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ERS是细胞应对各种压力的保护性反应。PERK作 [ 7 ] 张秋林,林慧婷,周格,等. 链脲佐菌素腹腔注射制作大
为 ERS 的关键传感器,在维持细胞稳态中发挥重要作 鼠2型糖尿病模型的方式与剂量研究[J]. 按摩与康复医
用。然而,PERK 的长期或过度激活会导致细胞功能紊 学,2023,14(2):77-80.
[15]
乱,并与多种代谢性疾病相关,包括 T2DM 。FOXO1 ZHANG Q L,LIN H T,ZHOU G,et al. The mode and
作为关键转录因子之一,在T2DM的发生发展中扮演着 dosage of streptozotocin intraperitoneal injection in estab‐
lishment of type 2 diabetes rat model[J]. Chin Manip Re‐
重要角色。具体而言,FOXO1 可通过抑制胰岛素信号
habil Med,2023,14(2):77-80.
传导及葡萄糖摄取、促进糖异生及脂质合成等机制,导
[ 8 ] 姜立娟 . 经典名方玉液汤通过 PI3K/AKT 信号途径改善
致糖脂代谢紊乱,引发 IR,增加 T2DM 及其并发症的发
2 型糖尿病胰岛素抵抗的作用及机制研究[D]. 长春:长
[16]
生风险 。当细胞发生氧化应激时,PERK被激活,进而
春中医药大学,2021.
使FOXO1磷酸化,增强其转录活性。激活的FOXO1一 JIANG L J. Study on the effect and mechanism of Yuye
方面可以诱导抗氧化酶的表达,发挥保护作用;另一方 decoction on insulin resistance of type 2 diabetes mellitus
面,过度激活FOXO1会加剧氧化应激和炎症反应,进一 through PI3K/AKT signaling pathway[D]. Changchun:
[17]
步损害胰岛β细胞功能,促进IR的发生发展 。本研究 Changchun University of Chinese Medicine,2021.
结果显示,经清血消脂降糖方干预后,T2DM 大鼠肝脏 [ 9 ] 李杲. 脾胃论[M]. 北京:中国中医药出版社,2019:1.
组织中 PERK、FOXO1 蛋白磷酸化水平降低,表明清血 LI G. Treatise on the spleen and stomach[M]. Beijing:
消脂降糖方可能通过抑制 PERK/FOXO1 信号通路调控 China Publishing House of Traditional Chinese Medi‐
T2DM大鼠炎症反应及氧化应激水平,改善IR。 cine,2019:1.
综上,清血消脂降糖方可调节 T2DM 大鼠糖脂代 [10] BO T,GAO L,YAO Z,et al. Hepatic selective insulin re‐
sistance at the intersection of insulin signaling and meta‐
谢、氧化应激和炎症水平,同时提高胰岛素敏感性,缓解
肝脏损伤,从而改善 IR,其作用机制可能与抑制 PERK/ bolic dysfunction-associated steatotic liver disease[J].Cell
Metab,2024,36(5):947-968.
FOXO1信号通路有关。本研究为清血消脂降糖方防治
[11] GAO D N,JIAO J,WANG Z P,et al. The roles of cell-
T2DM提供了实验依据,后续本课题组将深入研究其涉
cell and organ-organ crosstalk in the type 2 diabetes melli‐
及的分子机制。
tus associated inflammatory microenvironment[J]. Cyto‐
参考文献 kine Growth Factor Rev,2022,66:15-25.
[ 1 ] EFENDIĆ S,LUFT R,WAJNGOT A. Aspects of the [12] SCHIATTARELLA A,LOMBARDO M,MORLANDO M,
pathogenesis of type 2 diabetes[J]. Endocr Rev,1984,5 et al. The impact of a plant-based diet on gestational diabe‐
(3):395-410. tes:a review[J]. Antioxidants(Basel),2021,10(4):557.
[ 2 ] 中华医学会糖尿病学分会.胰岛素抵抗相关临床问题专 [13] NIE X,ZHAO Z,ZHANG X,et al. Endophytes alleviate
家共识:2022 版[J]. 中华糖尿病杂志,2022,14(12): drought-derived oxidative damage in Achnatherum inebrians
1368-1379. plants through increasing antioxidants and regulating host
Chinese Diabetes Society.Expert consensus on insulin re‐ stress responses[J].Microb Ecol,2024,87(1):73.
sistance:2022 edition [J]. Chin J Diabetes Mellit,2022,14 [14] HSIEH P S,HO H H,TSAO S P,et al. Multi-strain pro-
(12):1368-1379. biotic supplement attenuates streptozotocin-induced type-
[ 3 ] YARIBEYGI H,FARROKHI F R,BUTLER A E,et al. In‐ 2 diabetes by reducing inflammation and β-cell death in
sulin resistance:review of the underlying molecular rats[J]. PLoS One,2021,16(6):e0251646.
mechanisms[J]. J Cell Physiol,2019,234(6):8152-8161. [15] SHARMA R B,LANDA-GALVÁN H V,ALONSO L C.
[ 4 ] 宋林阳,胡依萌,徐焱成,等. 胰岛素抵抗的再认识[J]. 中 Living dangerously:protective and harmful ER stress
华糖尿病杂志,2022,14(12):1341-1347. responses in pancreatic β-cells[J]. Diabetes,2021,70(11):
SONG L Y,HU Y M,XU Y C,et al. Re-conceptualization 2431-2443.
of insulin resistance[J]. Chin J Diabetes Mellit,2022,14 [16] ZHANG T ,DONG H H .FoxO1:a conductor of insulin
(12):1341-1347. signaling to glucose and lipid metabolism[M]. Switzer‐
[ 5 ] HOTAMISLIGIL G S. Endoplasmic reticulum stress and land:Springer International Publishing,2016:79-99.
the inflammatory basis of metabolic disease[J]. Cell, [17] CHEN S F,HENDERSON A,PETRIELLO M C,et al.
2010,140(6):900-917. Trimethylamine N-oxide binds and activates PERK to pro‐
[ 6 ] DU H X,MA Y P,WANG X Q,et al. Advanced glycation mote metabolic dysfunction[J]. Cell Metab,2019,30(6):
end products induce skeletal muscle atrophy and insulin 1141-1151.e5.
resistance via activating ROS-mediated ER stress PERK/ (收稿日期:2024-07-18 修回日期:2024-12-09)
FOXO1 signaling[J]. Am J Physiol Endocrinol Metab, (编辑:林 静)
2023,324(3):1341-1347.
中国药房 2025年第36卷第1期 China Pharmacy 2025 Vol. 36 No. 1 · 29 ·