小檗碱调控PI3K/AKT信号通路干预糖尿病动脉硬化的实验研究

doi:10.3969/j.issn.1006-6233.2020.12.01

Abstract
Figure/Table
References (0)
Related Citation (2)

Download: PDF (2749 KB) HTML (1 KB)
Export: BibTeX | EndNote (RIS)

Abstract Objective: To investigate the expression level of PI3K/AKT signal pathway in the abdominal aorta of diabetic rats and the intervention mechanism of berberine. Methods: The SD rats were randomly divided into 3 groups, the normal control group, diabetic model group and berberine intervention group, 20 rats in each group. The diabetic rat model was established by intraabdominal injection of streptozotocin. The rats in berberine intervention group received berberine gastric perfusion with the dosage of 100mg·kg^-1·d^-1 while other 2 groups with the same dosage of normal saline after the model were established successfully. After 6 weeks, the blood glucose and lipid level were compared before and after intervention. The abdominal aorta were taken out and the PI3K, AKT, p21 expression level were detected by immunohistochemical technique. Results: The blood glucose level of diabetic model rats increased after modeling. The blood glucose level of the berberine intervention group decreased after pharmacological intervention and lower than that of the diabetic model group. There was no statistically significant difference of TC and TG between 3 groups before and after intervention. The expression level of PI3K, AKT in abdominal aorta were significant high while the level of p21 was low in the diabetic model group. BBR could decrease the level of blood glucose and inhibit the expression of PI3K, AKT while upregulating the level of p21 in abdominal aorta of diabetic rats. Conclusion: The activation of PI3K/AKT signal pathway may be one of the pathogenesis of DA. BBR may intervene the pathogenesis of DA by inhibiting cell proliferation by regulating the PI3K/AKT signal pathway.

Key words： Diabetic atherosclerosis PI3K/AKT signal pathway Berberine

	Service

	E-mail this article
	Add to my bookshelf
	Add to citation manager
	E-mail Alert
	RSS
	Articles by authors

Cite this article:

URL:

http://www.hbyxzzs.cn/EN/10.3969/j.issn.1006-6233.2020.12.01 OR http://www.hbyxzzs.cn/EN/Y2020/V26/I12/1937

[1] Cho NH,Shaw JE,Karuranga S, et al.IDF diabetes atlas: global estimates of diabetes prevalence for 2017 and projections for 2045[J].Diabetes Res Clin Pract,2018,138:271~281.
[2] 褚玉超,刘阳.黄连素治疗2型糖尿病及其并发症作用机制研究进展[J].中医药临床杂志,2019,31(3):408~412.
[3] Shirwaikar A, Shirwaikar A, Rajendran K, et al. In vitro antioxidant studies on the benzyl tetra isoquinoline alkaloid berberine[J]. Biol Pharm Bull, 2006,29(9):1906~1910.
[4] 张丽芬,吕仁和,黄文政.链脲佐菌素糖尿病肾病大鼠模型的建立及稳定性评价[J].中国比较医学杂志,2014,24(4):8~12,18.
[5] 韩莉,杨钦河,张玉佩,等.小檗碱对高脂饮食诱导非酒精性脂肪性肝病大鼠肝细胞脂质沉积的干预作用[J].中国中西医结合杂志,2015,35(3):314~319.
[6] Chandirasegaran G, Elanchezhiyan C, Ghosh K, et al. Berberine chloride ameliorates oxidative stress, inflammation and apoptosis in the pancreas of Streptozotocin induced diabetic rats[J]. Biomed Pharmacother, 2017,95:175~185.
[7] 李爱云,杨京,张昕宇,等.小檗碱治疗2型糖尿病降血糖机制的研究进展[J].中国实验方剂学杂志,2019,25(22):219~226.
[8] Monica Verdoia, Alon Schaffer, Ettore Cassetti, et al. Pasquale perrone-filardi,paolo marino,giuseppe de luca. glycosylated hemoglobin and coronary artery disease in patients without diabetes mellitus[J]. Am J Prev Med,2014,47(1):9~16.
[9] 谢俊,郭子宏.高血糖致动脉粥样硬化的机制研究及进展[J].中国老年保健医学,2018,16(3):124~127.
[10] Wang N, Han Y, Tao J, et al. Overexpression of CREG attenuates atherosclerotic endothelium apoptosis via VEGF/PI3K/AKT pathway[J]. Atherosclerosis, 2011,218(2):543~551.
[11] Xie S, Chen M, Yan B, et al. Identification of a role for the PI3K/AKT/mTOR signaling pathway in innate immune cells[J]. PLoS One, 2014,9(4):e94496.
[12] Boyle K B, Gyori D, Sindrilaru A, et al. Class IA phosphoinositide 3-kinase β and δ regulate neutrophil oxidase activation in response to Aspergillus fumigatus hyphae[J].Immunol, 2011,186(5):2978~2989.
[13] 孙亚男,黄小波,粱伟,等.陈皮、半夏对动脉粥样硬化小鼠PI3K-Akt通路、SOD、MDA、SA-β-gal水平的影响[J].首都医科大学学报,2018,39(6):805~809.
[14] Gulappa T, Reddy R S, Suman S, et al. Molecular interplay between cdk4 and p21 dictates G0/G1 cell cycle arrest in prostate cancer cells[J]. Cancer Lett, 2013,337(2):177~183.
[15] Beier I, Dusing R, Vetter H, et al. Epidermal growth factor stimulates Rac1 and p21-activated kinase in vascular smooth muscle cells[J]. Atherosclerosis, 2008,196(1):92~97.