阿魏酸对高糖诱导的肾小球系膜细胞炎症及自噬水平的影响*

doi:10.12047/j.cjap.6305.2022.085

摘要/Abstract

摘要： 目的: 通过观察阿魏酸对高糖诱导的肾小球系膜细胞炎症及自噬水平的影响,探讨阿魏酸对糖尿病肾病的保护作用及其可能机制。方法: 将SV40 MES 13细胞进行传代培养,随机分为:正常组(Control,5.6 mmol/L 葡萄糖)、甘露醇组(Man,30 mmol/L 甘露醇)、高糖组(HG,30 mmol/L 葡萄糖)、阿魏酸组(FA,30 mmol/L 葡萄糖 + 12.5、25、50、100、200 μmol/L 阿魏酸)。采用MTT法观察各组系膜细胞增殖情况;酶联免疫吸附试验(ELISA)法检测细胞上清液肿瘤坏死因子-α(TNF-α)、单核细胞趋化蛋白-1(MCP-1)和白介素-1β(IL-1β)的含量;免疫印迹法(Western blot)检测系膜细胞NLRP3、IL-1β、LC3-Ⅱ/Ⅰ、p62蛋白的表达水平。结果: ①与Control组相比,HG组肾小球系膜细胞增殖活力显著升高(P＜0.01),与HG组相比,不同浓度FA组的肾小球系膜细胞增殖活力则有不同程度的下降(P＜0.05~0.01);②与Control组相比,HG组细胞上清液中TNF-α、MCP-1和IL-1β含量均显著增加(P＜0.01),与HG组相比,FA组TNF-α、MCP-1和IL-1β含量均显著减少(P＜0.01);③与Control组相比,HG组细胞LC3-Ⅱ/Ⅰ比值减小,p62、NLRP3和IL-1β蛋白表达则均显著升高(P＜0.01),与HG组比较,FA组细胞LC3-Ⅱ/Ⅰ比值明显增大(P＜0.05),p62、NLRP3和IL-1β蛋白水平均显著降低(P＜0.01)。结论: FA可抑制高糖诱导的SV40 MES 13细胞异常增殖,FA可通过抑制炎症、提高自噬水平而保护系膜细胞。

关键词: 阿魏酸, 肾小球系膜细胞, 炎症, 自噬

Abstract: Objective: To investigate the protective effects and possible mechanisms of ferulic acid on diabetic nephropathy by observing the effects of ferulic acid on the level of inflammation and autophagy in glomerular mesangial cells induced by high glucose. Methods: SV40 MES 13 cells were cultured and randomly divided into the following groups: normal group (Control, 5.6 mmol/L glucose), mannitol group (Man, 30 mmol/L mannitol), high glucose group (HG, 30 mmol/L glucose), ferulic acid group (FA, 30 mmol/L glucose + 12.5, 25, 50, 100, 200 μmol/L ferulic acid), and the proliferation of SV40 MES 13 cells in each group was observed by MTT method. The levels of tumour necrosis factor-α (TNF-α), monocyte chemotactic protein-1 (MCP-1) and interleukin 1β(IL-1β)in cell supernatant were determined by enzyme-linked immunosorbent assay (ELISA). The expressions of NLRP3, IL-1β, LC3-II/I and p62 proteins in SV40 MES 13 cells were detected by Western blot. Results: ①The proliferative activity of SV40 MES 13 cells was significantly higher in the HG group compared to the control group (P＜0.01), while the proliferative activity of SV40 MES 13 cells was decreased to different degrees in the FA group compared to the HG group (P＜0.05～0.01). ②Compared to the control group, the levels of TNF-α, MCP-1 and IL-1β were increased significantly in the cell supernatant of HG group (P＜0.01). Compared with the HG group, the levels of TNF-α, MCP-1 and IL-1β were decreased significantly in the FA group (P＜0.01). ③Compared with the control group, LC3-II/Ⅰ protein expression was decreased in the HG group, while the levels of p62, NLRP3 and IL-1β protein were increased significantly (P＜0.01). Compared with the HG group, the expression of LC3-II/Ⅰ protein was elevated significantly (P＜0.05) in the FA group, while the levels of p62, NLRP3 and IL-1β protein in the FA group were decreased significantly (P＜ 0.01). Conclusion: FA can inhibit the abnormal proliferation of SV40 MES 13 cells induced by high glucose. FA can protect glomerular mesangial cells by inhibiting inflammation and increasing the level of autophagy.

Key words: Ferulic acid, glomerular mesangial cells, inflammation, autophagy

中图分类号:

R285.5

方情, 马汝玉, 贺英昊, 齐敏友. 阿魏酸对高糖诱导的肾小球系膜细胞炎症及自噬水平的影响^*[J]. 中国应用生理学杂志, 2022, 38(5): 453-457.

FANG Qing, MA Ru-yu, HE Ying-hao, QI Min-you. Effects of ferulic acid on inflammation and autophagy levels in glomerular mesangial cells induced by high glucose[J]. CJAP, 2022, 38(5): 453-457.

参考文献

[1] Umanath K, Lewis JB. Update on diabetic nephropathy: Core curriculum 2018[J]. Am J Kidney Dis, 2018, 71(6): 884-895.
[2] Tang SCW, Yiu WH. Innate immunity in diabetic kidney disease[J]. Nat Rev Nephrol, 2020, 16(4): 206-222.
[3] Liu X Q, Jiang L, Lei L, et al. Carnosine alleviates diabetic nephropathy by targeting GNMT, a key enzyme mediating renal inflammation and fibrosis[J]. Clin Sci (Lond), 2020, 134(23): 3175-3193.
[4] Yaribeygi H, Atkin SL, Sahebkar A. Interleukin-18 and diabetic nephropathy: A review[J]. J Cell Physiol, 2019, 234(5): 5674-5682.
[5] Sun L, Kanwar YS. Relevance of TNF-α in the context of other inflammatory cytokines in the progression of diabetic nephropathy[J]. Kidney Int, 2015, 88(4): 662-665.
[6] She H, He Y, Zhao Y, et al. Release the autophage brake on inflammation: The MAPK14/p38α-ULK1 pedal[J]. Autophagy, 2018, 14(6): 1097-1098.
[7] Levine B, Kroemer G. Biological functions of autophagy genes: A disease perspective[J]. Cell, 2019, 176(1-2): 11-42.
[8] Magee C, Grieve DJ, Watson CJ, et al. Diabetic nephropathy: a tangled web to unweave[J]. Cardiovasc Drugs Ther, 2017, 31(5-6): 579-592.
[9] Ghosh S, Basak P, Dutta S, et al. New insights into the ameliorative effects of ferulic acid in pathophysiological conditions[J]. Food Chem Toxicol, 2017, 103: 41-55.
[10] Ambothi K, Prasad N R, Balupillai A. Ferulic acid inhibits UVB-radiation induced photocarcinogenesis through modulating inflammatory and apoptotic signaling in Swiss albino mice[J]. Food Chem Toxicol, 2015, 82: 72-78.
[11] 王旭焘, 潘定一, 郭玮, 等. 阿魏酸对糖尿病大鼠肾脏足细胞nephrin、podocin蛋白表达的影响[J]. 中国应用生理学杂志, 2017, 33(6): 564-567.
[12] 万金艳, 龙宇, 张羽璐, 等. PI3K/Akt信号通路在糖尿病肾病中的作用及中药干预的研究进展[J]. 中草药, 2021, 52(12): 3705-3716.
[13] Ferrucci L, Fabbri E. Inflammageing: chronic inflammation in ageing, cardiovascular disease, and frailty[J]. Nat Rev Cardiol, 2018, 15(9): 505-522.
[14] Du Q, Fu YX, Shu AM, et al. Loganin alleviates macrophage infiltration and activation by inhibiting the MCP-1/CCR2 axis in diabetic nephropathy[J]. Life Sci, 2021, 272: 118808.
[15] 郭亚净, 任静, 刘寒, 等. MCC950对脑出血大鼠神经损伤的作用[J]. 中国应用生理学杂志, 2022, 38(1): 11-16.
[16] Wu M, Han W, Song S, et al. NLRP3 deficiency ameliorates renal inflammation and fibrosis in diabetic mice[J]. Mol Cell Endocrinol, 2018, 478: 115-125.
[17] Yamahara K, Yamahara M, Kume S. Role of autophagy in diabetic nephropathy[J]. Nihon Jinzo Gakkai Shi, 2017, 59(2): 50-57.
[18] 吕栋辉, 安方玉, 颜春鲁, 等. 中风胶囊对脑缺血/再灌注损伤模型鼠脑组织自噬相关蛋白表达的影响[J]. 中国应用生理学杂志, 2022, 38(1): 25-31.
[19] Zhang P, Fang J, Zhang J, et al. Curcumin inhibited podocyte cell apoptosis and accelerated cell autophagy in diabetic nephropathy via regulating Beclin1/UVRAG/Bcl2[J]. Diabetes Metab Syndr Obes, 2020, 13: 641-652.
[20] Choi ME. Autophagy in kidney disease[J]. Annu Rev Physiol, 2020, 82: 297-322.

阿魏酸对高糖诱导的肾小球系膜细胞炎症及自噬水平的影响^*

Effects of ferulic acid on inflammation and autophagy levels in glomerular mesangial cells induced by high glucose

PDF (PC)

可视化

摘要/Abstract

引用本文

使用本文

参考文献

相关文章 15

编辑推荐

Metrics

本文评价

[1]	王勇, 赵伟, 姜正林, 陈振华, 张欢. miR-125b-5p对创伤性脑损伤诱发大鼠认知功能障碍的干预作用及其机制^*[J]. 中国应用生理学杂志, 2022, 38(5): 424-429.
[2]	杜玥, 王志旺, 席建宏, 李济阳, 梁可克, 黄柯婷, 罗慧英. cAMP/Epac信号通路在当归治疗阴虚证慢性咳嗽中的作用^*[J]. 中国应用生理学杂志, 2022, 38(5): 475-479.
[3]	任彩佩, 张一楠, 吴亚俐, 都新新, 崔香丽. 白藜芦醇抑制肠癌细胞焦亡的作用^*[J]. 中国应用生理学杂志, 2022, 38(4): 326-331.
[4]	苗莹莹, 袁欢欢, 黄敏杰, 付升旗. 过表达微小RNA-130a-3P对LPS诱导心肌细胞损伤的干预作用及其机制^*[J]. 中国应用生理学杂志, 2022, 38(4): 335-340.
[5]	胡戈, 曹建民, 周海涛, 张静, 田一鸣, 宋滢洋, 蒋若雨. 黑果枸杞汁对大鼠酒精性肝损伤的保护作用^*[J]. 中国应用生理学杂志, 2022, 38(3): 241-246.
[6]	王肖婷, 汤一冰, 林青青, 王新雨, 宋正阳, 郝卯林, 钱巍, 王万铁. 细胞自噬在大鼠肺缺血/再灌注引发肝脏损伤中的作用^*[J]. 中国应用生理学杂志, 2022, 38(2): 102-107.
[7]	郭亚净, 任静, 刘寒, 李亭亭, 张帅, 王洪. MCC950对脑出血大鼠神经损伤的作用^*[J]. 中国应用生理学杂志, 2022, 38(1): 11-16.
[8]	吕栋辉, 安方玉, 颜春鲁, 李海龙, 王嘉玉, 石瑶, 袁灵青, 赵延真, 杨建新, 郭丹, 颉旺军. 中风胶囊对脑缺血/再灌注损伤模型鼠脑组织自噬相关蛋白表达的影响^*[J]. 中国应用生理学杂志, 2022, 38(1): 25-31.
[9]	白林林, 王志华, 宁学聪, 巩翠珂, 李爱敏, 段玉玲, 焦雨佼. IL-17A对慢性阻塞性肺疾病的干预作用及其机制^*[J]. 中国应用生理学杂志, 2021, 37(6): 584-588.
[10]	薛峰, 王辉, 许思多, 刘首挺, 龚永生, 范小芳. 左旋卡尼汀对脂多糖诱导小鼠肺微血管内皮细胞自噬和凋亡的影响^*[J]. 中国应用生理学杂志, 2021, 37(6): 589-593.
[11]	丁利平, 韩莹, 成祥, 赵彤, 朱玲玲, 廖红. 低氧联合LPS刺激对星形胶质细胞中炎性因子和BNIP3表达的影响^*[J]. 中国应用生理学杂志, 2021, 37(6): 632-637.
[12]	孙杨, 赵灿, 刘媛媛, 隋月林, 朱建忠. 辣木叶对糖尿病大鼠认知功能及海马神经细胞凋亡的影响^*[J]. 中国应用生理学杂志, 2021, 37(6): 638-643.
[13]	张岩岩, 刘华, 宋扬, 郭海艳. 白花蛇舌草多糖提取物对喉癌Hep-2细胞内质网自噬的影响^*[J]. 中国应用生理学杂志, 2021, 37(6): 660-664.
[14]	许骥, 方以群, 包晓辰, 袁恒荣, 王楠, 王芳芳. 核辐射对大深度快速上浮脱险致减压病大鼠相关指标的影响^*[J]. 中国应用生理学杂志, 2021, 37(5): 486-489.
[15]	杨云昊, 庞芳, 黄思琴, 杨之雪, 朱正威, 代攀, 郭啸, 廖冬梅, 唐成林. 电针对快速衰老小鼠肝脏自噬及脂质代谢的影响[J]. 中国应用生理学杂志, 2021, 37(4): 365-370.