Objective： To investigate the possible mechanism of San-Cao Granule（SCG, 三草颗粒） mediating antiliver fibrosis. Methods： A total of 60 male Sprague-Dawley rats were randomly divided into the normal control group,...Objective： To investigate the possible mechanism of San-Cao Granule（SCG, 三草颗粒） mediating antiliver fibrosis. Methods： A total of 60 male Sprague-Dawley rats were randomly divided into the normal control group, porcine serum-treated group, ursodesoxycholic acid（UDCA, 60 mg/kg）, SCG（3.6 g/kg） group, SCG（1.8 g/kg） group and SCG（0.9 g/kg） group, with 10 rats in each group. Liver fibrosis was induced with porcine serum by intraperitoneal injection for 8 weeks, except for the normal control group. Then, the rats in the three SCG-treated groups and UDCA group were administered SCG and UDCA respectively for 4 weeks. The serum levels of alanine transaminase（ALT）, aspartate transaminase（AST）, albumin（ALB）, total bilirubin（TBIL）, hyaluronic acid（HA）, laminin（LN）, and type Ⅳcollagen（ⅣC） were examined using commercial kits and hepatic histopathology was examined with hematoxylin and eosin and Masson staining. Moreover, the protein expression levels of high mobility group box-1 protein（HMGB1）, transforming growth factor β1（TGF-β1）, phosphorylated mothers against decapentaplegic homolog 3（p-Smad3）, Smad7, toll-like receptor 4（TLR4）, myeloid differentiation factor 88（My D88）, nuclear factor-kappa B（NF-κB） and α-smooth muscle actin（α-SMA） were determined by western blot, immunohistochemistry and real time quantitativereverse transcription polymerase. Results： Both SCG（3.6 and 1.8 g/kg） and UDCA significantly ameliorated the liver fibrosis induced by porcine serum as indicated by retarding the serum levels increasing of ALT, AST, TBIL, HA, LN and ⅣC and preventing the serum level reducing of ALB compared with the model group（all P〈0.01）. Meanwhile, the collagen deposition was attenuated by SCG and UDCA treatment. Furthermore, SCG markedly reduced the expressions of HMGB1, TGF-β1, p-Smad3, TLR4, My D88, NF-κB and α-SMA, and enhanced the expression of the Smad7 compared with the model group（all P〈0.01）. Conclusion： SCG ameliorates hepatic fibrosis possibly through inhibiting HMGB1, TLR4/NF-κB and TGF-β1/Smad signaling pathway.展开更多
文摘目的检测儿童社区获得性重症肺炎(SCAP)血清高迁移率族蛋白B1(HMGB1)、降钙素原(PCT)、Toll样受体4(TLR4)水平,并分析其对转归不良的预测价值。方法选取2019年6月至2023年6月于郑州市金水区总医院就诊的151例SCAP患儿,根据入院后28 d转归情况将其分为不良组、转归组。比较两组一般资料及入院时、入院48 h后血清HMGB1、PCT、TLR4水平;采用Logistic回归法分析SCAP患儿转归不良的影响因素,并绘制受试者工作特征曲线(ROC)分析入院时、入院后48 h血清HMGB1、PCT、TLR4单独及联合检测对转归不良的预测价值。结果SCAP患儿转归不良率为24.31%;不良组致病菌种类≥2种占比、急性生理学及慢性健康状况评分系统(APACHEⅡ)评分、机械通气占比及入院时、入院后48 h血清HMGB1、PCT、TLR4水平均高于转归组,年龄、氧合指数低于转归组,差异有统计学意义(P<0.05)。Logistic回归分析显示,年龄、致病菌≥2种、APACHEⅡ评分、机械通气及入院时、入院后48 h HMGB1、PCT、TLR4是SCAP患儿转归不良的影响因素,差异有统计学意义(P<0.05)。ROC曲线显示,入院时、入院后48 h HMGB1、PCT、TLR4联合检验的灵敏度高于单独检验,差异有统计学意义(P<0.05);三者单独检验与联合检验的特异度比较,差异无统计学意义(P>0.05);Pairwise算法检验显示,与HMGB1、PCT、TLR4单独检验比较,三者联合检验的曲线下面积(AUC)升高,差异有统计学意义(P<0.05)。结论入院时、入院后48 h血清HMGB1、PCT、TLR4水平与年龄、致病菌种类≥2种、APACHEⅡ评分、机械通气为SCAP患儿转归不良的影响因素,其中血清HMGB1、PCT、TLR4水平联合对转归不良具有较高的预测价值。
基金Supported by the Major Projects of the National Science and Technology(No.2012ZX10005010-002-002)the National Natural Science Foundation of China(No.81303120 and No.81173571)
文摘Objective： To investigate the possible mechanism of San-Cao Granule（SCG, 三草颗粒） mediating antiliver fibrosis. Methods： A total of 60 male Sprague-Dawley rats were randomly divided into the normal control group, porcine serum-treated group, ursodesoxycholic acid（UDCA, 60 mg/kg）, SCG（3.6 g/kg） group, SCG（1.8 g/kg） group and SCG（0.9 g/kg） group, with 10 rats in each group. Liver fibrosis was induced with porcine serum by intraperitoneal injection for 8 weeks, except for the normal control group. Then, the rats in the three SCG-treated groups and UDCA group were administered SCG and UDCA respectively for 4 weeks. The serum levels of alanine transaminase（ALT）, aspartate transaminase（AST）, albumin（ALB）, total bilirubin（TBIL）, hyaluronic acid（HA）, laminin（LN）, and type Ⅳcollagen（ⅣC） were examined using commercial kits and hepatic histopathology was examined with hematoxylin and eosin and Masson staining. Moreover, the protein expression levels of high mobility group box-1 protein（HMGB1）, transforming growth factor β1（TGF-β1）, phosphorylated mothers against decapentaplegic homolog 3（p-Smad3）, Smad7, toll-like receptor 4（TLR4）, myeloid differentiation factor 88（My D88）, nuclear factor-kappa B（NF-κB） and α-smooth muscle actin（α-SMA） were determined by western blot, immunohistochemistry and real time quantitativereverse transcription polymerase. Results： Both SCG（3.6 and 1.8 g/kg） and UDCA significantly ameliorated the liver fibrosis induced by porcine serum as indicated by retarding the serum levels increasing of ALT, AST, TBIL, HA, LN and ⅣC and preventing the serum level reducing of ALB compared with the model group（all P〈0.01）. Meanwhile, the collagen deposition was attenuated by SCG and UDCA treatment. Furthermore, SCG markedly reduced the expressions of HMGB1, TGF-β1, p-Smad3, TLR4, My D88, NF-κB and α-SMA, and enhanced the expression of the Smad7 compared with the model group（all P〈0.01）. Conclusion： SCG ameliorates hepatic fibrosis possibly through inhibiting HMGB1, TLR4/NF-κB and TGF-β1/Smad signaling pathway.
