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溪黄草水提物对四氯化碳诱导大鼠肝纤维化的保护作用及机制研究     被引量:17

Protective Effects and the Mechanism Study of Water Extract of Rabdosia serra on Hepatic Fibrosis Induced by Carbon Tetrachloride in Rats

文献类型:期刊文献

中文题名:溪黄草水提物对四氯化碳诱导大鼠肝纤维化的保护作用及机制研究

英文题名:Protective Effects and the Mechanism Study of Water Extract of Rabdosia serra on Hepatic Fibrosis Induced by Carbon Tetrachloride in Rats

作者:许琼梅[1];李跃龙[1];曹后康[1];陈春[1];王刚[1];朱依谆[1];张可锋[1,2]

第一作者:许琼梅

机构:[1]桂林医学院药物研究所;[2]甘肃中医药大学药学院

第一机构:桂林医学院药物研究所

年份:2018

卷号:29

期号:20

起止页码:2791

中文期刊名:中国药房

外文期刊名:China Pharmacy

收录:CSTPCD;;北大核心:【北大核心2017】;

基金:广西壮族自治区教育厅八桂学者专项经费项目(No.桂财教函[2017]143号)

语种:中文

中文关键词:溪黄草;水提物;肝纤维化;四氯化碳;氧化应激;炎症因子;转化生长因子β1;大鼠

外文关键词:Rabdosia serra;Water extract;Hepatic fibrosis;Carbon tetrachloride;Oxidative stress;Inflammatory factor;TGF-β1;Rats

摘要:目的:研究溪黄草水提物(RWE)对四氯化碳(CCl4)诱导大鼠肝纤维化(HF)的保护作用及其机制。方法:将60只雄性SD大鼠随机分为正常组、模型组、秋水仙碱组(0.12 mg/kg)和RWE低、中、高剂量组(4、8、16 g/kg,以生药量计),每组10只。除正常组大鼠腹腔注射橄榄油外,其余各组大鼠均腹腔注射40%CCl4橄榄油溶液以复制HF模型。自造模第1天起,各给药组大鼠均灌胃相应药物(10 mL/kg),正常组和模型组大鼠均灌胃等体积水,每天1次,连续6周。给药结束后,采用生化法或酶联免疫吸附测定法检测大鼠血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、透明质酸(HA)、层粘连蛋白(LN)、Ⅲ型前胶原(PCⅢ)、Ⅳ型胶原(Ⅳ-C)的含量以及肝组织中丙二醛(MDA)、超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、IL-1β的含量或活性;采用苏木精-伊红染色观察大鼠肝组织病理学变化;采用蛋白质印迹法检测大鼠肝组织中α-平滑肌肌动蛋白(α-SMA)、转化生长因子β1(TGF-β1)蛋白表达情况。结果:与正常组比较,模型组大鼠血清中ALT、AST、HA、LN、PCⅢ、Ⅳ-C的含量以及肝组织中MDA、TNF-α、IL-6、IL-1β的含量均显著升高(P<0.01),肝组织中SOD、GSH-Px的活性均显著降低(P<0.01);肝组织纤维化明显;肝组织中α-SMA、TGF-β1蛋白的相对表达量均显著升高(P<0.01)。与模型组比较,秋水仙碱组和RWE各剂量组大鼠血清中ALT、AST、HA、LN、PCⅢ、Ⅳ-C的含量以及肝组织中MDA、TNF-α、IL-6的含量,秋水仙碱组和RWE中、高剂量组大鼠肝组织中IL-1β的含量均显著降低(P<0.05或P<0.01),秋水仙碱组和RWE各剂量组大鼠肝组织中SOD、GSH-Px的活性均显著增强(P<0.05或P<0.01);肝组织纤维化程度明显减轻;肝组织中α-SMA、TGF-β1蛋白的相对表达量均显著降低(P<0.01)。结论:RWE对CCl4诱导的HF模型大鼠具有一定的保护作用,其作用机制可能与调节脂质代谢、减轻肝脂质过氧化损伤、抗氧化应激反应、抑制炎症因子释放及TGF-β1蛋白表达等有关。
OBJECTIVE:To study the protective effects and the mechanism of Rabdosia serra water extract(RWE)on hepatic fibrosis(HF)induced by carbon tetrachloride(CCl4)in rats.METHODS:Sixty male SD rats were randomly divided into normal group,model group,colchicine group(0.12 mg/kg),and RWE low-dose,medium-dose and high-dose groups(4,8,16 g/kg,by crude drug),with 10 rats in each group.Except for intraperitoneal injection of olive oil for normal group,other groups were given 40%CCl4 olive oil solution intraperitoneally to induce HF model.Since the first day of modeling,each treatment group was given relevant medicine(10 mL/kg)intragastrically,while normal group and model group were given constant volume of water intragastrically,once a day,for consecutive 6 weeks.After medication,biochemical process or ELISA were used to determine the contents of ALT,AST,HA,LN,PCⅢandⅣ-C in serum,the activities or contents of SOD,GSH-Px,MDA,TNF-α,IL-6 and IL-1βin liver tissue.Pathological changes of liver tissue in rats were observed by HE staining.The expression ofα-SMA and TGF-β1 in liver tissue were detected by Western blot.RESULTS:Compared with normal group,the contents of ALT,AST,LN,HA,PCⅢandⅣ-C in serum,the contents of MDA,TNF-α,IL-6 and IL-1βin liver tissue were all increased significantly in model group(P<0.01);the activities of SOD and GSH-Px in liver tissue were decreased significantly(P<0.01).Liver fibrosis was obvious,and the relative expression ofα-SMA and TGF-β1 were increased significantly(P<0.01).Compared with model group,the contents of ALT,AST,HA,LN,PCⅢandⅣ-C in serum as well as the contents of MDA,TNF-αand IL-6 in liver tissue in colchicines group and RWE groups,the contents of IL-1βin liver tissue of rats in colchicines group,RWE medium-dose and high-dose groups were all decreased significantly(P<0.05 or P<0.01).The activities of SOD and GSH-Px in liver tissue of rats were increased significantly in colchicines group and RWE groups(P<0.05 or P<0.01).The fibrosis degree of liver tissue was significantly reduced,while the relative expression ofα-SMA and TGF-β1 decreased significantly(P<0.01).CONCLUSIONS:RWE can protect CCl4-induced HF model rats,the mechanism of which may be associated with regulating lipid metabolism,relieving liver lipid peroxidation injury and anti-oxidative stress response,inhibiting the release of inflammatory factors and the expression of TGF-β1.

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