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1.广东药科大学附属第一医院中医科, 广州 510080
2.南方医科大学南方医院临床药学中心,广州 510515
硕士研究生。研究方向:中医药防治心血管疾病。 E-mail:ziyunwen1997@163.com
副研究员,硕士生导师,博士。研究方向:中医药防治心血管疾病。E-mail:huiyun1227@163.com
收稿日期:2023-11-16,
修回日期:2024-03-08,
录用日期:2024-03-28,
纸质出版日期:2024-05-30
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温紫云,韩倩倩,吕晴,等.水蛭对非酒精性脂肪肝病小鼠的保护作用及其机制[J].中国药房,2024,35(10):1193-1197.
WEN Ziyun,HAN Qianqian,LYU Qing,et al.Protective effect and mechanism of Hirudo on mice with non-alcoholic fatty liver disease[J].ZHONGGUO YAOFANG,2024,35(10):1193-1197.
温紫云,韩倩倩,吕晴,等.水蛭对非酒精性脂肪肝病小鼠的保护作用及其机制[J].中国药房,2024,35(10):1193-1197. DOI: 10.6039/j.issn.1001-0408.2024.10.07.
WEN Ziyun,HAN Qianqian,LYU Qing,et al.Protective effect and mechanism of Hirudo on mice with non-alcoholic fatty liver disease[J].ZHONGGUO YAOFANG,2024,35(10):1193-1197. DOI: 10.6039/j.issn.1001-0408.2024.10.07.
目的
2
探讨水蛭对非酒精性脂肪肝病(NAFLD)小鼠的保护作用及潜在机制。
方法
2
将雄性载脂蛋白E基因敲除(
ApoE
-/-
)小鼠随机分为模型组和水蛭低、高剂量组(0.45、0.9 g/kg),每组10只;另取同周龄野生型雄性C57BL/6J小鼠10只,作为对照组。对照组小鼠以基础维持饲料喂养,其余各组小鼠以高脂饲料喂养12周以建立NAFLD模型。第13周,各药物组小鼠灌胃相应药液,每天1次,连续8周。末次给药后,测定各组小鼠的体重、肝脏质量,并计算肝脏指数;检测其血清核因子κB(NF-κB)、肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)、IL-6、总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)水平;观察其肝组织病理形态学变化,并检测肝组织中过氧化物酶体增殖物激活受体γ(PPARγ)、沉默信息调节因子1(SIRT1)蛋白的表达情况。
结果
2
与对照组比较,模型组小鼠肝组织可见较多的脂肪空泡和炎症细胞浸润,并有明显的脂质堆积;其体重、肝脏质量及肝脏指数和血清NF-κB、TNF-α、IL-1β、IL-6、TC、TG、LDL-C水平均显著升高,血清HDL-C水平和肝组织中PPARγ、SIRT1蛋白的表达水平均显著降低(
P
<0.01)。与模型组比较,水蛭低、高剂量组小鼠肝组织病理改变均有所缓解;其体重、肝脏质量及肝脏指数和血清NF-κB、TNF-α、IL-1β、IL-6、TC、TG、LDL-C水平均显著降低,血清HDL-C水平和肝组织中PPARγ、SIRT1蛋白的表达水平均显著升高(
P
<0.05或
P
<0.01)。
结论
2
水蛭可能通过激活PPARγ、SIRT1蛋白的表达来调节肝脏脂质代谢、抑制炎症反应,从而发挥对NAFLD的改善作用。
OBJECTIVE
2
To explore the protective effects and potential mechanisms of
Hirudo
on mice with non-alcoholic fatty liver disease (NAFLD) in mice.
METHODS
2
The male
ApoE
-/-
mice were randomly divided into the model group and Hirudo low-dose and high-dose groups (0.45, 0.9 g/kg), with 10 mice in each group; another 10 wild-type male C57BL/6J mice were chosen as the control group. The control group was fed with basal maintenance chow and the remaining groups were fed with high-fat chow for 12 weeks to establish the NAFLD model. Each administration group was given corresponding solution intragastrically, once a day, for 8 consecutive weeks. In the 13th week, the body weight and liver weight of mice in each group were measured after the last medication, and the liver index was calculated; the serum levels of nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α), interle
ukin-1β (IL-1β), IL-6, total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) were detected; the liver pathomorphological changes were observed; the protein expressions of peroxisome proliferator-activated receptor γ(PPARγ) and silence information regulator type 1 (SIRT1) were detected.
RESULTS
2
Compared with the control group, the liver tissue of mice in the model group showed more fat vacuoles and infiltration of inflammatory cells, with significant lipid accumulation; the body weight, liver weight and liver index of the mice, and serum levels of NF-κB, TNF-α, IL-1β, IL-6, TC, TG and LDL-C significantly increased, while the serum level of HDL-C, the protein expressions of PPARγ and SIRT1 in liver tissues significantly decreased (
P
<0.01). Compared with the model group, the pathological changes in liver tissue of mice were all relieved in Hirudo low-dose and high-dose groups; the body weight, liver weight and liver index, the serum levels of NF-κB, TNF-α, IL-1β, IL-6, TC, TG and LDL-C decreased significantly, while the serum level of HDL-C, the protein expressions of PPARγ and SIRT1 in liver tissue all increased significantly (
P
<0.05 or
P
<0.01).
CONCLUSIONS
2
Hirudo can regulate liver lipid metabolism and inhibit inflammation by activating the protein expressions of PPARγ and SIRT1, thus having a significant ameliorative effect on NAFLD.
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