甘草苷对刀豆蛋白A诱导的实验性肝损伤的保护作用及机制  

Effect of Glycyrrhizin on experimental liver injury induced by concanavalin A

作　　者：文怡欣 鄂志野 张珊 聂影[1] 鞠宝玲[1] 张红军[1] WEN Yi-xin(Department of Immunology, Mudanjiang Medical University, Mudanjiang 157011, China)

机构地区：[1]牡丹江医学院免疫学教研室,黑龙江牡丹江157011

出　　处：《牡丹江医学院学报》2022年第3期16-19,79,共5页Journal of Mudanjiang Medical University

基　　金：黑龙江省省属高等学校基本科研业务费项目(2020-KYYWF-0781)。

摘　　要：目的 探讨甘草苷(Liquiritin,Liq)对刀豆蛋白A(Concanavalin A,ConA)诱导的实验性肝损伤的保护作用及作用机制。方法 将ICR小鼠雌雄各半随机分为四组:对照组、ConA模型组、药物治疗中剂量组(ConA+Liq40 mg/kg)、药物治疗高剂量组(ConA+Liq80 mg/kg)。对照组给予等量的生理盐水,其余组均通过小鼠尾静脉注射ConA(10 mg/kg)1次/7 d,共6次建立肝损伤模型,第28天开始药物治疗中剂量组按40 mg/kg、药物治疗高剂量组按80 mg/kg体重灌胃,1次/d,连续治疗14 d,第42天后处死小鼠,收集样本待检;采用全自动生化仪检测血清丙氨酸氨基转移酶(alanine aminotransferase,ALT)、天门冬氨酸氨基转移酶(aspartate aminotransferase,AST)水平;HE染色观察肝脏病理学改变;Masson染色分析肝脏组织中胶原纤维的表达;实时荧光定量PCR(QuantitativeReal-TimePCR,qRT-PCR)检测实验动物肝组织Ⅰ型胶原(CollagenⅠ,col1a1)、α-平滑肌激动蛋白(α-smooth muscle actin,α-SMA)和激活素A(ActivinA)、激活素受体2A(Activin A Receptor TypeⅡ,ACVR2A)及Smad2的mRNA表达情况。结果 与对照组相比,ConA模型组ALT与AST水平明显升高,与ConA模型组相比,药物治疗中剂量组以及药物高剂量组组小鼠的ALT和AST均有所下降(P<0.05);ConA模型组的组织切片染色可见肝脏小叶结构破坏,有大片组织坏死,细胞肿胀,伴有脂肪变性,药物治疗组中剂量组与药物高剂量组损伤明显减轻;与对照组相比,ConA模型组的胶原含量增加,与ConA模型组比较,药物治疗组中剂量组与药物高剂量组的胶原含量减少(P<0.05);与对照组相比,ConA模型组中col1a1以及α-SMA、Smad2、ActivinA、ACVR2A的mRNA表达上升,与ConA模型组相比,药物治疗中剂量组以及药物治疗高剂量组可明显下调实验动物肝组织col1a1以及α-SMA的mRNA表达,还可下调Smad2、ActivinA、ACVR2A的mRNA表达(P<0.05)。结论 Liq能有效缓解ConA诱导的肝损伤,具有肝脏保护作用,其机制可�Objective To explore the protective effect and mechanism of Liquiritin(Liq) on experimental liver injury induced by A(Concanavalin A(ConA). Methods ICR mice were randomly divided into four groups: control group, ConA model group, middle dose group(ConA+Liq40 mg/kg) and high dose group(ConA+Liq80 mg/kg). The control group was given the same amount of normal saline, and the other groups were injected with ConA(10 mg/kg) once a day for 7 days with 6 times in total through the tail vein of mice to establish the liver injury model. From the 28 th day, the drug treatment group with 40 mg/kg in the middle dose and the drug treatment group with 80 mg/kg in the high dose were given intragastrically once a day for 14 days, and the mice were killed after the 42 day, and samples were collected for examination. The levels of serum alanine aminotransferase(ALT) and aspartate aminotransferase(AST) were detected by automatic biochemical analyzer. Pathological changes of liver were observed by HE staining. Masson staining was used to analyze the expression of collagen fibers in liver tissue. The mRNA expression of collagen Ⅰ(col1 a1), α-smooth muscle actin(α-SMA), activin A,(Activin A receptor type ⅡACVR2 A) and Smad2 in experimental animal liver tissues was detected by qRT-PCR. Results Compared with the control group, the levels of ALT and AST in ConA model group were significantly increased, while the levels of ALT and AST in mice in middle dose group and high dose group were decreased(P<0.05). Tissue section staining of ConA model group showed that the liver lobule structure was damaged, with large tissue necrosis, cell swelling and fatty degeneration, and the damage of middle dose group and high dose group in drug treatment group was significantly reduced. Compared with the control group, the collagen content of ConA model group increased, while the collagen content of middle-dose group and high-dose group decreased(P<0.05). Compared with the control group, the mRNA expressions of col1 a1, α-SMA, Smad2, Activin A and A

关 键 词：LIQUIRITIN CONA 免疫性肝损伤 HSC ActivinA 

分 类 号：R285.5[医药卫生—中药学]