Interventional effect and mechanism of 1，8-cineole on pancreatic β cell ferroptosis induced by type 2 diabetes
- VernacularTitle:1，8-桉叶油素对2型糖尿病胰岛β细胞铁死亡的干预作用及机制
- Author:
Hong YANG
1
,
2
;
Pengyan REN
2
,
3
;
Yongxin CHEN
2
,
3
;
Yuting YAO
2
,
3
;
Shiquan GAN
2
,
3
;
Jia LIU
1
;
Tingting CHEN
1
;
Bao ZHANG
1
;
Xiangchun SHEN
2
,
3
;
Yue LI
1
Author Information
1. Dept. of Pharmacy，Guiyang Maternal and Child Health Care Hospital/Guiyang Children’s Hospital，Guiyang 550003，China
2. Key Laboratory of Optimal Utilization of Natural Medicine Resources，Guizhou Medical University，Guiyang 561113，China
3. College of Pharmacy，Guizhou Medical University，Guiyang 561113，China
- Publication Type:Journal Article
- Keywords:
1，8-cineole;
type 2 diabetes;
pancreatic β cell;
ferroptosis
- From:
China Pharmacy
2024;35(3):290-295
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To study the interventional effect and mechanism of 1，8-cineole on pancreatic β cell ferroptosis induced by type 2 diabetes. METHODS In vitro ferroptosis model was established in pancreatic β cells of mice by using high glucose. The effects of low-dose and high-dose 1，8-cineole （0.25， 0.5 μmol/L） on the level of Fe2+ in pancreatic β cells were investigated. The effects of 1，8-cineole （0.5 μmol/L） combined with ferroptosis inducer Erastin （20 μmol/L） and ferroptosis inhibitor Ferrostatin-1 （20 μmol/L） on the protein expressions of glutathione peroxidase-4 （GPX4） and cyclooxygenase-2 （COX2） were also detected. The type 2 diabetes model mice were established by feeding high-sugar and high-fat diet combined with intraperitoneal injection of streptozotocin. The effects of low-dose and high-dose 1，8-cineole （50， 200 mg/kg） on the pathological morphology of pancreatic tissue， the content of iron as well as the protein expressions of GPX4 and COX2 were investigated. RESULTS The results of the cell experiment showed that compared with the model group， pretreatment with 1，8-cineole significantly reduced intracellular Fe2+ levels and upregulated GPX4 protein expression， while downregulated COX2 protein expression in pancreatic β cells （P＜0.05）. After combining with Ferrostatin-1， the expression trends of the above two proteins were the same， while there was no statistically significant difference after combining with Erastin. The results of animal experiments showed that compared with the model group， after intervention with 1，8-cineole， the structure of the pancreatic islets in mice recovered intact and their morphology improved； the iron content of pancreatic tissue and protein expression of COX2 were decreased significantly （P＜0.05）， while protein expression of GPX4 was increased significantly （P＜0.05）. CONCLUSIONS 1，8-cineole could ameliorate pancreatic β cell injury induced by diabetes， the mechanism of which may be related to reducing intracellular iron deposition and regulating ferroptosis-related proteins.
