage of Li increases are attributed to electrostatic doping induced by charge transfer between Li atoms and I atoms, as supported by the charge doping simulation. The tunable robust magnetic anisotropy may open new promising applications of CrI3–based materials in spintronic devices.

To study the dispersion characteristic of photonic crystal, the eigen-equations matrix of the light transmitting in is gotten in plane-wave expansion method, then the dispersion curves are calculated for two dimensional air-hole-type square photonic crystal respectively. And the influence on the band structures caused by oblique incidence also is studied by change incidence angle. The results of calculations demonstrate that: For two dimensional square structure photonic crystals, the shape of the band structures of TE mode is very similar to that of TM mode, but their positions of band gaps are different, especially the first band gap of TE mode in the square structure in direction is completely staggered with that of the TM mode. Moreover, we get the conclusion that the width of band gap enlarges with the increasing radius of the hole in square photonic crystal in direction.

AIM: To investigate the effect of activin A on the extracelluar matrix secretion of rat hepatic stellate cell. METHODS: Hepatic stellate cells were isolated and purified from normal male Sprague-Dawley rat liver by a combination of pronase-collagenase perfusion and density gradient centrifugation. Passaged hepatic stellate cells were divided randomly into eight groups: control group(A group), ACTA 1 μg/L group (B group), ACTA 10 μg/L group(C group), ACTA 100 μg/L group (D group), TGF β1 10 μg/L group(E group), TGF β1 10 μg/L plus ACTA 1 μg/L group(F group), TGF β1 10 μg/L plus ACTA 10 μg/L group(G group), TGF β1 10 μg/L plus ACTA 100 μg/L group(H group). 24 h after incubation secretion of procollagen , collagen and mRNA of collagen in hepatic stellate cells were detected by radioimmunoassays and semi-quantitative RT-PCR method respectively. RESULTS: Extracellular matrix secretion in passaged hepatic stellate cells was enhanced by activin A according to its concentration, the capacity of extracellular matrix secretion by 100 μg/L activin A was equal to that of 10 μg/L TGF β1, extracellular matrix secretion and type collagen mRNA expression in passaged hepatic stellate cells was enhanced by activin A and TGFβ1 in a synergistic manner. CONCLUSION: Activin A may contribute to hepatic fibrogenesis. Liu QH, Li DG, Huang X, You HN, Pan Q, Xu LM, Xu QF, Lu HM. Effect of Activin on extracelluar matrix secretion in isolated rat hepatic stellate cell. Shijie Huaren Xiaohua Zazhi 2003;11(6):745-748

Playing a central role in hepatic fibrosis, hepatic stellate cell (HSC) has made itself the major target of research. The limited supply of HSC, however, can not meet the ever growing need of experiment. Establishment and identification of novel immortalized HSC line thus may be urgently required.Primary HSCs were isolated from a normal adult male Sprague-Dawley rat by in situ perfusion with collagenase IV and pronase E, and then were purified by single-step density gradient centrifugation with nycodenz. Once they reached total activation in culture, a new immortalized myofibroblast-like HSC line was established through cellular cloning. Its characteristics were identified by means of immunocytochemical staining, light microscopy, transmission electron microscopy, and growth curve analysis.The novel HSC line, termed HSC-PQ, had a doubling time of about 75 hours in the Dulbecco's modified Eagle medium (DMEM) containing 20% fetal bovine serum. Most of the main morphological characteristics of the differentiated primary HSC could be detected in HSC-PQ cell, while functional features of activated HSC such as alpha-smooth muscle actin, desmin, collagen type I, collagen type III, fibronectin, laminin and other extracellular matrix proteins could also be found in it except for collagen type IV. In contrast, fat droplets and autofluorescence of vitamin A disappeared in the HSC-PQ line. This cell line had been maintained in culture for over 30 passages and more than 1 year with little alternation in biological characteristics.A new rat HSC line (HSC-PQ) has been successfully established. It consistently retains the characteristics of activated primary HSC, and has proved to be immortalized.

Somafostatin receptors (SSTRs) have been suggested to involve in mediating the effect of somatostatin on hepatic stellate cells (HSCs) in an activation-dependent way. We, therefore, try to investigate the relationship between expression of SSTRs and activation of rat HSCs.HSCs were isolated from rats by in situ perfusion and single-step density gradient centrifugation. SSTR1-5 mRNA levels in the differentiated first passage HSCs were detected by means of a reverse transcription polymerase chain reaction. On the other hand, hepatic fibrosis was induced in adult male Sprague-Dawley rats by carbon tetrachloride intoxication, and the expression of SSTR1-5 in normal as well as fibrotic livers was measured by immunohistochemical staining.SSTR mRNA and SSTR could not be found in freshly isolated rat HSCs or normal rat liver. However, SSTR1-3 mRNA appeared as HSCs became wholly activated, and could also be identified on the membrane of activated HSCs in the perisinusoid space, fibrous septa, etc.The expression of SSTR1-3 in the rat HSC is closely related to its activation. This may reflect one of the main negative regulation mechanisms in the course of HSC activation.

To investigate the pathway via which 17beta-estradiol (beta-Est) exerts suppressive effects on rat hepatic fibrosis.In vivo study was done in CCl4-induced female hepatofibrotic rats. Fibrosis-suppressive effect of beta-Est (20 microg/kg/d) was evaluated in intact and ovariectomized rat models. Six weeks after the treatment, all the rats were sacrificed and specimens of serum or liver tissue were collected for the studies. Serum liver enzymes, fibrosis markers and estradiol levels were determined by standard enzymatic methods, ELISA and RIA, respectively. Degrees of fibrosis and areas of hepatic stellate cells (HSCs) positive for alpha-smooth muscle actin (alpha-SMA) in the liver were determined by van Gieson (VG) stain and immunohistochemistry. In vitro studies, HSCs were isolated by a combination of pronase-collagenase perfusion and density gradient centrifugation. First-passage HSCs were randomly divided into 10 groups, and different concentrations of beta-Est, 2-hydroxyestradiol (2OHE) or 2-methoxyestradiol (2MeOE) were separately added to the cell groups. After incubation for 72 h, the degree of cell proliferation, collagen production, alpha-SMA or estrogen receptor (ER) expression was determined by MTT assay, ELISA and immunohistochemistry, respectively.Beta-Est treatment reduced aspartate aminotransferase (AST), alanine aminotransferase (ALT), hyaluronic acid (HA) and type IV collagen (C IV) in sera, suppressed hepatic collagen content, decreased the areas of HSCs positive for alpha-SMA significantly in both intact and ovariectomized female hepatofibrotic rats. There was a negative correlation between the percentage of fibrotic area of liver tissue and the serum estradiol level; the calculated correlation coefficient was -0.57 (P0.01). Beta-Est and its metabolites concentration-dependently (10(-9) mol/L-10(-7) mol/L) inhibited HSC proliferation and collagen synthesis. At the concentration of 10(-7) mol/L, they could inhibit alpha-SMA expression. The order of potency was 2MeOE2OHEbeta-Est.Beta-Est may suppress hepatic fibrosis probably via its biologically active metabolites.

To investigate the therapeutic effects and mechanism of octreotide on experimental hepatic fibrosis in rats.Hepatofibrotic rats models were established with carbon tetrachloride. All the experimental rats were divided into four groups: normal control group, pre-and post-treatment model group, and octreotide-treated group in which the rats were injected subcutaneously with octreotide at the dose of 50ng/100g, twice daily, for thirty days. Serum levels of hyaluronic acid (HA), laminin (LN) and pro-collagen type III peptide (PCIII) were detected by radioimmunoassay. Hepatic fibrosis scoring grade was assessed through Van-Gieson staining and observed under light microscope. Protein expression levels of alpha-smooth muscle actin (alpha-SMA) and transforming growth factor beta1 (TGFbeta1) were determined with immunohistochemical staining method. Messenger RNA (mRNA) levels of collagen type I and PCIII were detected by reverse transcription polymerase chain reaction.Serum levels of HA (ng/L), LN (microg/L) and PCIII (ng/L) in pre- and post-treatment model groups were higher than those in normal control group (121.8+/-9.5 and 110.3+/-13.4 vs. 33.1+/-3.7, 85.7+/-12.1 and 78.2+/-7.9 vs. 37.1+/-6.3, 35.9+/-3.5 and 33.7+/-2.6 vs. 15.6+/-2.8, respectively, tor = 9.41, P0.05), and there was no significant difference between the two model groups. Concentrations of HA (55.8ng/L+/-7.2ng/L), LN (43.1microg/L+/-3.4microg/L) and PCIII (27.8ng/L+/-3.4ng/L) decreased significantly in octreotide-treated group, compared with those in model groups (tor=2.76, P0.05). With histological analysis, fibrotic scoring grade in octreotide-treated group was obviously ameliorated, compared with that in model groups (chi2or = 3.97, P0.05). Imaging analysis revealed that alpha-SMA and TGFbeta1 immunohistological staining areas were markedly shrinked in octreotide-treated group (tor = 2.47, P0.05). In two model groups, PCIII and type I mRNA levels significantly up-regulated as compared with those in normal group (tor = 9.27, P0.001), and they were inhibited by octreotide markedly (tor = 2.47, P0.05).Octreotide can inhibit hepatic stellate cells transforming into myofibroblasts, down-regulate TGFbeta1, collagen type I and PCIII transcriptions, so that it has therapeutic effects on experimental hepatic fibrosis.

AIM:To investigate effect of losartan, an AT1 receptor antagonist, on hepatic fibrosis induced by CCl(4); and to determine whether or not AT1 receptors are expressed on hepatic stellate cells. METHODS AND RESULTS:Fifty male Sprague-Dawley rats, weighing (180 plus minus20)g, were randomized into five groups (control group, model group, and three losartan treated groups), in which all rats were given the subcutaneous injection of 40% CCl(4)(every 3 days for 6 weeks) except for rats of control group. Rats of losartan-treated groups were treated with losartan (20 mg/kg, 10 mg/kg, 5 mg/kg, daily gavage). After 6 weeks liver tissue and serum samples of all rats were examined. Serum hyaluronic acid (HA), procollagen type III (PC III) were detected by radioimmunoassays. van Giesion collagen staining was used to evaluate the extracellular matrix of rats with liver fibrosis. The expression of AT1 receptors, transforming growth factor-beta (TGF-beta), and alpha-smooth muscle actinalpha-SMA) in liver tissue were determined by immunohistochemical techniques. Compared with model group, serum ALT and AST of losartan-treated groups were significantly reduced (italict = 4.20,P0.01 and italict = 4.57,P0.01). Serum HA and PC III also had significant differences (italict = 3.53,P0.01 and t=2.20, P0.05). The degree of fibrosis was improved by losartan and correlated with the expressions of AT1 receptors, TGF-beta, and alpha-SMA in liver tissue.CONCLUSION:AT1 receptor antagonist, losartan, could limit the progression of the hepatic fibrosis induced by CCl(4). The mechanism may be related to the decrease in the expression of AT1 receptors and TGF-beta, ameliorating the injury of hepatocytes; activation of local renin-angiotensin system might relate to hepatic fibrosis; and during progression of fibrosis, activated hepatic stellate cells might express AT1 receptors.

AIM: To examine the expression of activin A, a member of the transforming growth factor (TGF-β) superfamily, recently has been reported to beoverexpressed in liver cirrhosis, in the course of carbon tetrachloride-induced rat hepatic fibrosis. METHODS: Hepatic fibrosis was induced in rats by subcutaneous injections of 40% carbon tetrachloride oily solution for a period of 1 to 7 weeks. At the end of 1, 2, 3, 4, 5, 6 and 7 weeks after carbon tetrachloride injections, the rats were killed in group (6-10 rats each time) for study. The activin A messenger RNA expression and its protein localization were assessed by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry. RESULTS: The normal rat liver expressed activin A mRNA and protein, and its expression was transiently decreased and became undetectable after carbon tetrachloride injections for 2 or 3 weeks and then increased gradually. After injection of carbon tetrachloride for 6 and 7 weeks, activin A mRNA and protein expressions were significantly enchanced in rat liver. Compared with that of the normal rat liver. Activin A mRNA expression levels in rats receiving carbon tetrachloride injections for 6 and 7 weeks were 1.6 and 2.2 times that of those in normal rat liver respectively (0.456 ± 0.094 vs 0.286 ± 0.0670, P < 0.01; 0.620 ± 0.134 vs 0.286 ± 0.0670, P < 0.01). Immunohistochemistry showed that activin A expressed in hepatocytes of normal liver, and its expression was decreased in rats receiving carbon tetrachloride for 2 or 3 weeks. Compared with normal liver, activin A expression distribution mode changed in fibrotic liver, being increased significantly in hepatocytes around fibrotic areas. CONCLUSION: Activin A expression was increased in late stage of hepatic fibrosis, and this may be involved in hepatic fibrosis formation in this period.

AIM: To assess the effects of somatostatin on proliferation and apoptosis of activated rat hepatic stellate cells (HSCs). METHODS: HSCs isolated from the livers of adult Sprague-Dawley rats (weighing 400-500 g) by in situ perfusion and purified by single-step density gradient centrifugation with Nycodenz, became activated after 10 days’ cultivation. Then the apoptotic rate of HSCs treated with different doses of somatostatin for 72 h, was assayed by acridine orange/ ethidium bromide fluorescent staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, transmission electron microscopy and flow cytometry, while the proliferation of HSCs was measured by MTT assay. Furthermore, the mechanisms of somatostatin were investigated by cytodynamic analysis. RESULTS: Somatostatin at the concentration of 10-6-10-9 mol/L could decrease the proliferative rate, and promote the apoptosis of activated rat HSCs in a dose-dependent way. Its action was most significant when the concentration reached 10-6 mol/L or 10-7 mol/L (P < 0.05-0.01). An obvious cell-cycle arrest (G0/G1 arrest) was the important way for somatostatin to exert its action. CONCLUSION: Antiproliferative and proapoptotic effects of low-dose somatostatin on activated rat HSCs can be obtained. These findings reveal its potential antifibrotic action.