Neuroprotection via maintenance or increase of antioxidants and neurotrophic factors in ischemic gerbil hippocampus treated with tanshinone I.
- Author:
Joon Ha PARK
1
;
Ok Kyu PARK
2
;
Bingchun YAN
3
;
Ji Hyeon AHN
1
;
In Hye KIM
1
;
Jae-Chul LEE
1
;
Seung-Hae KWON
2
;
Ki-Yeon YOO
4
;
Choong Hyun LEE
5
;
In Koo HWANG
6
;
Jung Hoon CHOI
7
;
Moo-Ho WON
8
;
Jong-Dai KIM
9
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Antioxidants; metabolism; Blotting, Western; Brain Ischemia; drug therapy; metabolism; Brain-Derived Neurotrophic Factor; metabolism; Diterpenes, Abietane; therapeutic use; Gerbillinae; Hippocampus; metabolism; Immunohistochemistry; Insulin-Like Growth Factor I; metabolism; Male; Nerve Growth Factors; metabolism; Superoxide Dismutase; metabolism; Superoxide Dismutase-1
- From: Chinese Medical Journal 2014;127(19):3396-3405
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDDanshen (Radix Salvia miltiorrhizae) has been used as a traditional medicine in Asia for treatment of various microcirculatory disturbance related diseases. Tanshinones are mainly hydrophobic active components, which have been isolated from Danshen and show various biological functions. In this study, we observed the neuroprotective effect of tanshinone I (TsI) against ischemic damage in the gerbil hippocampal CA1 region (CA1) after transient cerebral ischemia and examined its neuroprotective mechanism.
METHODSThe gerbils were divided into vehicle-treated-sham-group, vehicle-treated-ischemia-group, TsI-treated-sham-group, and TsI-treated-ischemia-group. TsI was administrated intraperitoneally three times (once a day for three days) before ischemia-reperfusion. The neuroprotective effect of TsI was examined using H&E staining, neuronal nuclei (NeuN) immunohistochemistry and Fluoro-Jade B staining. To investigate the neuroprotective mechanism of TsI after ischemia-reperfusion, immunohistochemical (IHC) and Western blotting analyses for Cu, Zn-superoxide dismutase (SOD1), Mn-superoxide dismutase (SOD2), brain-derived neurotrophic factor (BDNF) and insulin-like growth factor-I (IGF-I) were performed.
RESULTSTreatment with TsI protected pyramidal neurons from ischemia-induced neuronal death in the CA1 after ischemia-reperfusion. In addition, treatment with TsI maintained the levels of SOD1 and SOD2 as determined by IHC and Western blotting in the CA1 after ischemia-reperfusion compared with the vehicle-ischemia-group. In addition, treatment with TsI increased the levels of BDNF and IGF-I determined by IHC and Western blotting in the TsI-treated-sham-group compared with the vehicle-treated-sham-group, and their levels were maintained in the stratum pyramidale of the ischemic CA1 in the TsI-treated-ischemia-group.
CONCLUSIONTreatment with TsI protects pyramidal neurons of the CA1 from ischemic damage induced by transient cerebral ischemia via the maintenance of antioxidants and the increase of neurotrophic factors.