Inhibitory effect of Astragalus membranaceus root on matrix metalloproteinase‐1 collagenase expression and procollagen destruction in ultraviolet B‐irradiated human dermal fibroblasts by suppressing nuclear factor kappa‐B activity

Objectives The root of Astragalus membranaceus, regarded as a tonic in traditional Korean medicine, has been prescribed for long periods to treat chronic illness by boosting the immune system. Ultraviolet (UV) irradiation causes damage to skin connective tissue by degrading collagen, which is a major structural component of the extracellular matrix. Such damage is considered to be a cause of the wrinkling observed in premature ageing of the skin. This study has investigated the photo‐protective effect of A. membranaceus on UVB radiation‐induced activation of nuclear factor kappa‐B (NF‐κB) activity in human dermal fibroblasts. Methods Hs68 fibroblast cells cultured with various concentrations of A. membranaceus were exposed to UVB (40 mJ/cm²). Activation of NF‐κB P65 and expression of matrix metalloproteinase‐1 (MMP‐1) and type 1 procollagen were measured by Western blotting. Translocation of NF‐κB P65 and MMP‐1 regulation were also examined by immunocytochemistry. Key findings Western blotting and immunocytochemistry results showed that A. membranaceus inhibited UVB‐induced translocation of NF‐κB P65 and MMP‐1 expression. The data suggested that A. membranaceus restored type 1 procollagen synthesis by inhibiting NF‐κB P65 activity and MMP‐1 expression in UVB‐exposed human dermal fibroblasts. Conclusion A. membranaceus is a candidate for use in skin protection from UVB‐induced skin inflammation and photoageing.     

Suppressive effects of<Emphasis Type="Italic">Platycodon grandiflorum</Emphasis> on the progress of carbon tetrachloride-lnduced hepatic fibrosis

The suppressive effects of Platycodi Radix (Changkil: CK), the root of Platycodon grandiflorum A. DC (Campanulaceae), on the progress of acute carbon tetrachloride (CCl4)-induced hepatic fibrosis were investigated in the rat. CK significantly suppressed CCl4-induced hepatic necrosis and inflammation, as determined by the serum enzymatic activities of alanine and aspartate aminotransferase and serum tumor necrosis factor-alpha levels, in dose-dependent manners. In addition, the increased hepatic fibrosis after acute CCl4 treatment was suppressed by the administration of CK. CK also significantly prevented the elevation of hepatic alpha1 (I) procollagen (type I collagen) mRNA and alpha-smooth muscle actin (alpha-SMA) expressions in the liver of CCl4-intoxicated rats and also suppressed the induction of alpha-SMA and type I collagen in cultured hepatic stellate cells, in dose-dependent manners. These results suggest that the suppressive effects of CK against the progress of acute CCl4-induced hepatic fibrosis possibly involve mechanisms related to its ability to block both hepatic inflammation and the activation of hepatic stellate cells.     

Chronic moderate alcohol consumption relieves high‐fat high‐cholesterol diet‐induced liver fibrosis in a rat model

Nonalcoholic fatty liver disease is a worldwide health issue and chronic alcohol consumption may have different effects on this disease. This study explored the role of chronic moderate alcohol consumption on high‐fat high‐cholesterol (HFHC) diet‐induced liver fibrosis in a rodent model. Male Sprague–Dawley rats were divided into five groups: standard chow group, standard chow plus Er Guo Tou (EGT, a Chinese spirit made from fermented cereals) group, HFHC group, HFHC plus EGT group, and HFHC plus pure ethanol (EtOH) group. Rats were fed standard chow or HFHC chow for 12 weeks. EGT or pure ethanol was administrated at a daily dose of 4 g/kg body weight via intra‐gastric gavage from week 4. At the end of week 12, hematoxylin and eosin staining, Sirius red and immunohistochemistry of liver sections were examined. The hepatic expression of F4/80, TNF‐α, IL‐1β, IL‐6, CXCL1, CXCL2, α‐SMA, Collagen, TGF‐β, MMP2, MMP9, and TIMP1 was calculated. Both moderate EGT and pure ethanol did not increase plasma endotoxin in the portal vein comparing with the FHFC group. EGT and pure ethanol did not improve hepatic inflammation, but ameliorated liver fibrosis in histology. Moderate EGT and pure ethanol ameliorated HFHC diet‐induced activation of Kupffer cells and hepatic stellate cells. In conclusion, chronic moderate EGT and pure ethanol could ameliorate HFHC diet‐induced liver fibrosis.     

Potential protective effects of a traditional Chinese herb,Litsea coreana Levl., on liver fibrosis in rats

Objectives It was found that total flavonoids from Litsea coreana Levl. (TFLC), which is a traditional Chinese medicine, had a preventive effect against hepatic steatosis in our previous study. This study was designed to evaluate whether TFLC could improve liver fibrosis in rats. Methods The liver fibrosis model rats were treated with composite factors of high‐fat emulsion (10 ml/kg) via gavage accompanied by a subcutaneous injection of low‐dose CCl₄. Thirty rats were given composite factors plus TFLC (100, 200, 400 mg/kg), respectively, for 8 weeks. Key findings The results showed that TFLC (200 and 400 mg/kg) treatment significantly reduced the elevation of liver index (liver weight/body weight) and spleen index (spleen weight/body weight), alanine transaminase, aspartate aminotransferase, hyaluronic acid, laminin, procollagen III N‐terminal peptide, procollagenase IV and hydroxyproline. In addition, TFLC treatment improved the morphologic changes of hepatic fibrosis, suppressed expression of α‐smooth muscle actin, collagen I, transforming growth factor (TGF)‐β1 and TGFβ receptor (TGFβR)1, and increased peroxisome proliferator‐activated receptor‐γ expression in the liver of hepatic fibrosis rats. Conclusions In conclusion, TFLC is able to ameliorate liver injury and protect rats from liver fibrosis. This process may be related to inhibiting the expression of transforming growth factor‐β1 and increasing the expression of peroxisome proliferator‐activated receptor‐γ.     

The CD147/MMP‐2 signaling pathway may regulate early stage cardiac remodelling in spontaneously hypertensive rats

Previous studies have reported that decreased matrix metalloproteinase‐2 (MMP‐2) is associated with early stage (age 8–16 weeks) ventricular remodelling in spontaneously hypertensive rats (SHR). We hypothesized that inhibited CD147/MMP‐2 signalling might down‐regulate MMP‐2 expression and augment remodelling in spontaneously hypertensive rats. Twenty‐nine male SHR (8 weeks) were randomly assigned to SHR, CD147, and CD147+DOX groups. The control group included eight age‐matched WKY rats. CD147 and CD147+DOX groups received recombinant human CD147 (600 ng/kg in 1.5 mL saline, weekly). The SHR and WKY groups received the vehicle. The CD147+DOX group also received doxycycline, an inhibitor of MMPs (daily, 30 mg/kg in 1.5 mL saline, iG). On day 56 echocardiography and left ventricular mass index (LVWI) measurements were collected and histological sections were stained for cell and collagen content. Myocardium MMP‐2, TIMP‐1, CD147, and collagens types I and III were estimated by western blot. CD147 and the ratio of MMP‐2/TIMP‐1 were lower in SHR than WKY rats (P<.05). Myocyte hypertrophy, partial fibre breaks, plasmolysis, necrosis and collagen content (collagen volume fraction [CVF], I and III) in SHR were above control levels (P<.05). CD147 rats showed CD147, MMP‐2 and MMP‐2/TIMP‐1 were increased (P<.05), CVF, LVWI, and collagen I and III were decreased (P<.05) and myocyte morphology was improved. CD147 levels did not differ between CD147+DOX and CD147 groups, CVF, collagens type I and III and partial fiber breaks were more abundant in CD147+DOX (P<.05). In summary, an inhibited CD147/MMP‐2 pathway was associated with early stage cardiac remodelling, and CD147 supplementation may attenuate this response.     

TGF‐β1 mediated Smad signaling pathway and EMT in hepatic fibrosis induced by Nano NiO in vivo and in vitro

Nickel oxide nanoparticles (Nano NiO) bears hepatotoxicity, while whether it leads to liver fibrosis remains unclear. The aim of this study was to establish the Nano NiO‐induced hepatic fibrosis model in vivo and investigate the roles of transforming growth factor β1 (TGF‐β1) in Smad pathway activation, epithelial‐mesenchymal transition (EMT) occurrence, and extracellular matrix (ECM) deposition in vitro. Male Wistar rats were exposed to 0.015, 0.06, and 0.24 mg/kg Nano NiO by intratracheal instilling twice a week for 9 weeks. HepG2 cells were treated with 100 μg/mL Nano NiO and TGF‐β1 inhibitor (SB431542) to explore the mechanism of collagen formation. Results of Masson staining as well as the elevated levels of type I collagen (Col‐I) and Col‐III suggested that Nano NiO resulted in hepatic fibrosis in rats. Furthermore, Nano NiO increased the protein expression of TGF‐β1, p‐Smad2, p‐Smad3, alpha‐smooth muscle actin (α‐SMA), matrix metalloproteinase9 (MMP9), and tissue inhibitors of metalloproteinase1 (TIMP1), while decreased the protein content of E‐cadherin and Smad7 in rat liver and HepG2 cells. Most importantly, Nano NiO‐triggered the abnormal expression of the abovementioned proteins were all alleviated by co‐treatment with SB431542, implying that TGF‐β1‐mediated Smad pathway, EMT and MMP9/TIMP1 imbalance were involved in overproduction of collagen in HepG2 cells. In conclusion, these findings indicated that Nano NiO induced hepatic fibrosis via TGF‐β1‐mediated Smad pathway activation, EMT occurrence, and ECM deposition.     

Ito cells and fibrogenesis in chronic alcoholic liver disease.

The relationships between the number of Ito cells; serum N-terminal type III procollagen and laminin; clinical and biochemical parameters of liver function derangement; histomorphometrically assessed total amount of liver fibrosis; and daily ethanol intake were studied in 43 patients affected by chronic alcoholic liver disease (10 cirrhotics). Significant correlations were found between serum laminin and N-terminal type III procollagen and histological, clinical and biochemical data of liver function derangement, but no correlation was found between the aforementioned parameters and the percentage of Ito cells, which in turn seemed to be related to ethanol ingestion.     

Gypsophila elegans isoorientin-2″-O-α-l-arabinopyranosyl ameliorates porcine serum-induced immune liver fibrosis by inhibiting NF-κB signaling pathway and suppressing HSC activation

The present study was to investigate the inhibitory effect of Gypsophila elegans isoorientin-2″-O-α-l-arabinopyranosyl (GEI) on hepatic stellate cells (HSCs), to reveal the underlying mechanism of GEI against hepatic fibrosis. Our study showed that GEI significantly alleviated liver injury induced by porcine serum (PS) in rats; it notably alleviated collagen accumulation as evidenced by a significant decrease in the levels of collagen biomarkers including hyaluronic acid, laminin, hydroxyproline and procollagen III N-terminal peptide. Moreover, GEI treatment markedly decreased the secretion of inflammatory cytokines by inhibiting the NF-κB pathway and significantly inhibited the generation of excessive extracellular matrix (ECM) components by restoring the balance between matrix metalloproteinases (MMPs) and tissue inhibitor of matrix metalloproteinases (TIMPs). Additionally, the cell experiments in vitro showed that GEI strongly inhibited HSC proliferation, migration and clonogenicity and markedly induced HSC apoptosis. Moreover, GEI caused cell cycle arrest at G2 phase. In conclusion, our study demonstrates that GEI significantly alleviates PS-induced hepatic fibrosis by inhibiting the NF-κB pathway, restoring the balance between MMPs and TIMPs, and suppressing HSC activation.     

The therapeutic effects of tectorigenin on chemically induced liver fibrosis in rats and an associated metabonomic investigation

The aim of this study was to investigate the effects of tectorigenin on chemically induced liver fibrosis in rats. Liver fibrosis was induced in rats with carbon tetrachloride, a diet high in fat, cholesterol and alcohol in the drinking water. Our results indicate that tectorigenin treatment significantly inhibited the increases in the activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and the increases in the serum levels of hyaluronate (HA), laminin (LN) and procollagen III N-terminal peptide (PIIIP); tectorigenin treatment also significantly inhibited the increases in the amount of collagen in the livers of the fibrogenic rats. Chemically induced liver fibrosis caused a drop in the serum albumin concentration and a decrease in the ratio of albumin to globulin (A/G). Tectorigenin caused a remarkable increase at a dose of 30 mg/kg, but only a slight increase at the lower doses. Tectorigenin was also able to inhibit the increase in the liver lipid peroxidation (LPO), as well as the decrease in the activities of liver superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), caused by liver fibrosis. In addition, we present a related metabolic profile determined, using a (1)H NMR spectroscopy and multivariate pattern recognition techniques. The results were consistent with the pathological examination, liver function analysis and liver fibrosis marker analysis. Furthermore, tectorigenin does not cause acute toxicity.     

慢性病毒性乙型肝炎患者血清肝纤维化指标检测的临床意义

目的 探讨慢性病毒性乙型肝炎(乙肝)患者血清肝纤维化指标水平与临床的关系.方法 应用放射免疫法及化学发光法检测146例慢性病毒性乙型肝炎患者及40例健康人(对照组)血清肝纤维化指标血清透明质酸(HA)、Ⅳ型胶原(Ⅳ-C)、层粘连蛋白(LN)及Ⅲ型前胶原(PCⅢ)水平,并就上述指标与临床肝功能指标关系进行分析.结果 慢性乙肝患者血清HA、Ⅳ-C、LN、PCⅢ水平均不同程度高于对照组(P＜0.05或P＜0.01),在不同病程之间差异有统计学意义(P＜0.05或P＜0.01);慢性乙肝患者血清Ⅳ-C、PCⅢ水平与血浆PT呈正相关,HA、Ⅳ-C、LN水平与Alb呈负相关,HA水平与TBil呈正相关,PCⅢ水平与ALT呈正相关,LN水平与CHE呈负相关.结论 检测慢性病毒性乙型肝炎患者血清HA、Ⅳ-C、LN、PCⅢ水平,可反映肝纤维化进展情况和肝功能损害程度.     

The role of matrix metalloproteinase inhibitors in ischemia-reperfusion injury in the liver

Liver ischemia-reperfusion injury is characterized by cell necrosis and apoptosis and by profound modifications in the extracellular matrix (ECM). During the complex series of events that take place both during ischemia and when normal blood flow is restored (reperfusion), a concerted regulation of release and activation of matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) mainly by stellate cells, Kupffer cells and inflammatory cells leads first to endothelial cell injury and subsequent infiltration of neutrophils into the wounded area. Later, MMP activation causes degradation of extracellular matrix components of the liver, mainly collagen and fibronectin, altering tissue architecture. The fibrosis that can result after liver injury is also dependent on the imbalance between MMPs and TIMPs and to new collagen deposition. Several experimental models of liver ischemia-reperfusion injury have demonstrated protective effects of MMP inhibitors in terms of cell necrosis, apoptosis and rearrangement of the extracellular matrix. This review summarizes current knowledge of MMP biology, with particular attention to the most recent evidence of novel, non-extracellular matrix MMP substrates involved in inflammation and cell cycle regulation. An overview of MMP and TIMP expression and activation in hepatic ischemia-reperfusion injury is provided. The analysis of such provides a rational basis for MMP inhibition as a viable strategy to prevent liver injury.     

Protective effects of Phyllanthus amarus on fibrotic markers during alcohol and polyunsaturated fatty acid-induced toxicity

Alcoholic liver disease (ALD) remains a major problem, with significant morbidity and mortality worldwide. One of the serious consequences of ALD is hepatic fibrosis. This happens when the matrix synthesis rate exceeds that of matrix degradation. Matrix metalloproteinases (MMPs) and tissue inhibitors of matrix metalloproteinases (TIMPs) play a key role in matrix remodeling. Disruption of MMP/TIMP balance can lead to excessive accumulation of extracellular matrix components resulting in severe liver injury. The focus of the present study is to analyze the effect of Phyllanthus amarus on MMP and TIMPs activity in alcohol and thermally oxidized polyunsaturated fatty acid (PUFA)-induced hepatic fibrosis. Male albino Wistar rats were used for the study. The matrix metalloproteinase expression was found to be significantly decreased and the levels of TIMPs and the collagen were significantly increased in alcohol + thermally oxidized PUFA-treated rats. Administration of Phyllanthus amarus extract significantly decreased the levels of collagen and TIMPs; and positively modulated the expression of MMPs. From this study, we conclude that Phyllanthus amarus effectively modifies alcohol + thermally oxidized PUFA-induced fibrosis.     

Invasive and non-invasive monitoring of hepatitis C virus-induced liver fibrosis: alternatives or complements?

Chronic hepatitis C virus (HCV) infection results in the development of liver fibrosis and cirrhosis in 20 to 25% of patients. The main task of the physician when examining a patient with a verified HCV infection is to identify the activity of inflammatory and necrotic processes in the liver, as well as the stage of fibrosis, and the reversibility of detected changes. Along with other clinical and laboratory parameters, this plays a major role in forecasting the course of hepatitis, as well as determines the therapeutic approach in each specific case. Liver biopsy remains the best way to assess the severity of chronic hepatitis C. The risk of developing cirrhosis depends on the stage (degree of fibrosis) and the grade (degree of inflammation and necrosis) observed in the initial liver biopsy. Non-invasive diagnostic approaches attempt to evaluate the serum markers of fibrogenesis. Biochemical markers of fibrosis scoring include thrombocyte counts, the prothrombin time, ratio of alaninaminotransferase (ALT) and aspartataminotransferase (AST) levels, the level of g-glutamyl transferase and the quantity of blood serum albumin. Another set of markers is based on the detection of molecular junctions that activate fibrosis, or participate in the generation of the liver extracellular matrix. The most applicable include hyaluronic acid (HA), type IV collagen (IV-C), N-terminal propeptide of type III procollagen (PIIIP), metalloproteinases (MMP), inhibitors of metalloproteinases (TIMP), and growth-transforming factor betta (GTFbeta). The review discusses the clinical significance of each of the criteria and possibility of their combination in the non-invasive monitoring of liver fibrosis.     

Adenosine A2A receptor occupancy stimulates collagen expression by hepatic stellate cells via pathways involving protein kinase A, Src, and extracellular signal-regulated kinases 1/2 signaling cascade or p38 mitogen-activated protein kinase signaling pathway

Prior studies indicate that adenosine and the adenosine A2A receptor play a role in hepatic fibrosis by a mechanism that has been proposed to involve direct stimulation of hepatic stellate cells (HSCs). The objective of this study was to determine whether primary hepatic stellate cells produce collagen in response to adenosine (via activation of adenosine A2A receptors) and to further determine the signaling mechanisms involved in adenosine A2A receptor-mediated promotion of collagen production. Cultured primary HSCs increase their collagen production after stimulation of the adenosine A2A receptor in a dose-dependent fashion. Likewise, LX-2 cells, a human HSC line, increases expression of procollagen alphaI and procollagen alphaIII mRNA and their translational proteins, collagen type I and type III, in response to pharmacological stimulation of adenosine A2A receptors. Based on the use of pharmacological inhibitors of signal transduction, adenosine A2A receptor-mediated stimulation of procollagen alphaI mRNA and collagen type I collagen expression were regulated by signal transduction involving protein kinase A, src, and mitogen-activated protein kinase kinase/extracellular signal-regulated kinase (erk), but surprisingly, adenosine A2A receptor-mediated stimulation of procollagen alphaIII mRNA and collagen type III protein expression depend on the activation of p38 mitogen-activated protein kinase (MAPK), findings confirmed by small interfering RNA-mediated knockdown of src, erk1, erk2, and p38 MAPK. These results indicate that adenosine A2A receptors signal for increased collagen production by multiple signaling pathways. These results provide strong evidence in support of the hypothesis that adenosine receptors promote hepatic fibrosis, at least in part, via direct stimulation of collagen expression and that signaling for collagen production proceeds via multiple pathways.     

Hydroxysafflor yellow A protects against chronic carbon tetrachloride-induced liver fibrosis

Hydroxysafflor yellow A (HSYA) was isolated from the dried flower of Carthamus tinctorius L. which was extensively used in traditional Chinese medicine to treat cirrhosis. However, the potential protective effect of HSYA in liver fibrosis is still unknown. In the present study, we investigated the effects of HSYA in rats with carbon tetrachloride (CCl4)-induced liver fibrosis. Sprague-Dawley (SD) rats were subjected to biweekly CCl4 injections over 12 weeks, while controls were given isovolumetric injections of olive oil. HSYA was given in a daily dose of 5 mg/kg by means of intraperitoneal concurrent with CCl4. Hepatic fibrosis was quantified by digital analysis of Masson's trichrome stained slides and hydroxyproline content. mRNA expression was quantified by real-time polymerase chain reaction (PCR), and protein was quantified by western blot or enzyme-linked immunosorbent assay (ELISA). CCl4 treatment induced micronodular liver fibrosis with a pronounced deposition of collagen fibers. HSYA significantly reduced liver fibrosis. HSYA down regulates α-smooth muscle actin (SMA), collagen α type I, matrix metalloproteinases (MMP)-9, and tissue inhibitors of metalloproteinases (TIMP)-1 gene expression. This was accompanied by a decreased expression of transforming growth factor (TGF)-β1 and phosphorylation of Smad4. These results indicate that HSYA might be a promising antifibrotic agent in chronic liver disease.     

Diallyl trisulfide attenuates carbon tetrachloride-caused liver injury and fibrogenesis and reduces hepatic oxidative stress in rats

Liver fibrosis represents a frequent event following chronic insult to trigger wound healing reactions with accumulation of extracellular matrix (ECM) components in the liver. Activation of hepatic stellate cells (HSCs) is the pivotal event during liver fibrogenesis. The process of HSC activation is accompanied by enhanced expression of a series of marker proteins and pro-fibrogenic signal molecules. Natural products have been an important source of antifibrotic remedies. The present study aims to evaluate the in vivo effects of diallyl trisulfide (DATS), the primary component derived from garlic, on carbon tetrachloride (CCl₄)-induced injury and fibrosis in rats. Our results showed that DATS improved liver histological architecture and decreased hepatic enzyme levels, but did not significantly affect cytochrome P450 2E1 activity in vivo. DATS also attenuated collagen deposition and inhibited HSC activation in the rat fibrotic liver demonstrated by reduced expression of α-smooth muscle actin, α1(I) procollagen, and fibronectin—three key markers of HSC activation—and by downregulation of transforming growth factor-β receptor 1, platelet-derived growth factor-β receptor, and epidermal growth factor receptor—three key receptors transmitting pro-fibrogenic pathways. In addition, DATS ameliorated hepatic oxidative stress by diminishing the levels of lipid peroxides and malondialdehyde and enhancing glutathione content. These data collectively revealed that DATS protected the rat liver from CCl₄-caused injury and fibrogenesis in vivo, which was associated with inhibition of HSC activation and attenuation of oxidative stress. Our results suggested DATS as a promising antifibrogenic candidate for the prevention and treatment of liver fibrosis.     

ARFI技术与血清铁、铁蛋白和肝纤维化四项检测在肝纤维化及肝硬化诊断中的相关性

目的：探讨声脉冲辐射力成像技术（ acoustic radiation force impulse imaging ,ARFI）、血清铁、铁蛋白及肝纤维化四项指标（Ⅲ型前胶原、Ⅳ型胶原、层黏蛋白、透明质酸）在诊断肝纤维化及肝硬化中的相关性。方法在2013年6-10月期间,选取20例正常者作为对照组和53例肝纤维化、肝硬化作为观察组。所有研究对象均进行上述7项指标的检测,比较对照组和观察组组间测量指标的差异;将观察组ARFI测量值与血清铁、铁蛋白、肝纤维化四项指标进行相关性分析。结果观察组的ARFI、血清铁、铁蛋白、Ⅲ型前胶原、Ⅳ型胶原、层黏蛋白和透明质酸的测值均高于对照组（ P均＜0.01）;观察组的ARFI分别与透明质酸（r＝0．48,P＜0．01）、层黏蛋白（r＝0．44,P＜0．01）、Ⅳ型胶原（r＝0．41,P＜0．01）和血清铁（r＝0.33,P＜0.05）均存在正相关;但与Ⅲ型前胶原（r＝0．07,P＞0．05）和铁蛋白（r＝0．12,P＞0．05）不存在相关性。结论 ARFI技术可无创反映肝组织的弹性硬度,且与透明质酸、层黏蛋白、Ⅳ型胶原、血清铁相关性良好,对肝纤维化及肝硬化的诊断具有一定临床价值。     

金雀异黄素和槲皮素对大鼠肝星状细胞增殖、胶原合成及Ⅰ型原胶原nRNA水平的影响(英文)

目的:研究金雀异黄素和槲皮素对HSC-T6大鼠肝星状细胞增殖和胶原合成及Ⅰ型原胶原mRNA表达的影响。方法:细胞增殖和胶原合成分别采用结晶紫染色法和[~3H]-脯氨酸掺入法。原胶原mRNA水平用RT-PCR法测定。结果:金雀异黄素(25-70μmol/L)和槲皮素(6.25-50μmol/L)浓度依赖抑制HSC-T6细胞增殖和胶原合成,对Ⅰ型原胶原mRNA表达也有抑制作用。结论:金雀异黄素和槲皮素抑制肝星状细胞增殖和胶原合成可能对肝纤维化有保护作用。