生物
细胞生物学
细胞迁移
p38丝裂原活化蛋白激酶
细胞生长
庆大霉素保护试验
雪旺细胞
MAPK/ERK通路
免疫印迹
信号转导
细胞
生物化学
基因
作者
Yong Zhang,Yanfen Niu,Qiuyan Weng
出处
期刊:Tissue & Cell
[Elsevier]
日期:2022-10-31
卷期号:79: 101967-101967
标识
DOI:10.1016/j.tice.2022.101967
摘要
The proliferation and migration of Schwann cells is pivotal to peripheral nerve injury (PNI) repair. Recent studies have revealed that Ginkgetin has neuroprotective effects. Hence, we focused on identifying whether Ginkgetin could regulate the proliferation and migration of Schwann cells, thereby contributing to the repair of PNI. Rat Schwann cells RSC96 were treated with different concentrations of Ginkgetin. Short hairpin RNA targeting phosphatidylinositol glycan anchor biosynthesis class F (shPIGF) was employed to investigate the effects of PIGF on Ginkgetin-induced RSC96 cells. Viability of RSC96 cells was estimated via cell counting kit-8 (CCK-8) assay and proliferation of the cells was assessed by 5-ethynyl-2'-deoxyuridine (EdU) assay. Migration was estimated via wound healing assay and invasion was evaluated through transwell assay. Western blot was employed to test the expressions of PIGF, protein-38 (p38), and phosphorylated p-38 (p-p38). Ginkgetin (50 or 100 μg/ml) increased the viability, proliferation, migration, and invasion of RSC96 cells, up-regulated PIGF expression and raised the ratio of p-p38/p38, which were all reversed by PIGF silencing. Ginkgetin promotes proliferation, migration, and invasion of Schwann cells via PIGF/p38 MAPK signaling pathway.
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