加味四君子汤通过调控Fibulin-5,p-Akt表达抗脑缺血大鼠神经细胞失巢凋亡机制
作者：
陈岩岩;李花;刘旺华;唐冰镕;李宇翔;...
期刊：
中国实验方剂学杂志 ,2021年27(01):112-120 ISSN：1005-9903
通讯作者：
Li, H.
作者机构：
[陈岩岩; 李宇翔; 李花; 刘旺华; 王浩瞩; 唐冰镕] Key Laboratory of Diagnostics of Chinese Medicine in Hunan Province, Hunan University of Chinese Medicine, Changsha, 410208, China
通讯机构：
[Li, H.] K;Key Laboratory of Diagnostics of Chinese Medicine in Hunan Province, China
关键词：
加味四君子汤;脑缺血再灌注;失巢凋亡;纤维蛋白-5(Fibulin-5);磷酸化蛋白激酶B(p-Akt)
摘要：
目的:探讨加味四君子汤对大鼠脑缺血再灌注(I/R)损伤后缺血侧海马区脑组织纤维蛋白-5(Fibulin-5),磷酸化蛋白激酶B(p-Akt)的表达及对神经细胞失巢凋亡的影响。方法:将60只SPF级雄性SD大鼠随机分为假手术组、模型组、依达拉奉组(3.2 mg·kg~(-1)),加味四君子汤高、中、低剂量组(19.08,9.54,4.77 g·kg~(-1))。采用线栓法制备大鼠大脑中动脉栓塞(MCAO)模型,7 d后处死大鼠,处死前进行神经功能缺损评分,采用苏木素-伊红(HE)染色进行组织病理学观察,原位末端标记法(TUNEL)染色检测神经细胞凋亡指数,免疫组化法和蛋白免疫印迹法(Western blot)检测缺血侧海马区脑组织Fibulin-5及p-Akt蛋白表达情况。结果:神经功能缺损评分结果显示,与假手术组比较,模型组大鼠神经功能缺损评分显著升高(P<0.01);与模型组比较,依达拉奉组、加味四君子汤高、中、低剂量组大鼠神经功能缺损评分均明显降低(P<0.05,P<0.01)。免疫组化结果显示,与假手术组比较,模型组大鼠Fibulin-5,p-Akt蛋白表达,神经细胞凋亡指数均明显增高(P<0.05,P<0.01);与模型组比较,依达拉奉组、加味四君子汤高、中、低剂量组大鼠Fibulin-5,p-Akt蛋白表达均明显增加(P<0.05,P<0.01),神经细胞凋亡指数均明显降低(P<0.05,P<0.01)。Western blot结果显示,与假手术组比较,模型组Fibulin-5,p-Akt蛋白相对表达显著下调(P<0.01);与模型组比较,依达拉奉组、加味四君子汤高、中、低剂量组Fibulin-5,p-Akt蛋白表达均明显上升(P<0.05, P<0.01)。结论:加味四君子汤可能通过稳定神经元细胞外基质(ECM)Fibulin-5,从而增加了ECM对细胞的黏附作用,促进p-Akt蛋白的表达,从而抑制神经细胞凋亡,保护脑缺血损伤。
语种：
中文
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《黄帝内经》阙部面诊思想初探
作者：
蒋诗倩;李花;刘旺华;李宇翔;陈岩岩
期刊：
北京中医药大学学报 ,2020年43(04):280-283 ISSN：1006-2157
作者机构：
湖南中医药大学中医学院 湖南410208;[李宇翔; 陈岩岩; 李花; 刘旺华; 蒋诗倩] 湖南中医药大学
关键词：
黄帝内经;阙;眉间;面诊
摘要：
根据《黄帝内经》原文及后世与阙部面诊相关的论述,从辨体质、别风痹、候脏腑、察五色4个方面探讨了《黄帝内经》阙部面诊思想的主要内容,发现此部以丰隆为体质强,所别之风乃外感病邪袭于皮毛肺表之病机,痹乃经络气血凝滞之病机,所候脏腑有肺、心、肝3种说法,五色察病可有阴阳寒热与五行生克2种模式,并列举了阙部五色常见病证,以期为《黄帝内经》理论研究和分部面诊学说研究提供新思路。
语种：
中文
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Protein arginine methyltranferase-1 induces ER stress and epithelial-mesenchymal transition in renal tubular epithelial cells and contributes to diabetic nephropathy.
作者：
Chen, Yin-Yin;Peng, Xiao-Fei;Liu, Guo-Yong;Liu, Jin-Song;Sun, Lin;...
期刊：
Biochimica et Biophysica Acta - Molecular Basis of Disease ,2019年1865(10):2563-2575 ISSN：0925-4439
通讯作者：
He, Li-Yu
作者机构：
[Chen, Yin-Yin] Hunan Normal Univ, Dept Nephrol, Hunan Prov Peoples Hosp, Lab Kidney Dis, Changsha 410005, Hunan, Peoples R China.;[Peng, Xiao-Fei] Cent S Univ, Dept Rheumatol & Immunol, Xiangya Hosp 2, Changsha 410011, Hunan, Peoples R China.;[Liu, Guo-Yong] Changde Vocat Tech Coll, Affiliated Hosp 1, Dept Nephrol, Changde 415000, Peoples R China.;[Liu, Jin-Song] Hunan Univ Chinese Med, Dept Nephrol, Chinese Med & Western Med Hosp, Changsha 410011, Hunan, Peoples R China.;[He, Li-Yu; Sun, Lin; Liu, Hong; Xiao, Li] Cent S Univ, Dept Nephrol, Xiangya Hosp 2, Changsha 410011, Hunan, Peoples R China.
通讯机构：
[He, Li-Yu] C;Cent S Univ, Dept Nephrol, Xiangya Hosp 2, Key Lab Kidney Dis & Blood Purificat Hunan, 139 Renmin Rd, Changsha 410011, Hunan, Peoples R China.
关键词：
Diabetic nephropathy;ER stress;Epithelial-mesenchymal transition;Fibrosis;PRMT1
摘要：
Background: In this study, we examined the association of PRMT1 with ER stress and epithelial-mesenchymal transition (EMT), two critical pathogenic mechanisms leading to DN development, in proximal tubular epithelial cells (PTECs). Methods: The level of PRMT1 was compared between the serum from DN patients and healthy individuals by ELISA, and between renal tissues of DN mice and normal mice using RT-qPCR and immunohistochemistry. Using high-glucose-treated PTEC cell line, HK2 cells as the model system, the significance of PRMT1 in ER stress and EMT was assessed by shRNA targeting PRMT1 (sh-PRMT1) and/or by overexpressing PRMT1. Mechanistic studies focused on three major pathways controlling ER stress: protein kinase R-like ER kinase (PERK), inositol requiring-1α (IRE1α), and activating transcription factor 6 (ATF6). Results: PRMT1 was up-regulated in the serum of DN patients and renal tissues of DN mice. High glucose administration induced elevation of PRMT1 expression in HK2 cells in vitro, accompanied with ER stress and EMT activation. PRMT1 knockdown attenuated high glucose-induced ER stress and apoptosis by inactivating PERK and ATF6, but not IRE1α. PRMT1 activated ATF6 by recruiting H4R3me2as to the promoter. Furthermore, PRMT1-induced ER stress was concomitant with the activation of an EMT-like state. Specifically, inhibition of ATF6, but not PERK blocked PRMT1-induced EMT in high-glucose-treatment HK2 cells. Conclusions: By activating ER stress, PRMT1 essentially regulates the apoptosis and EMT of PTECs in response to diabetic milieu. Thus, targeting PRMT1 may alleviate both tissue injury and renal fibrosis, and thus benefit the treatment of DN. © 2019 Elsevier B.V.
语种：
英文
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