详细信息
红芪多糖对非酒精性脂肪肝病细胞模型的干预效果 被引量:3
Intervention effect of hedysarum polybotrys polysacchcaide on cell model of non-alcoholic fatty liver disease
文献类型:期刊文献
中文题名:红芪多糖对非酒精性脂肪肝病细胞模型的干预效果
英文题名:Intervention effect of hedysarum polybotrys polysacchcaide on cell model of non-alcoholic fatty liver disease
作者:张磊[1,2,3];万生芳[1];李亚玲[1]
第一作者:张磊
机构:[1]甘肃中医药大学基础医学院,兰州甘肃730000;[2]甘肃中医药大学敦煌医学与转化教育部重点实验室,兰州甘肃730000;[3]福建中医药大学中医证研究基地,福建福州350122
第一机构:甘肃中医药大学基础医学院(敦煌医学研究所)
年份:2023
卷号:39
期号:2
起止页码:206
中文期刊名:中国临床药理学杂志
外文期刊名:The Chinese Journal of Clinical Pharmacology
收录:CSTPCD;;北大核心:【北大核心2020】;CSCD:【CSCD2023_2024】;
基金:2021年度甘肃省科技计划基金资助项目(21JR1RA274);敦煌医学与转化教育部重点实验室开放课题基金资助项目(DHYX20-04)。
语种:中文
中文关键词:红芪多糖;非酒精性脂肪肝病;细胞凋亡;葡萄糖调节蛋白78;固醇调节元件结合蛋白-1
外文关键词:hedysarum polybotrys polysacchcaide;non-alcoholic fatty liver disease;apoptosis;glucose regulated protein 78;sterol regulatory element binding protein-1
摘要:目的 观察红芪多糖(HPS)对高浓度脂肪酸复制的非酒精性脂肪肝病(NAFLD)细胞模型的干预效果。方法 用1.2 mmol·L^(-1)脂肪酸培养LO-2细胞复制NAFLD细胞模型。将细胞分为正常组(细胞正常培养)、模型组(复制NAFLD细胞模型)、阳性对照组(复制模型后加入192μmol·L^(-1)硫辛酸),实验组(复制模型后加入100 mg·L^(-1)HPS),各组细胞均培养24 h。用GPO-PAP酶法检测细胞三酰甘油(TG)含量;用流式细胞技术检测细胞凋亡率;用蛋白质印迹(Western blot)法和逆转录定量聚合酶链反应检测肝细胞GRP78、SREBP-1蛋白和mRNA的表达水平。结果 正常组、模型组、阳性对照组、实验组肝细TG含量分别为(0.30±0.07),(0.87±0.28),(0.61±0.20)和(0.57±0.22)mmol·g^(-1);这4组细胞凋亡率分别为(3.70±0.46)%,(7.73±0.72)%,(4.03±1.22)%和(4.77±0.57)%;这4组GRP78 mRNA表达水平分别为1.00±0.00,1.54±0.08,1.12±0.10和1.13±0.08;这4组SREBP-1c mRNA表达水平分别为1.00±0.00,1.41±0.04,1.15±0.06和1.10±0.04;这4组GRP78蛋白表达水平分别为0.43±0.02,1.14±0.02,0.60±0.03和0.77±0.04;这4组SREBP-1蛋白表达水平分别为0.65±0.06,1.31±0.04,0.96±0.04和1.14±0.05。上述指标,模型组与正常组比较,差异均有统计学意义(均P<0.05);阳性对照组、实验组与模型组比较,差异均有统计学意义(均P<0.05)。结论 HPS可能通过调控GRP78、SREBP-1表达,减少肝细胞脂质合成,减轻内质网应激,减少肝细胞凋亡,从而保护肝细胞。
Objective To observe the intervention effect of hedysarum polybotrys polysacchcaide(HPS) on the cell model of non-alcoholic fatty liver disease induced by high concentration of fatty acid. Methods The cells were cultured with 1.2 mmol·L^(-1)fatty acids to replicate the non-alcoholic fatty liver disease cell model.The cell were divided into normal group(complete medium), model group(1.2 mmol·L^(-1)fatty acid solution), positive control group(1.2 mmol·L^(-1)fatty acid solution+ 192 μmol·L^(-1)alpha-lipoic acid) and experimental group(1.2 mmol·L^(-1)fatty acid solution+100 mg·L^(-1)HPS), culture for 24 h. The content of triglyceride(TG) was detected by GPO-PAP enzyme method;the apoptosis rate was detected by flow cytometry;the expressions of GRP78,SREBP-1 protein in hepatocytes were detected by Western blot. Results The contents of TG in hepatocytes of normal group, model group, control group and experimental group were( 0. 30 ± 0. 07),( 0. 87 ± 0. 28),( 0. 61 ± 0. 20) and( 0. 57 ± 0. 22) mmol·g^(-1),respectively;the apoptosis rates in these four groups were( 3. 70 ± 0. 46) %,( 7. 73 ± 0. 72) %,( 4. 03 ± 1. 22) % and( 4. 77 ± 0. 57) %,respectively;the levels of GRP78 mRNA in these four groups were 1. 00 ± 0. 00,1. 54 ± 0. 08,1. 12 ± 0. 10 and 1. 13 ± 0. 08,respectively;the levels of SREBP-1c mRNA in these four groups were 1. 00 ± 0. 00,1. 41 ± 0. 04,1. 15 ± 0. 06 and 1. 10 ± 0. 04,respectively;the protein expression of GRP78 in these four groups were 0. 43 ± 0. 02,1. 14 ± 0. 02,0. 60 ± 0. 03 and0. 77 ± 0. 04,respectively;the protein expressions of SREBP-1 in these four groups were 0. 65 ± 0. 06,1. 31 ± 0. 04,0. 96 ± 0. 04 and 1. 14 ± 0. 05,respectively. Compared with the normal group,there were significant differences in the above indexes of model group( all P < 0. 05);compared with the model group,there were significant differences in the above indexes of control group and experimental group( all P < 0. 05). Conclusion HPS may protect hepatocytes by regulating the expression of GRP78 and SREBP-1,reducing lipid synthesis of hepatocytes,reducing endoplasmic reticulum stress and reducing hepatocyte apoptosis.
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