Effect of Jianpi Huogu Formula on function damage of vascular endothelial cells induced by glucocorticoid.
10.19540/j.cnki.cjcmm.20211116.401
- Author:
Teng-Teng XU
1
;
Jin-Xia WANG
1
;
Rui-Rui MING
1
;
Chao YANG
1
;
Luo-Chang-Ting FANG
1
;
Xiao-Xiao WANG
1
;
Zhi-Xing HU
1
;
Wei-Heng CHEN
2
;
Chun-Fang LIU
1
;
Na LIN
1
Author Information
1. Institute of Chinese Materia Medica, China Academy of Chinese Medical Sciences Beijing 100700, China.
2. the Third Affiliated Hospital of Beijing University of Chinese Medicine Beijing 100029, China.
- Publication Type:Journal Article
- Keywords:
Jianpi Huogu Formula(JPHGF);
methylprednisolone sodiumsuccinate(MPS);
steroid-induced avascular necrosis of femoral head(SANFH);
vascular endothelial cells
- MeSH:
Animals;
Glucocorticoids/pharmacology*;
Human Umbilical Vein Endothelial Cells;
Humans;
Neovascularization, Pathologic/metabolism*;
Rats;
Rats, Sprague-Dawley;
Vascular Endothelial Growth Factor A/metabolism*
- From:
China Journal of Chinese Materia Medica
2022;47(6):1625-1631
- CountryChina
- Language:Chinese
-
Abstract:
This study aimed to observe the intervention effect of Jianpi Huogu Formula(JPHGF) on the functional damage of vascular endothelial cells caused by glucocorticoid, and explore its action mechanism from the PI3 K/Akt and mitogen activated protein kinase(MAPK) signaling pathways. The extracted thoracic aorta ring of normal SD rats were intervened first with vascularendothelial growth factor(VEGF, 20 μg·L-1) and/or sodium succinate(MPS, 0. 04 g·L-1) in vitro and then with JPHGF(8, 16, and 32 μg·L-1) for five mcontinuous ethylpdays, rednisolofollowed nebythe statistics of the number, length, and area of microvessels budding fromvascular rings. In addition, the human umbilical vein endothelial cells(HUVECs) induced by VEGF(20 μg·L-1) were added with MPS(0. 04 g·L-1) and then with JPHGF(8, 16, and 32 μg·L-1) for observing the migration, invasion, and luminal formation abilities of HUVECs in the migration, invasion and luminal formation experiments. The protein expression levels of PI3 K, p-Akt, p-JN K, and p-ERK in HUVECs were assayed by Western blot. The results showed that JPHGF dose-dependently improved the num-ber,length, and area of microvessels in MPS-induced rat thoracic aortic ring, reversed the migration, invasion and lumen formation abiliti es of HUVECs reduced by MPS, and up-regulated the protein expression levels of PI3 K, p-Akt, and p-JNK in HUVECs. All thesehave suggested that JPHGF exerts the protective effect against hormone-induced damage to the angiogenesis of vascular endothelial cells by activating the PI3 K/Akt and MAPK signaling pathways, which has provided reference for exploring the mechanism of JPHGF in treating s teroid-induced avascular necrosis of femoral head(SANFH) and also the experimental evidence for enriching the scientific connotationof spleen-invigorating and blood-activating therapy.
