Protective function of compound Danshen injection on stress-induced gastric mucosal damage of rats / 国际中医中药杂志

Objective To investigate the effects of compound Danshen injection on stress-induced gastric mucosal damage and its mechanism.Methods Sprague Dawley rats were used to establish immersion restraint cold stress model.50 SD rats were randomly divided into five groups(n=10 per group):① the normal control group; ② the stress model group; ③ the group treated with low dose of compound Danshen injection(50 mg/kg) ; ④ the group treated with medial dose of compound Danshen injection(100 mg/kg) ; ⑤the group treated with high dose of compound Danshen injection (200 mg/kg).The gastric mucosal ulcer index (UI),the level of malondialdehyde (MDA) in gastric mucosa,the activity of superoxide dismutase (SOD),and plasma intedeukin-1beta (IL-1β)content were detected.Results Compared with the normal control group [(0.7± 0.4) mm,(0.25 ± 0.03)nmol/mg,and (246.5 ± 45.4)Nu/mg],the stress model group exhibited a markedly increase in gastric mucosal UI[(28.4±4.5)mm](P＜0.01) and MDA level [(0.60±0.08)nmol/mg](P＜0.01) and a decrease in the activity of gastric mucosal SOD [(122.5 ±14.2) Nu/mg] (P＜0.01).In addition,an elevated level of plasma IL-1β[(31.6±8.4) pg/ml vs (8.5±3.1) pg/ml] (P＜0.01) was observed in the stress model group.Pretreatment with compound Danshen injection dose-dependently attenuated the gastric mucosal damage,characterized by a markedly decrease in gastric mucosal UI [(22.8 ± 3.7)mm、(12.2 ±3.5)mm,(6.2 ± 1.6)mm] and MDA level [(0.52 ± 0.07)nmol/mg,(0.32 ± 0.06)nmol/mg,(0.28 ±0.03)nmol/mg] and an increase in the activity of gastric mucosal SOD[(135.2± 13.6)Nu/mg,(220.7±33.5)Nu/mg,(251.2±23.7)Nu/mg] (P＜0.01).Meanwhile,compound Danshen injection reduced the content of plasma IL-1β[(27.2±7.5)pg/ml,(13.5±5.3)pg/ml,(9.3±4.4)pg/ml] (P＜0.01).Conclusion Compound Danshen injection exhibits preventive protection on the stress-induced gastric mucosal damage by water immersion restraint cold stress in SD rats,the mechanism of which might be linked to its inhibition of gastric mucosal oxidation stress and the reduced release of inflammatory mediator IL-1β.

The change of the hepatic fibrosis and pigment deposition in mice schistosomal liver fibrosis treated with combination of Anluohuaxian pilule and interferon-γ / 中华传染病杂志

Objective To evaluate efficacy and mechanism of Anluohuaxian pilule combined with interferon-γ in the treatment of schistosomal liver fibrosis. To preliminarily study on the relationship of pigment deposition in liver and schistosomal liver fibrosis. Methods Thirty Kunming mice were divided into the normal control group, the infection control group and the combination of Anluohuaxian pilule and Interferon-γ treated group. Schistosomal liver fibrosis model was established by infection with 40 Schistosoma japonicum cercariae. The treated group was treated by combination of Anluohuaxian pilule and Interferon-γ for 8 weeks. The changes of pigment deposition and hepatic egg granuloma in Schistosoma japonicum infected mice were observed. Expressions of collagen Ⅰ and Ⅲ were detected by immunohistochemistry. Transforming growth factor (TGF)-β1 was detected by fluorescent polymerase chain reaetion(PCR). Histopathology and computer image analysis were applied to evaluate the change in the liver tissues. Results The amount of pigment deposition in liver was related to the expression of TGF-β1 mRNA (correlation coefficient = 0. 8). Compared to the infection control group, combination of Anluohuaxian pilule and Interferon-γ can lessen hepatic fibrosis(P<0.05). The combination therapy can also make pigment deposition less and hepatic granuloma smaller than the infection control group(P<0. 05). Conclusions Pigment deposition in liver is related to the expression of TGF-β 1. Combination of Anluohuaxian pilule and Interferon-γ can lessen hepatic fibrosis in mice infected with Schistosoma japonicum. It's one mechanism to of the combination therapy down-regulate the expression of collagen Ⅰ, Ⅲ and TGF-β 1.

Differential Gene Expression Profiles in Acute Hepatic Failure Model in Mice Infected with MHV-3 Virus Intervened by Anti-hepatic Failure Compound / 华中科技大学学报（医学）（英德文版）

Differential gene expression profiles in Balb/cJ mouse model of acute hepatic failure in- fected with MHV-3 virus intervened by anti-hepatic failure compound (AHFC) and the changes of cytokines regulated by genes were investigated. The Balb/cj mice were divided into AHFC-intervened group and control group randomly. Acute hepatic failure model of Balb/cJ mice infected with MHV-3 virus was established. The survival rate in the two groups was observed. It was found that the survival rate in the AHFC-intervened group and control group was 90% and 50% re- spectively 48 h after intrapefitoneal injection of MHV-3 (P<0.05). Before and after the experiment, the cytokines in peripheral blood of the survival mice were determined, and RNA was extracted from survival mouse liver tissue for the analysis of the differential gene expression by a 36 kb mouse oli- gonuleotide DNA array. In all the genes of microarray there were 332 genes expressed differently in the two groups, in which 234 genes were up-regulated and 78 genes down-regulated. Through clustering analysis, the differential expression of immune related genes, including TNF receptor superfamily, Kctd9, Bcl-2, Fg12, IL-8, IL-6, IFN-γ, TNF-α etc. might be related with the curative effectiveness of AHFC. It was suggested that AHFC can balance the immune state of mouse model of acute hepatic failure infected with MHV-3 virus mainly through regulating the expression of immune related genes, decrease the immune damage and inhibit liver cell apoptosis of mouse acute hepatic failure model obviously so as to increase the survival rate of mouse models of acute hepatic failure.

Differential gene expression profiles in acute hepatic failure model in mice infected with MHV-3 virus intervened by anti-hepatic failure compound / 华中科技大学学报（医学）（英德文版）

Differential gene expression profiles in Balb/cJ mouse model of acute hepatic failure infected with MHV-3 virus intervened by anti-hepatic failure compound (AHFC) and the changes of cytokines regulated by genes were investigated. The Balb/cj mice were divided into AHFC-intervened group and control group randomly. Acute hepatic failure model of Balb/cJ mice infected with MHV-3 virus was established. The survival rate in the two groups was observed. It was found that the survival rate in the AHFC-intervened group and control group was 90% and 50% respectively 48 h after intraperitoneal injection of MHV-3 (P<0.05). Before and after the experiment, the cytokines in peripheral blood of the survival mice were determined, and RNA was extracted from survival mouse liver tissue for the analysis of the differential gene expression by a 36 kb mouse oligonucleotide DNA array. In all the genes of microarray there were 332 genes expressed differently in the two groups, in which 234 genes were up-regulated and 78 genes down-regulated. Through clustering analysis, the differential expression of immune related genes, including TNF receptor superfamily, Kctd9, Bcl-2, Fgl2, IL-8, IL-6, IFN-gamma, TNF-alpha etc. might be related with the curative effectiveness of AHFC. It was suggested that AHFC can balance the immune state of mouse model of acute hepatic failure infected with MHV-3 virus mainly through regulating the expression of immune related genes, decrease the immune damage and inhibit liver cell apoptosis of mouse acute hepatic failure model obviously so as to increase the survival rate of mouse models of acute hepatic failure.