A preliminary study on the mechanism of 7-HEC on high altitude cerebral edema
10.12206/j.issn.2097-2024.202205090
- VernacularTitle:7-羟乙基白杨素对高原脑水肿的作用机制初探
- Author:
Zhiqun SHI
1
,
2
;
Yingchun GAO
3
;
Dongmei ZHANG
3
;
Keming CHEN
4
;
Linlin JING
3
;
Huiping MA
1
,
2
Author Information
1. No. 940 Hospital of Joint Logistics Support Force of the PLA Key Laboratory of the Plateau Medicine
2. College of pharmacy, Gansu university of Chinese Medicine, Lanzhou 730000, China.
3. No. 940 Hospital of Joint Logistics Support Force of the PLA Key Laboratory of the Plateau Medicine.
4. No. 940 Hospital of Joint Logistics Support Force of the PLA Fundamental Medical Science Research Laboratories, Lanzhou 730050, China.
- Keywords:
high altitude cerebral edema;
oxidative stress;
apoptosis;
cycle;
autophagy
- From:
Journal of Pharmaceutical Practice and Service
2022;40(5):399-402
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the possible mechanism of 7-hydroxyethyl chrysin (7-HEC) on high altitude cerebral edema (HACE). Methods A rat model of high altitude cerebral edema was established. The activity of superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in rat brain tissues were measured. The expression levels of apoptosis, cell cycle and autophagy related proteins were detected by Western blotting to explore the protective effect of 7-HEC on high altitude cerebral edema and its mechanism. Results Compared with the control group, the content of MDA in the brain tissue of the hypoxia model group was significantly up-regulated; the activity of SOD was significantly down-regulated, the relative expression of CyclinD1, CyclinE1, CDK6 and CDK2, apoptotic proteins Bcl-2, PARP, and autophagy protein LC3-B were down-regulated; and the relative expression of apoptotic protein Bax and autophagy protein P62 were up-regulated; the difference was statistically significant (P<0.05); Compared with the hypoxia model group, the content of MDA was down-regulated and the activity of SOD was significantly up-regulated in the 7-HEC administration group. The relative expression of CyclinD1, CyclinE1, CDK6, CDK2, apoptotic proteins Bcl-2, PARP, autophagy protein LC3-B was up-regulated and the relative expression of apoptotic proteins Bax and the relative expression of autophagy protein P62 was down-regulated in the 7-HEC administration group. The difference was statistically significant (P<0.05). Conclusion 7-HEC has a certain protective effect on high altitude cerebral edema, and its mechanism may be related to the regulation of cell cycle, autophagy, apoptosis and oxidative stress pathways.
