Effect of tanshinone IIA pretreatment on IL-1β and RelA mRNA expression in rats with focal cerebral ischemia.
- Author:
Wei-yin CHEN
1
;
Cheng-ming SUN
;
Hui-ming WANG
;
Mei HUANG
;
Guan-xiang ZHU
;
Bi-de ZHU
;
Fu-you LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Anti-Inflammatory Agents, Non-Steroidal; pharmacology; therapeutic use; Antioxidants; pharmacology; therapeutic use; Brain Ischemia; drug therapy; metabolism; Diterpenes, Abietane; pharmacology; therapeutic use; Infarction, Middle Cerebral Artery; drug therapy; metabolism; Interleukin-1beta; genetics; metabolism; Male; RNA, Messenger; genetics; metabolism; Rats; Reperfusion Injury; prevention & control; Transcription Factor RelA; genetics; metabolism
- From: Journal of Southern Medical University 2010;30(9):2115-2118
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of tanshinone IIA (TS IIA) pretreatment on the expression of the inflammatory factor IL-1β and RelA mRNA in rats with focal cerebral ischemia.
METHODSA total of 100 adult male SD rats were randomly divided into 6 groups, namely the model, ischemic preconditioning (IPC), TSIIA preconditioning, TSIIA treatment, sham-operated, and blank control groups. In the former 4 groups, rat models of focal cerebral ischemia were established with corresponding treatments. The expressions of IL-1β and RelA mRNA in each group were detected using RT-PCR.
RESULTSAll the groups showed expressions of IL-1β and RelA mRNA with the exception of the blank control group. Compared to the model group, TSIIA preconditioning group, TSIIA treatment group, and IPC group all had significantly reduced expression of IL-1β and RelA mRNA (P < 0.05). The expressions were lower in IPC group than in TSIIA preconditioning group and TSIIA treatment group(P < 0.05), and no significant difference was found in the expressions between the latter two groups.
CONCLUSIONThe protective effect of pretreatment with TS IIA against cerebral ischemia is related to the reduction of IL-1β and RelA mRNA expressions.