Mechanism of pterostilbene reducing oxidative damage in endothelial cells in mouse hepatic sinus
- Author:
Lei YAO
1
;
Jian DU
1
;
Hai-Jian CAI
2
;
Zhen-Hai TANG
2
;
Deng LIU
3
;
Li-Jian CHEN
3
Author Information
- Publication Type:Journal Article
- Keywords: fenestration; HO-1; ischemic/reperfusion; LSECs; pterostilbene; scanning electron microscope
- From: Chinese Pharmacological Bulletin 2023;39(2):310-314
- CountryChina
- Language:Chinese
- Abstract: Aim To explore the mechanism of the natural phenolic compound pterostilbene(PTE)in the protection of liver ischemic/reperfusion. Methods A total of 40 C57 mice were divided into control group,model group,drug delivery group and treatment group and a 70% liver ischemic/reperfusion(ischemic 60 min)model was established,then primary LSECs were isolated by perfusion and digestion. Hepatic structural disruption was observed by HE staining. The ultrastructure of hepatic sinus endothelial cells was observed by transmission electron microscopy(TEM). The structure of LSECs fenestrae was observed by scanning electron microscopy(SEM). The expression level of heme oxygenase 1(HO-1)in LSECs was detected by Western blot. Results HE staining showed that PTE protected against hepatic ischemic injury. TEM observed that PTE had a protective effect on hepatic sinus endothelial cells,and the number of LSECs fenestrae in the blank control group was larger and the number of fenestrae in the liver I/R model group was reduced. The number of LSECs fenestrae in the liver I/R model group treated with PTE increased compared with the untreated liver I/R model group. Western blot result showed that PTE was able to induce HO-1 expression in LSECs. Conclusions PTE alleviates oxidative damage of endothelial cells in mouse hepatic sinus by inducing HO-1expression,and protects the liver from ischemia/reperfusion injury.
