大麻二酚对高糖诱导小鼠肾脏足细胞系MPC5细胞凋亡的保护作用

苏静华, 焦婷, 韩宁, 苏静克, 党瑞杰, 李琳, 张海松

武警医学 ›› 2022, Vol. 33 ›› Issue (4) : 303-306.

PDF(739 KB)
PDF(739 KB)
武警医学 ›› 2022, Vol. 33 ›› Issue (4) : 303-306.
论著

大麻二酚对高糖诱导小鼠肾脏足细胞系MPC5细胞凋亡的保护作用

  • 苏静华1, 焦婷2, 韩宁3, 苏静克3, 党瑞杰4, 李琳4, 张海松2
作者信息 +

Protective effect of cannabidiol on high glucose-induced podocytes MPC5 apoptosis

  • SU Jinghua1, JIAO Ting2, HAN Ning3, SU Jingke3, DANG Ruijie4, LI Lin4, ZHANG Haisong2
Author information +
文章历史 +

摘要

目的 探讨大麻二酚(cannabidiol, CBD)对高糖环境中小鼠足细胞系MPC5细胞凋亡的影响。方法 将MPC5细胞分为对照组(Vehicle)、高糖组(high glucose, HG)和CBD组。CCK-8试剂盒检测MPC5细胞的增殖活性,流式细胞术检测MPC5细胞的凋亡率,Western blot检测裂孔膜蛋白Nephrin与凋亡相关蛋白Bax及Bcl-2的表达情况。结果 与Vehicle组相比,HG组明显抑制MPC5增殖并促进其凋亡[(25.27±2.15)% vs. (8.43±0.70) %];而CBD干预显著促进高糖环境中MPC5增殖且抑制凋亡[(12.83±1.05)% vs. (25.27±2.15) %; P<0.05]。同时,CBD干预显著升高高糖环境中MPC5细胞Nephrin蛋白的表达[(0.77±0.06) vs. (0.32±0.10)],降低促凋亡蛋白Bax与抗凋亡蛋白Bcl-2的蛋白表达比[(1.02±0.09) vs. (12.30±0.09)]。结论 CBD能缓解高糖诱导的MPC5细胞凋亡。

Abstract

Objective To investigate the effect of cannabidiol (CBD) on podocytes MPC5 apoptosis induced by high glucose.Methods MPC5 cells were randomly divided into vehicle group, high glucose (HG) group and CBD group. CCK-8 method was used to access cell proliferation, flow cytometry was used to evaluate apoptotic rate, and western blot was used to investigate protein level of Nephrin and apoptosis-related proteins Bax and Bcl-2.Results Compared with the Vehicle group, HG significantly inhibited MPC5 proliferation and promoted MPC5 apoptosis [(25.27±2.15)% vs. (8.43±0.70)%], while CBD obviously promoted MPC5 proliferation and inhibited MPC5 apoptosis [(12.83±1.05)% vs. (25.27±2.15)%; P<0.05] in the high glucose environment. Meanwhile, CBD administration increased Nephrin expression [(0.77±0.06) vs. (0.32±0.10)], and reduced Bax/Bcl-2 [(1.02±0.09) vs. (12.30±0.09); P<0.05].Conclusions CBD attenuates high glucose-induced MPC5 apoptosis.

关键词

大麻二酚 / 高糖 / 足细胞 / 细胞凋亡

Key words

cannabidiol / high glucose / podocyte / cell apoptosis

引用本文

导出引用
苏静华, 焦婷, 韩宁, 苏静克, 党瑞杰, 李琳, 张海松. 大麻二酚对高糖诱导小鼠肾脏足细胞系MPC5细胞凋亡的保护作用[J]. 武警医学. 2022, 33(4): 303-306
SU Jinghua, JIAO Ting, HAN Ning, SU Jingke, DANG Ruijie, LI Lin, ZHANG Haisong. Protective effect of cannabidiol on high glucose-induced podocytes MPC5 apoptosis[J]. Medical Journal of the Chinese People Armed Police Forces. 2022, 33(4): 303-306
中图分类号: R285.5   

参考文献

[1] 吕晓楠,宗春辉,董 铮. 低聚原花青素对糖尿病肾病大鼠足细胞上皮-间质转化的抑制作用[J]. 武警医学, 2021,32(7):616-619.
[2] 贺明娟,梅 稳,林 梅. 艾塞那肽对高糖诱导的小鼠足细胞损伤的保护作用及机制研究[J]. 中华糖尿病杂志, 2021,13(1):80-86.
[3] He M, Li Y, Wang L, et al. MYDGF attenuates podocyte injury and proteinuria by activating Akt/BAD signal pathway in mice with diabetic kidney disease[J]. Diabetologia, 2020,63(9):1916-1931.
[4] Fouda M A, Ruben P C. Protein kinases mediate anti-inflammatory effects of cannabidiol and estradiol against high glucose in cardiac sodium channels[J]. Front Pharmacol, 2021,12:668657.
[5] 宋贤奎, 谢冠博,吴 宁, 等. 大麻二酚对口腔颌面部炎性痛的镇痛作用及机制研究[J]. 实用口腔医学杂志, 2021,37(3):307-311.
[6] Rajesh M, Mukhopadhyay P, Bátkai S, et al. Cannabidiol attenuates cardiac dysfunction, oxidative stress, fibrosis, and inflammatory and cell death signaling pathways in diabetic cardiomyopathy[J]. J Am Coll Cardiol, 2010,56(25):2115-2125.
[7] Lehmann C, Fisher N B, Tugwell B, et al. Experimental cannabidiol treatment reduces early pancreatic inflammation in type 1 diabetes[J]. Clin Hemorheol Microcirc, 2016,64(4):655-662.
[8] Fouda M A, Ghovanloo M R, Ruben P C. Cannabidiol protects against high glucose-induced oxidative stress and cytotoxicity in cardiac voltage-gated sodium channels[J]. Br J Pharmacol, 2020,177(13):2932-2946.
[9] Mei W, Zhu B, Shu Y, et al. GDF11 protects against glucotoxicity-induced mice retinal microvascular endothelial cell dysfunction and diabetic retinopathy disease[J]. Mol Cell Endocrinol, 2021,537:111422.
[10] Susztak K, Raff A C, Schiffer M, et al. Glucose-induced reactive oxygen species cause apoptosis of podocytes and podocyte depletion at the onset of diabetic nephropathy[J]. Diabetes, 2006,55(1):225-233.
[11] Chuang P Y, Yu Q, Fang W, et al. Advanced glycation endproducts induce podocyte apoptosis by activation of the FOXO4 transcription factor[J]. Kidney Int, 2007,72(8):965-976.
[12] 王亚荣, 董兆珵,张 娜,等. 黄芪菟箭合剂对高糖诱导的足细胞损伤及凋亡的影响[J].山西医科大学学报, 2021,52(5):612-618.
[13] Gruden G, Barutta F, Kunos G, et al. Role of the endocannabinoid system in diabetes and diabetic complications[J]. Br J Pharmacol, 2016,173(7):1116-1127.
[14] Jourdan T, Szanda G, Rosenberg A Z, et al. Overactive cannabinoid 1 receptor in podocytes drives type 2 diabetic nephropathy[J]. Proc Natl Acad Sci U S A, 2014,111(50):E5420-E5428.
[15] Barutta F, Corbelli A, Mastrocola R, et al. Cannabinoid receptor 1 blockade ameliorates albuminuria in experimental diabetic nephropathy[J]. Diabetes, 2010,59(4):1046-1054.
[16] Barutta F, Piscitelli F, Pinach S, et al. Protective role of cannabinoid receptor type 2 in a mouse model of diabetic nephropathy[J]. Diabetes, 2011,60(9):2386-2396.
[17] Janiak P, Poirier B, Bidouard J P, et al. Blockade of cannabinoid CB1 receptors improves renal function, metabolic profile, and increased survival of obese Zucker rats[J]. Kidney Int, 2007,72(11):1345-1357.

基金

中国博士后科学基金资助项目(2019T120977)


PDF(739 KB)

Accesses

Citation

Detail

段落导航
相关文章

/