Publications (9)16.14 Total impact
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Article: Total glucosides of Danggui Buxue Tang attenuates bleomycin-induced pulmonary fibrosis via inhibition of extracellular matrix remodelling.
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ABSTRACT: This study was designed to investigate the antifibrosis effects and possible mechanism of action of total glucosides of Danggui Buxue Tang (DBTG) on bleomycin-induced pulmonary fibrosis in rats. DBTG was extracted from Radix Astragali and Radix Angelicae Sinensis. Pulmonary fibrosis was induced by intratracheal instillation of bleomycin (5 mg/kg) in Wistar rats. Subsequently, the rats received daily intragastric administration of DBTG (16, 32 or 64 mg/kg per day) or cortisone (3 mg/kg) 1 day after bleomycin instillation for 4 weeks. Histological changes in the lung were evaluated by hematoxylin and eosin and Masson's trichrome staining. Markers of fibrosis in serum were determined by radioimmunoassay. The mRNA expression of metalloproteinases 1 and 9 (MMP-1, MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) in lung tissue were detected by reverse transcription PCR. DBTG administration attenuated the degree of alveolitis and lung fibrosis, and markedly reduced the elevated levels of hyaluronic acid, laminin, type III procollagen and type IV collagen in serum. DBTG decreased the mRNA levels of MMP-9 and TIMP-1. MMP-1 expression was only moderately decreased by DBTG. DBTG had an inhibitory effect on bleomycin-induced pulmonary fibrosis and its effect may be associated with the ability of DBTG to inhibit the synthesis of extracellular matrix and balance the MMP/TIMP-1 system.The Journal of pharmacy and pharmacology. 06/2012; 64(6):811-20. -
Article: Antifibrosis effects of total glucosides of Danggui-Buxue-Tang in a rat model of bleomycin-induced pulmonary fibrosis.
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ABSTRACT: The present study examined the antifibrosis effects of DBTG (total glucosides of Danggui-Buxue-Tang) on bleomycin-induced pulmonary injury and fibrosis in rats. Animals were randomly divided into six groups: (1) saline control group; (2) Bleomycin group in which rats were endotracheally instillated with bleomycin (5mg/kg); (3-5) Bleomycin and DBTG group, in which DBTG were given to rats daily (16.32 or 64mg/kg/day, i.g.) one day after bleomycin injection for 4 weeks until the end of the treatment; (6) Bleomycin and positive control group. Animals were sacrificed at 7, 14, and 28 days post bleomycin administration and lungs were removed. Lung specimens were stained with hematoxylin and eosin (HE) and Masson trichrome for histological evaluation of lung injury and fibrosis by light microscopy. Body weight and lung index from various groups were measured, as well as TNF-α, TGF-β1 and type I collagen concentrations in lung homogenates. DBTG reduced bleomycin-induced weight loss, decreased the lung index and histological evidence supported the ability of DBTG to attenuate bleomycin-induced lung fibrosis and consolidation. DBTG could partly dose-dependently decrease TNF-α and TGF-β1 activity, as well as it decrease type I collagen expression in lung tissues. The findings of the present study provide evidence that DBTG may serve as a novel target for potential therapeutic treatment of lung fibrosis.Journal of ethnopharmacology 03/2011; 136(1):21-6. · 2.32 Impact Factor -
Article: [Effects of losartan and simvastatin on collagen content, myocardial expression of MMP-2 mRNA, MMP-9 mRNA and TIMP-1 mRNA, TIMP-2 mRNA in pressure overload rat hearts].
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ABSTRACT: To investigate the effects of simvastatin(Sim) and losartan(Los) on cardiac fibrosis and myocardial expression of MMP-2 mRNA, MMP-9 mRNA and TIMP-1 mRNA, TIMP-2 mRNA in pressure overloaded rat hearts. The pressure overload model was induced by descending aortic constriction (DAC) in rats. SD rats were randomized into 6 groups (n = 20 each): normol control group, control sham group, DAC group, Los group (DAC + Los, 5 mg/kg), Sim group (DAC + Sim, 2 mg/kg), Los + Sim group (DAC + Los + Sim, Los 5 mg/kg, Sim 2 mg/kg). Water, Los or Sim drug was administrated by gavage daily beginning from day 5 after operation for 30 days. Collagen was measured on Masson stained myocardial sections, and the level of MMP-2 mRNA, MMP-9 mRNA and TIMP-1 mRNA, TIMP-2 mRNA in left ventricle were detected by RT-PCR. Collagen volume fraction (CVF) in DAC group was significantly higher than the normal control and sham groups (P < 0.01) which could be significantly reduced by Los and Sim (P < 0.05), especially in DAC + Los + Sim group (P < 0.01). The levels of myocardial MMP-2 mRNA, MMP-9 mRNA and TIMP-1 mRNA, TIMP-2 mRNA were also significantly higher in DAC group than in normal control and sham groups (P < 0.01). Treatment Sim and Los alone and especially in combination significantly decreased the TIMP-1 mRNA, TIMP-2 mRNA expressions (P < 0.01) while MMP-2 mRNA, MMP-9 mRNA levels remained unchanged (P > 0.05). Upregulation of myocardial MMP-2 mRNA, MMP-9 mRNA and TIMP-1 mRNA, TIMP-2 mRNA expressions might contribute to myocardial fibrosis in this model, Sim and Los significantly inhibited myocardial fibrosis possibly by downregulating myocardial TIMP-1 mRNA, TIMP-2 mRNA expressions in this model.Zhonghua xin xue guan bing za zhi [Chinese journal of cardiovascular diseases] 10/2009; 37(10):887-91. -
Article: Antiinflammatory and immunoregulatory effects of total glucosides of Yupingfeng powder.
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ABSTRACT: Yupingfeng, a traditional Chinese complex prescription, has been used efficaciously in China for the cure and prevention of inflammatory diseases related to immunodeficiency such as allergic rhinitis and chronic bronchitis. However, the active components of this prescription remain unclear. The present study focused on investigating the antiinflammatory and immunoregulatory effects of the glucosidic extract from Yupingfeng. We tested animal models for ear swelling induced by dimethylbenzene in mice; palm swelling induced by carregeenin and granuloma induced by cotton pellet in rats; level of haemolysin, antibody generation by the splenic cells, delayed hypersensitivity and T cell subsets in spleen of immunosuppressed mice. Glucosidic extract of 24 mg/kg, 48 mg/kg and 96 mg/kg significantly inhibited mice's ear swelling induced by dimethylbenzene. Similarly glucosidic extract of 16 mg/kg, 32 mg/kg and 64 mg/kg inhibited rats' palm swelling induced by carregeenin and granuloma induced by cotton pellet. Glucosidic extract of 24 mg/kg, 48 mg/kg and 96 mg/kg improved the IgM level in serum and level of haemolysin in splenocytes in mice immunosuppressed by cyclophosphamide. Delayed hypersensitivity in mice suppressed by cyclophosphamide was enhanced by glucosidic extract of 24 mg/kg, 48 mg/kg and 96 mg/kg. These results suggested that Yupingfeng could recover humoral and cellular immune function in mice with immunosuppression. Glucosidic extract of 48 mg/kg and 96 mg/kg significantly resisted the immunosuppressive mice ear swelling and maintained it at nearly normal level. The enhanced, delayed hypersensitivity actions of glucosidic extract, suppressed by cyclophosphamide, might be brought about by inducing TH cell and regulating T lymphocytes subset. The glucosidic extract from Yupingfeng has antiinflammatory and immunoregulation action, suggesting that these glucosides are the principal active components of the traditional Chinese prescription Yupingfeng.Chinese medical journal 08/2009; 122(14):1636-41. · 0.86 Impact Factor -
Article: Synergism of simvastatin with losartan prevents angiotensin II-induced cardiomyocyte apoptosis in vitro.
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ABSTRACT: Increasing evidence suggests that cardiomyocyte apoptosis has an important role in the transition from compensatory cardiac remodelling to heart failure. The synergistic effect of statins (3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors) and angiotensin II (Ang II) type 1 receptor antagonists reduces the incidence of cardiovascular events. However, the anti-apoptotic potential of the synergism between losartan and simvastatin in heart failure remains unexplored. Here, we demonstrate that Ang II-induced apoptosis is prevented by losartan and simvastatin in neonatal cardiomyocytes. The in-vitro cardiomyocyte apoptosis model was established by co-culturing neonate rat cardiomyocytes with Ang II. Cell viability was analysed by the MTT assay. Cell apoptosis was evaluated using fluorescence microscopy and flow cytometry. Apoptosis-related proteins Bax and Bcl-2 expressions were measured by flow cytometry detection. Incubation with 10(-7) M Ang II for 48 h increased cardiomyocyte apoptosis and decreased cell viability. Losartan (10(-5) M) and simvastatin (10(-5) M), either alone or in combination, significantly decreased Ang II-induced cardiomyocyte apoptosis and increased cell viability. The q values calculated by the probability sum test were 1.31 for cardiomyocyte apoptosis and 1.21 for cell viability. Ang II induced a significant increase in Bax protein expression, whereas Bcl-2 protein expression was decreased. Losartan alone or in combination with simvastatin blocked the increased Bax expression and increased Bcl-2 expression. However, simvastatin had no such effect. Our data provide the first evidence that synergism of simvastatin with losartan prevents angiotensin II-induced cardiomyocyte apoptosis in vitro. Synergism between simvastatin and losartan may provide a new therapeutic approach to the prevention of cardiac remodelling.Journal of Pharmacy and Pharmacology 05/2009; 61(4):503-10. · 2.17 Impact Factor -
Article: Leptin stimulates alpha1(I) collagen expression in human hepatic stellate cells via the phosphatidylinositol 3-kinase/Akt signalling pathway.
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ABSTRACT: Leptin has been recognized as a profibrogenic hormone in the liver and is involved in collagen type I formation by activated hepatic stellate cells (HSCs) in response to fibrogenic substances, but the molecular signal mechanisms by which leptin promotes liver fibrogenesis through upregulation of collagen type I expression is not clear. We investigated whether leptin-induced collagen type I is mediated by the Janus kinase-phosphatidylinositol 3-kinase-Akt (JAKs-PI3K-Akt) pathway in a human HSC cell line, LX-2. LX-2 cells were treated with or without various inhibitors in the presence of leptin. Leptin increased alpha1(I) collagen mRNA and protein. JAK1, PI3K and Akt were activated after leptin stimulation. AG490, a JAK inhibitor, blocked JAK1 phosphorylation accompanied by inhibition of PI3K and Akt activation as well as alpha1(I) collagen mRNA expression, indicating a JAK1-dependent mechanism. Wortmannin, a PI3K inhibitor, prevented PI3K and Akt activation and resulted in suppression of alpha1(I) collagen mRNA expression, suggesting a PI3K-mediated process. These changes were reproduced by overexpression of the dominant-negative p85alpha mutant. A443654.3, an Akt inhibitor, opposed Akt activation, leading to downregulation of alpha1(I) collagen mRNA. Overexpression of the dominant-negative Akt mutant led to similar alterations. Leptin has a direct action on liver fibrogenesis by stimulating alpha1(I) collagen production in activated HSC. The process appears to be mediated by the PI3K/Akt pathway through activated JAK1.Liver international: official journal of the International Association for the Study of the Liver 12/2007; 27(9):1265-72. · 3.82 Impact Factor -
Article: Anti-oxidative effect of triterpene acids of Eriobotrya japonica (Thunb.) Lindl. leaf in chronic bronchitis rats
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ABSTRACT: The study was to evaluate the effect of triterpene acids of Eriobotrya japonica (Thunb.) Lindl. leaf (TAL) on expression of antioxidative mediators by alveolar macrophages (AM) in rats with chronic bronchitis (CB), CB was induced by endotracheal instillation of lipopolysaccharedes (LPS) followed by Bacillus Calmette–Guérin (BCG) injection through caudal vein 1 week later. Treatment groups received TAL at there different doses (50, 150, or 450 mg/kg daily, intragastrically (i.g.)) or dexamethasone (1.2 mg/kg daily i.g.) for 2 weeks, 7 days after LPS injection. AM were then isolated and incubated. Superoxide dismutase (SOD) and methylene dianiline (MDA) levels in AM were measured by commercial kits; meanwhile, heme oxygenase-1 (HO-1) expression and its mRNA expression in AM were detected by immunocytochemistry and RT–PCR, respectively. HO-1 activity of the lung was also detected by a specific biochemistry reaction. The levels of MDA and HO-1 expressed by cultured AM and the HO-1 activity in the lung of the TAL groups were significantly lower than those from the CB group without treatment (p < 0.01 and p < 0.05, respectively), while the SOD levels were increased in a dose-dependent manner by TAL treatment. These results suggest that TAL inhibits HO-1 expression and MDA production and up-regulates SOD expression in AM from CB rats, which might be one of molecular mechanisms of its anti-inflammatory effects in CB rats.Life Sciences 05/2006; · 2.53 Impact Factor -
Article: Pharmacokinetics and tissue distribution of 5-fluorouracil encapsulated by galactosylceramide liposomes in mice.
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ABSTRACT: To study the pharmacokinetics and tissue distribution of 5-fluorouracil encapsulated by galactosylceramide liposomes (5-Fu-GCL) in mice. The concentration of 5-fluorouracil (5-Fu) in serum was detected by high performance liquid chromatography after 5-Fu-GCL (80, 40, 20 mg/kg) and free 5-Fu (40 mg/kg) were injected intravenously into mice. The tissue distribution of 5-Fu-GCL (40 mg/kg) and free 5-Fu (40 mg/kg) was investigated, and concentration-time profile of the two preparations in the liver were studied. Data were analyzed by 3p97 program. Serum concentration-time curves of 5-Fu-GCL and free 5-Fu conformed to one compartment model of first order absorption. 5-Fu-GCL at 80, 40, and 20 mg/kg had T(1/2Ke) of 25.8+/-4.2, 27.3+/-4.4, and 28.2+/-5.6 min; C0 of 24.9+/-4.9, 17.7+/-3.6, and 11.5+/-2.7 mg/L; and AUC of 990.0+/-45.2,622.5+/-38.3, and 340.4+/-25.6 mg x min x L(-1), respectively. In contrast free 5-Fu at 40 kg/mg had T(1/2Ke) of 15.8+/-2.2 min, C0 of 35.8+/-6.2 mg/L, AUC of 639.0+/-35.9 mg x min x L(-1). The tissue distribution of 5-Fu-GCL in the liver and immune organs was significantly increased, while in heart and kidney it was remarkably decreased. The AUC of 5-Fu-GCL in the liver was 3 times higher than that of free 5-Fu. The pharmacokinetics and tissue distribution of 5-Fu-GCL appears to be linear-related and dose-dependent, and exhibits sustained-release and hepatic target characteristics.Acta Pharmacologica Sinica 03/2005; 26(2):250-6. · 1.95 Impact Factor -
Article: Gastroprotective effect and mechanism of amtolmetin guacyl in mice.
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ABSTRACT: To investigate the gastroprotective effect and mechanism of amtolmetin guacyl (AMG, MED15) in mice. Male and female Kunming strain mice, weighing 18-22 g, were utilized in the experiment. Normal or ethanol-induced gastric mucosal damage models in mice were successfully established to investigate the gastroprotective effect and mechanism of AMG. In the experiment of gastric mucosal damage after repeated treatment with AMG, the mice were randomly divided into 5 groups: normal group, 3 AMG groups receiving (75, 150 and 300 mg/kg), and tolmetin group receiving 90 mg/kg. The mice were randomly divided into 6 groups as follows: normal group, model group, AMG groups with doses of 75, 150 and 300 mg/kg, respectively, and tolmetin group with a dose of 90 mg/kg in ethanol-induced gastric mucosal damage experiment. The severity of gastric mucosal lesions was scored from 0 to 5. Gastric tissue sections were stained with hematoxylin and eosin (HE) and examined under light microscopy. Also gastric tissue sections were stained with uranyl acetate and lead citrate, and examined under electron microscopy. In addition, nitric oxide (NO) and malondialdehyde (MDA) contents, and nitric oxide synthase (NOS) and superoxide dismutase (SOD) activities in the stomach tissue homogenates were measured by biochemical methods. Repeated treatment with AMG (75, 150 and 300 mg/kg) for 7 d did not induce any appreciable mucosal damage, and the average score was not significantly different from that of normal mice. In contrast, tolmetin (90 mg/kg) produced significant gastric mucosal lesions compared with the normal group (P<0.01). AMG (75, 150 and 300 mg/kg) significantly reduced the severity of gastric lesions induced by ethanol in a dose-dependent manner as compared with the model group (P<0.05, AMG 75 and 150 mg/kg vs model; P<0.01, AMG 300 mg/kg vs model). Light and electron microscopy revealed that AMG (150 and 300 mg/kg) induced minimal changes in the surface epithelium layer, without vascular congestion or leucocyte adherence. AMG (75,150 and 300 mg/kg) demonstrated dose-dependent gastroprotective effects on mice in our study. AMG (75, 150 and 300 mg/kg) could significantly increase NO content and NOS level in the stomach homogenates of mice compared with the model group (P<0.05, AMG 75 mg/kg and 150 mg/kg groups vs model group; P<0.01, AMG 300 mg/kg vs model group) respectively. Moreover, AMG (150 and 300 mg/kg) not only significantly increased SOD activities but also obviously decreased the MDA content in the stomach homogenates of mice.World Journal of Gastroenterology 01/2005; 10(24):3616-20. · 2.47 Impact Factor
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2006
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Anhui Medical University
Hefei, Anhui Sheng, China
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