Baicalin protects rat brain microvascular endothelial cells injured by oxygen-glucose deprivation via anti-inflammation
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- 作者：Peng Zhang ; Jincai Hou ; Jianhua Fu ; Dan Li ; Cuixiang Zhang ; Jianxun Liu
- 关键词：Baicalin ; Brain microvascular endothelial cells ; Inflammation ; NF-¦ÊB
- 刊名：Brain Research Bulletin
- 出版年：2013
- 出版时间：August, 2013
- 年：2013
- 卷：97
- 期：Complete
- 页码：8-15
- 全文大小：1810 K
文摘
Baicalin, which is isolated from Scutellariae Radix, has been evidenced to possess several pharmacological effects. The present study focuses on the in vitro protective effect of baicalin on oxygen-glucose deprivation (OGD) injured brain microvascular endothelial cells (BMECs) via anti-inflammation and mechanisms against BMECs damaged by OGD. Cultured primary rat BMECs were exposed to baicalin at the concentrations of 100 ¦ÌM (high dose) and 10 ¦ÌM (low dose) for 6 h after a 2 h OGD. The effects of baicalin were evaluated in terms of (i) cell viability; (ii) lactate dehydrogenase (LDH) leakage rate; (iii) levels of TNF-¦Á, IL-1¦Â, IL-6 in culture media; (iv) protein expressions of p-MEK6, p-MEK1/2, p-ERK, p-I¦ÊB¦Á, NF-¦ÊB p65, p-IKK¦Á, p-IKK¦Â and p-p38; and (v) nuclear translocation of NF-¦ÊB p65 and p-I¦ÊB¦Á. The results showed that OGD treatment could reduce cell viability, increase LDH leakage rate, increase the levels of TNF-¦Á, IL-1¦Â and IL-6 in the culture media. These effects were suppressed by baicalin with high or low dose. In addition, baicalin could notably down-regulate the phosphorylation of proteins in MAPK signaling pathway such as p-MRK1/2, p-ERK and p-p38. While low dose of baicalin could significantly suppress the phosphorylation of proteins in NF-§ÜB signaling pathway such as p-IKK¦Á, p-IKK¦Â and p-I¦ÊB¦Á. Furthermore, baicalin at 10 ¦ÌM could remarkably inhibit nuclear transcriptional activity triggered via NF-¦ÊB p65 and p-I¦ÊB¦Á in BMECs. In conclusion, baicalin displays a protective effect on OGD-injured BMECs in vitro by attenuating inflammatory factors via down-regulated the MAPK and NF-¦ÊB signaling pathway.