Lithium chloride inhibits neural cell apoptosis and nuclear factor kappa B protein expression in rats with intracerebral hemorrhage
10.3760/cma.j.issn.1671-8925.2009.08.011
- VernacularTitle:氯化锂预处理对脑出血后血肿周围神经细胞凋亡及核因子κB表达的抑制作用
- Author:
An-Min LIU
1
;
Rong-Kang MAI
;
Wang-Qing CAI
;
Mei-Guang ZHENG
;
Zhen HU
;
Fang-Cheng LI
Author Information
1. 中山大学附属第二医院
- Keywords:
Intracerebral hemorrhage;
Lithium;
Apoptosis;
Nuclear factor kappa B;
Inflammatory response
- From:
Chinese Journal of Neuromedicine
2009;8(8):798-801,809
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the effects of lithium chloride (LiCl) on neural cell apoptosis, inflammatory response and expression of nuclear factor kappa B (NF-κB) protein in rats with intracerebral hemorrhage (ICH). Methods Fifty-four male SD rats were randomized into sham-operated, ICH and LiCl treatment groups (n=18), and in the latter two groups, ICH was induced by injection of collagenase Ⅳ into the internal capsule, and phosphate buffer solution was injected in the sham-operated group. Seven days before ICH, the rats in LiCl group received intraperitoneal injection of 1 mmol/kg LiCl once daily till the rats were sacrificed. Brain tissue specimens were collected at 1, 3, and 7 d after ICH to observe neural cell apoptosis, inflammatory response and expression of NF-κB in rat brain using terminal dUTP nick end-labeling (TUNEL), HE staining and immunohistochemistry, respectively. Results Compared with the ICH model group, the rats in LiCl treatment group showed significantly reduced number of TUNEL-positive cells in the brain tissues around the hematoma at 1, 3, and 7 days after ICH (P<0.05). NF-κB protein expression was observed 1 day after ICH, which reached the peak level on day 3 and lowered 7 days after ICH. LiCl treatment significantly lowered the expression of NF-κB protein in comparison with that in ICH group (P<0.05) and obviously ameliorated the inflammatory responses in the brain tissues. Conclusion LiCl provides neuroprotection against ICH by inhibiting neural cell apoptosis and reducing inflammatory response through down-regulation of NF-κB expression.
